ORIGINAL_ARTICLE
Cognitive outcome of traumatic brain injury in elderly patients
Objective: To assess the cognitive outcome of traumatic brain injury in elderly patients. Design: a prospective study. Methodsthis study was conducted on 50 elderly patients exposed to TBI in sohag university hospital and 50 patients exposed to TBI but less than 65 years used as a control. IntroductionTraumatic brain injury (TBI) is a significant problem in older adults,and is associated with changes in the brain that affect the cognition(Sapoznik et al 2006) ResultsDuring the study period, 50 elderly patients with TBI were followed up for cognitive outcome, 12 patients (24%) were associated with cognitive deficits. Conclusion: TBI in elderly patients is associated with cognitive deficits post injury
https://smj.journals.ekb.eg/article_34180_098e5b4b5fe65a6499ab1d2b135998d6.pdf
2018-01-01
11
13
10.21608/smj.2018.34180
Traumatic brain injury
elderly patients
cognitive outcome
geriatric trauma
prognosis
Momen
Almamoun
momenmohamed@med.sohag.edu.eg
1
Department of Neurosurgery , Faculty of Medicine, Sohag University.
AUTHOR
Magda
Ali
magda_ali@med.sohag.edu.eg
2
Department of public health and community medicine, Faculty of Medicine, Sohag University.
AUTHOR
Ahmed
EL Sayed
3
Department of Neurosurgery , Faculty of Medicine, Sohag University.
AUTHOR
Roshdy
Elkhayat
4
Department of Neurosurgery , Faculty of Medicine, Assuit University.
AUTHOR
1- Kempermann, G., Gast, D., & Gage, F. H. (2002). Neuroplasticity in old age: Sustained fivefold induction of hippocampal neurogenesis by long-term environmental enrichment. Annals of Neurology, 52(2), 135–143
1
2- Patel HC, Bouamra O, Woodford M, et al (2010). Clinical article: mortality associated with severe head injury in the elderly. ActaNeurochir (Wien). (2010).
2
3- Sapoznik, S., Ivenshitz, M., & Segal, M. (2006). Age-dependent glutamate induction of synaptic plasticity in cultured hippocampal neurons. Learning and Memory, 13(6), 719-727.
3
4- Senathi-Raja, D., Ponsford, J., & Schonberger, M. (2010). The association of age and time postinjury with long-term emotional outcome following traumatic brain injury. Journal of Head Trauma and Rehabilitation, 25(5), 330-338.
4
5- Wheelen-Goodinson, R., Ponsford, J. L., Schonberger, M., & Johnston, L. (2010). Predictors of psychiatric disorders following traumatic brain injury. Journal of Head Trauma and Rehabilitation, 25(5), 320-3.
5
ORIGINAL_ARTICLE
METABOLIC SYNDROME INPATIENTS WITH RHEUMATOID ARTHRITIS
Objectives:To determine the prevalence of metabolic syndrome (MetS) in patients with rheumatoid arthritis (RA) and to evaluate the relation between parameters of MetS and clinical aspects of RA. Design: Cross-sectional study. Patients:Patients with rheumatoid arthritis (RA) according to 2010 ACR/EULAR classification criteria for RA (n = 150). Methods: Demographic data, arthritis history, medical and therapeutic history were evaluated. Height, weight, BMI, waist circumference (WC) and blood pressure (BP) were recorded. Disease activity was evaluated using DAS28 (ESR). Immunological investigations included RF, ESR, CRP, and anti-CCP. Fasting blood glucose and lipid profile were measured.The patient was diagnosed as having MetS according to 3 definitions; ATPIII (2004), IDF (2005), and JIS (2009). Results:Prevalence of MetS in rheumatoid patients was 48% (ATPIII definition), 52 % (IDF definition), and 46 % (JIS definition with Egyptian cut-off of WC), respectively. The most prevalent component of MetS was central obesity (75.3- 92 % according to the used definition).DAS28 was significantly higher in patients with MetS with higher number of tender joints and VAS (0-100) and most rheumatoid patients with MetS (68 %) had high disease activity. Conclusions:The increased prevalence of MetS components in RA patients, suggests greater attention be given to modifiable risk factors, including improvement of dietary habits, physical activity and blood pressure control.
https://smj.journals.ekb.eg/article_34303_d944f5a7466f79980580bfa5e68b4ef3.pdf
2018-01-01
15
26
10.21608/smj.2018.34303
Rheumatoid Arthritis
Metabolic syndrome
DAS28
Hanan
Mohammed Abo-Zeid
hanan_abozaid@med.sohag.edu.eg
1
Department of Rheumatology, Rehabilitation and Physical medicine - Faculty of Medicine- Sohag University.
AUTHOR
Ebtesam
Ali Fayez
ebtsamkhalaf@med.sohag.edu.eg
2
Department of Rheumatology, Rehabilitation and Physical medicine - Faculty of Medicine- Sohag University.
AUTHOR
Ali
Kasem
3
Department of Internal Medicine- Faculty of Medicine- Sohag University
AUTHOR
Esam
Abo Al-Fadl
essam_mohamed@med.sohag.edu.eg
4
Department of Rheumatology, Rehabilitation and Physical medicine - Faculty of Medicine- Sohag University.
AUTHOR
REFERENCES
1
1. Smolen JS, Aletaha D and Mcinnes IB: Rheumatoid arthritis.Lancet. 2016; 388(10055): 2023-2038.
2
2. Silman AJ and Pearson JE: Epidemiology and genetics of rheumatoid arthritis.Arthritis Res. 2002; 4 Suppl 3: S265-72.
3
3. Kramer HR and Giles JT: Cardiovascular disease risk in rheumatoid arthritis: progress, debate, and opportunity.Arthritis Care Res (Hoboken). 2011; 63(4): 484-99.
4
4. Lopez-Mejias R, Castaneda S, Gonzalez-Juanatey C, Corrales A, Ferraz-Amaro I: Cardiovascular risk assessment in patients with rheumatoid arthritis: The relevance of clinical, genetic and serological markers.Autoimmun Rev. 2016; 15(11): 1013-1030.
5
5. Rochlani Y, Pothineni NV, Kovelamudi S and Mehta JL: Metabolic syndrome: pathophysiology, management, and modulation by natural compounds.Ther Adv Cardiovasc Dis. 2017: 1753944717711379.
6
6. Tune JD, Goodwill AG, Sassoon DJ and Mather KJ: Cardiovascular consequences of metabolic syndrome.Transl Res. 2017; 183: 57-70.
7
7. Zhang J, Fu L, Shi J, Chen X, Li Y: The risk of metabolic syndrome in patients with rheumatoid arthritis: a meta-analysis of observational studies.PLoS One. 2013; 8(10): e78151.
8
8. Parra-Salcedo F, Contreras-Yanez I, Elias-Lopez D, Aguilar-Salinas CA and Pascual-Ramos V: Prevalence, incidence and characteristics of the metabolic syndrome (MetS) in a cohort of Mexican Mestizo early rheumatoid arthritis patients treated with conventional disease modifying anti-rheumatic drugs: the complex relationship between MetS and disease activity.Arthritis Res Ther. 2015; 17: 34.
9
9. Kerekes G, Nurmohamed MT, Gonzalez-Gay MA, Seres I, Paragh G: Rheumatoid arthritis and metabolic syndrome.Nat Rev Rheumatol. 2014; 10(11): 691-6.
10
10. Lee SG, Kim JM, Lee SH, Kim KH, Kim JH: Is the frequency of metabolic syndrome higher in South Korean women with rheumatoid arthritis than in healthy subjects? Korean J Intern Med. 2013; 28(2): 206-15.
11
11. Karvounaris SA, Sidiropoulos PI, Papadakis JA, Spanakis EK, Bertsias GK: Metabolic syndrome is common among middle-to-older aged Mediterranean patients with rheumatoid arthritis and correlates with disease activity: a retrospective, cross-sectional, controlled, study.Ann Rheum Dis. 2007; 66(1): 28-33.
12
12. Aletaha D, Neogi T, Silman AJ, Funovits J, Felson DT: 2010 rheumatoid arthritis classification criteria: an American College of Rheumatology/European League Against Rheumatism collaborative initiative.Ann Rheum Dis. 2010; 69(9): 1580-8.
13
13. Jung YO and Kim HA: Recent paradigm shifts in the diagnosis and treatment of rheumatoid arthritis.Korean J Intern Med. 2012; 27(4): 378-87.
14
14. Grundy SM, Brewer HB, Cleeman JI, Smith SC and Lenfant C: Definition of metabolic syndrome: Report of the National Heart, Lung, and Blood Institute/American Heart Association conference on scientific issues related to definition.Circulation. 2004; 109(3): 433-8.
15
15. Alberti KG, Zimmet P and Shaw J: Metabolic syndrome--a new world-wide definition. A Consensus Statement from the International Diabetes Federation.Diabet Med. 2006; 23(5): 469-80.
16
16. Alberti KG, Eckel RH, Grundy SM, Zimmet PZ, Cleeman JI: Harmonizing the metabolic syndrome: a joint interim statement of the International Diabetes Federation Task Force on Epidemiology and Prevention; National Heart, Lung, and Blood Institute; American Heart Association; World Heart Federation; International Atherosclerosis Society; and International Association for the Study of Obesity.Circulation. 2009; 120(16): 1640-5.
17
17. Assaad-Khalil SH, Mikhail MM, Aati TA, Zaki A, Helmy MA: Optimal waist circumference cutoff points for the determination of abdominal obesity and detection of cardiovascular risk factors among adult Egyptian population.Indian J Endocrinol Metab. 2015; 19(6): 804-10.
18
18. De Oliveira BM, Medeiros MM, De Cerqueira JV, De Souza Quixada RT and De Oliveira IM: Metabolic syndrome in patients with rheumatoid arthritis followed at a University Hospital in Northeastern Brazil.Rev Bras Reumatol Engl Ed. 2016; 56(2): 117-25.
19
19. Gomes KWP, Luz AJP, Felipe MRB, Beltrao LA, Sampaio AXC: Prevalence of metabolic syndrome in rheumatoid arthritis patients from Northeastern Brazil: Association with disease activity.Mod Rheumatol. 2017: 1-6.
20
20. La Montagna G, Cacciapuoti F, Buono R, Manzella D, Mennillo GA: Insulin resistance is an independent risk factor for atherosclerosis in rheumatoid arthritis.Diab Vasc Dis Res. 2007; 4(2): 130-5.
21
21. Toms TE, Panoulas VF, John H, Douglas KM and Kitas GD: Methotrexate therapy associates with reduced prevalence of the metabolic syndrome in rheumatoid arthritis patients over the age of 60- more than just an anti-inflammatory effect? A cross sectional study.Arthritis Res Ther. 2009; 11(4): R110
22
22. Santos MJ, Vinagre F, Silva JJ, Gil V and Fonseca JE: Cardiovascular risk profile in systemic lupus erythematosus and rheumatoid arthritis: a comparative study of female patients.Acta Reumatol Port. 2010; 35(3): 325-32.
23
23. Dao HH, Do QT and Sakamoto J: Increased frequency of metabolic syndrome among Vietnamese women with early rheumatoid arthritis: a cross-sectional study.Arthritis Res Ther. 2010; 12(6): R218.
24
24. Baker JF, Mehta NN, Baker DG, Toedter G, Shults J: Vitamin D, metabolic dyslipidemia, and metabolic syndrome in rheumatoid arthritis.Am J Med. 2012; 125(10): 1036 e9-1036 e15.
25
25. Karakoc M, Batmaz I, Sariyildiz MA, Tahtasiz M, Cevik R: The relationship of metabolic syndrome with disease activity and the functional status in patients with rheumatoid arthritis.J Clin Med Res. 2012; 4(4): 279-85.
26
26. Ormseth MJ, Lipson A, Alexopoulos N, Hartlage GR, Oeser AM: Association of epicardial adipose tissue with cardiometabolic risk and metabolic syndrome in patients with rheumatoid arthritis.Arthritis Care Res (Hoboken). 2013; 65(9): 1410-5.
27
27. Salinas MJ, Bertoli AM, Lema L, Saucedo C, Rosa J: Prevalence and correlates of metabolic syndrome in patients with rheumatoid arthritis in Argentina.J Clin Rheumatol. 2013; 19(8): 439-43.
28
28. Rostom S, Mengat M, Lahlou R, Hari A, Bahiri R: Metabolic syndrome in rheumatoid arthritis: case control study.BMC Musculoskelet Disord. 2013; 14: 147.
29
29. Zafar ZA, Mahmud TH, Rasheed A and Wagan AA: Frequency of metabolic syndrome in Pakistani cohort of patients with rheumatoid arthritis.J Pak Med Assoc. 2016; 66(6): 671-6.
30
30. Pandey PK, Swami A, Biswas TK and Thakuria R: Prevalence of metabolic syndrome in treatment naive rheumatoid arthritis and correlation with disease parameters.Arch Rheumatol. 2017; 32(1): 46-52.
31
31. Goshayeshi L, Saber H, Sahebari M, Rezaieyazdi Z, Rafatpanah H: Association between metabolic syndrome, BMI, and serum vitamin D concentrations in rheumatoid arthritis.Clin Rheumatol. 2012; 31(8): 1197-203.
32
32. Da Cunha VR, Brenol CV, Brenol JC, Fuchs SC, Arlindo EM: Metabolic syndrome prevalence is increased in rheumatoid arthritis patients and is associated with disease activity.Scand J Rheumatol. 2012; 41(3): 186-91.
33
33. Sahebari M, Goshayeshi L, Mirfeizi Z, Rezaieyazdi Z, Hatef MR: Investigation of the association between metabolic syndrome and disease activity in rheumatoid arthritis.Scientific World J. 2011; 11: 1195-205.
34
34. Chung CP, Oeser A, Solus JF, Avalos I, Gebretsadik T: Prevalence of the metabolic syndrome is increased in rheumatoid arthritis and is associated with coronary atherosclerosis.Atherosclerosis. 2008; 196(2): 756-63.
35
35. Abourazzak FE, Mansouri S, Najdi A, Tahiri L, Nejjari C: Prevalence of metabolic syndrome in patients with rheumatoid arthritis in Morocco: a cross-sectional study of 179 cases.Clin Rheumatol. 2014; 33(11): 1549-55.
36
36. Panoulas VF, Douglas KM, Milionis HJ, Stavropoulos-Kalinglou A, Nightingale P: Prevalence and associations of hypertension and its control in patients with rheumatoid arthritis.Rheumatology (Oxford). 2007; 46(9): 1477-82.
37
37. Bajraktari IH, Rexhepi S, Berisha I, Lahu A, Kryeziu A: Prevalence of Asymptomatic Arterial Hypertension and Its Correlation with Inflammatory Activity in Early Rheumatoid Arthritis.Open Access Maced J Med Sci. 2017; 5(5): 641-644.
38
38. Erum U, Ahsan T and Khowaja D: Lipid abnormalities in patients with Rheumatoid Arthritis.Pak J Med Sci. 2017; 33(1): 227-230.
39
39. Galarza-Delgado DA, Azpiri-Lopez JR, Colunga-Pedraza IJ, Cardenas-De La Garza JA, Vera-Pineda R: Prevalence of comorbidities in Mexican mestizo patients with rheumatoid arthritis.Rheumatol Int. 2017.
40
40. Van Breukelen-Van Der Stoep DF, Van Zeben D, Klop B, Van De Geijn GJ, Janssen HJ: Marked underdiagnosis and undertreatment of hypertension and hypercholesterolaemia in rheumatoid arthritis.Rheumatology (Oxford). 2016; 55(7): 1210-6.
41
41. Ruscitti P, Ursini F, Cipriani P, Liakouli V, Carubbi F: Poor clinical response in rheumatoid arthritis is the main risk factor for diabetes development in the short-term: A 1-year, single-centre, longitudinal study.PLoS One. 2017; 12(7): e0181203.
42
ORIGINAL_ARTICLE
Relation Between SF-36, mHAQ Scores and Disease Activity in Rheumatoid Arthritis
Objective: To investigate the relationship between quality of life (QOL) and disease activity in patients with rheumatoid arthritis (RA). Methods: 200 patients with RA were included in the study. Data were obtained by questionnaires and laboratory investigation. Disease Activity Score (DAS-28) was calculated for assessment of disease activity. Separate dimensions and physical and mental summary scores of the Short form Health survey (SF-36) and Health Assessment Questionnaire (HAQ) were compared to study the relationship between QOL and disease activity in patients with rheumatoid arthritis. Results: There was a significant association between DAS-28 and QOL scores. Conclusions: RA has a significant effect on the health related quality of life of patients, and its activity is ditectly related to worse QOL.
https://smj.journals.ekb.eg/article_34316_9635f867d1a2b276ca954d7462e85c14.pdf
2018-01-01
27
29
10.21608/smj.2018.34316
Rheumatoid Arthritis
quality of life
DAS-28
SF-36
Aya
Gmal
1
Specialist of Rheumatology and Rehabilitation Faculty of Medicine .Assiut University
AUTHOR
Nagwa
Ahmad
nagwa_ahmed@med.sohag.edu.eg
2
Debartment of Biochemistry, Faculty of Medicine, Sohag University.
AUTHOR
Mohammed
AI
3
Debartment of Rheumatology and Rehabilitation Faculty of Medicine Sohag.
AUTHOR
Nihal
F
4
Debartment Rheumatology and Rehabilitation Faculty of Medicine .Assiut University.
AUTHOR
Anna Paula Ribeiro Campos; Cinthia Maria Silva; Shamyr Sulyvam de Castro; Cristiane Vitaliano Graminha, Depression and quality of life in rheumatoid arthritis individuals and stable health individuals: a comparative study. Fisioter. Pesqui. 2013;20(4).
1
Cader MZ, Filer A, Hazlehurst J, et al. Performance of the 2010 ACR/EULAR criteria for rheumatoid arthritis: comparison with 1987 ACR criteria in a very early synovitis cohort Ann Rheum Dis 2011; 70:949–55.
2
Weinblatt ME, Keystone EC, Furst DE, Kavanaugh AF, Chartash EK, Segurado OG. Long term efficacy and safety of adalimumab plus methotrexate in patients with rheumatoid arthritis: ARMADA 4 year extended study. Ann Rheum Dis 2006;65:753–9.
3
Costa AFC, Brasil MAA, Papi JA, Azevedo MNL. Depressão, ansiedade e atividade de doençan aartrite rheumatoid. Rev Bras Reumatol. 2008;48(1):7-11.
4
Aletaha D, Neogi T, Silman AJ, et al. 2010 rheumatoid arthritis classification criteria: an American College of Rheumatology/ Euro-pean League Against Rheumatism collaborative initiative. Ann Rheum Dis. 2010;69:1580–1588.
5
Castrejón1, A.M. Ortiz1, R. García-Vicuña1, J.P. Lopez-Bote1, A. Humbría1, L. Carmona2, I. Gonzalez-Alvaro1 sedimentation rate equivalent when estimating the 28-jointdisease activity score in rheumatoid arthritis? Clinical and Experimental Rheumatology 2008; 26: 769-775.
6
Haroon N, Aggarwal A, Lawrence A et al. Impact of rheumatoid arthritis on quality of life. Mod Rheumatol. 2007;17:290–5.
7
ORIGINAL_ARTICLE
Word Finding Difficulty Test Design and Standardization
OBJECTIVE: The aim of this study is to design a new test for assessment of word finding difficulty in children in order to better assess and manage this problem. SUBJECTS AND METHODS: The test was designed and included pictures of different semantic groups. It was revised by Phoniatric experts. Then it was applied on a group of 50 normal children and a group of 25 DLD children with age range of 5-10 years with average or below average IQ. . RESULTS: The test consists of 7 sections. Validity of the test was examined by content validity, contrasted group validity and internal consistency validity. The results showed significant difference between scores of normal children and DLD children in all sections of the test. . CONCLUSION: Word finding difficulty test is suitable and easy applicable to assess word finding difficulty in children. It will help in accurate assessment of these children and therefore putting suitable plan for
https://smj.journals.ekb.eg/article_34658_c6a36a03f8a5e453d360a1f72657918e.pdf
2018-01-01
31
41
10.21608/smj.2018.34658
1.Adel, H.M., Hegazi, M.A., Saber, A.S. (2014): Word Naming Speed in Specific Language Impairment Children. Ain Shams University, Cairo, Egypt.
1
2.Alt, M., and Plante, E.(2006). Factors that influence lexical and semantic fast mapping of young children with specific language impairment.Journal of Speech, Language,and Hearing Research,49,941-954.
2
3. Connor, L.T. and Obler, L.k. (2002): Anomia. In Ramachandron, V Encyclopedia of the human brain. New York: Academic Press.
3
4.Dockrell, J.E., Messer, D., George, R. and Wilson,G., (1998):Children's word finding difficulties-prevalence,presentation and naming problems.International Journal of language and Communicative disorders;33:445-454.
4
5.Faust, M., Dimitrovski, L. and Davidi, S. (1997): Naming difficulties in language disabled children: preliminary findings with the application of the tip of the tongue paradigm. Journal of Speech, language and Hearing. Research; 40:1026-1036.
5
6.German, D.J. (1998): Prevalence estimates for word finding difficulty in LD students. Implications for assessment/instructional accommodations. Paper presented at the Learning Disabilities Association, Washington.
6
7. German, D. J. (2000b)The Test of Word finding, Second Edition (TWF- 2). Austin, TX: Pro Ed
7
8. German, D.J. and Newman, R.S. (2005): Word Finding Based Oral Reading Errors, Paper presented at the International Congress of the Study of Child Language (ICSAL), Berlin, Germany.
8
9. Hanoura, M.A. (2002): Stanford-Binet Intelligence Test: Arabic Version. Cairo, Anglo Press.
9
10.Howard, D. and Gatehouse, C. (2006): Distinguishing semantic and lexical word retrieval deficits in people with aphasia. Aphasiology; 20(9):921-950.
10
11. Jeffry A and Coady (2013): Rapid Naming by Children with and without specific language impairment. Journal of Speech, Language, and Hearing Research; 56: 604-617.
11
12.Kail, R.(1994). A method for studying the generalized slowing hypothesis in children with specific language impairment. Journal of Speech and Hearing Research,37,418-421
12
13.Kail, R.,&Leonard, L. B.(1986).Word-finding abilities in language-impaired children (ASHA Monographs Number 25). Rockville,MD: American Speech-Language-Hearing Association.
13
14.Khedr,A.A., Hegazi, M.A., Saber, A.S.,Nassar,J.F.(2009):Word finding difficulties in communication disorders. Ain Shams University, Cairo, Egypt.
14
15.Kotby, M.N., Bassiouni, S., El Zomor, M. and Mohsen, E. (1985): Pilot study for standardization of an articulation test. Proc 10th Annu Ain-Shams Med Congr, Cairo.
15
16.Kotby, M.N., Khairy, A., Baraka, M., Rifaie, N. and El Shoubary, A. (1995): Language testing of Arabic speaking children. Proceedings of the XXIII World Congress of International Association of Logopedics and Phoniatrics. Cairo; August 6-10.
16
17.Leonard, L. B.,Nippold, M. A., Kail, R. and Hale, C. A.(1983): Picture naming in language impaired children, Differentiating lexical storage from retrieval. Journal of Speech and Hearing Research, 26, 609-615.
17
18.Mainela-Arnold, E., Evans, J. L.,& Coady, J. A.(2008). Lexical representations in children with SLI: Evidence from a frequency- manipulated gating task. Journal of Speech Language,and Hearing Research,51,381-393.
18
19.Mainela-Arnold, E., Evans, J. L.,& Coady, J.(2010). . Explaining lexical semantic deficits in specific language impairment: The role of phonological similarity, phonological working memory,and lexical inhibition. Joumal of Speech,Language,and Hearing Research,53,1742-1756
19
20.Roach, A., Schwartz, M.F., Martin, N., Grewal, R.S. and Brecher, A.(1996): The Philadelphia Naming Test: Scoring and rationale. Clinical Aphasiology. ; 24:121–133.
20
21.Thompson, C.K., Lukic, S., King, M.C., Mesulam, M.M. and Weintraub, S. (2012): Verb and noun deficits in stroke-induced and primary progressive aphasia: The Northwestern Naming Battery. Aphasiology. ; 26(5): 632–
21
ORIGINAL_ARTICLE
Virtual CT Colonography: Technique and findings: Single Institute experience.
Colorectal cancer is the second leading cause of death due to malignancy in industrialized counties. It is argued that most large bowel malignancies arise from preexisting adenormas. Computed tomographic (CT) colonography is a noninvasive, rapidly evolving technique that has been shown in some studies to be comparable with conventional colonoscopy for the screening of colorectal cancer. However, widespread colorectal screening and preventive efforts aimed at detecting disease in this early stage are opposed by several practical obstacles, including limited resources, and poor patient acceptance and therefore poor compliance (1-2). Patients and methods
https://smj.journals.ekb.eg/article_34677_aaf935fbbdfbfc5d6ec38ea248a8bb24.pdf
2018-01-01
45
52
10.21608/smj.2018.34677
Hossam
saro
hossam.salah@med.sohag.edu.eg
1
AUTHOR
khaled
Alkhayat
khaled_mohamed@med.sohag.edu.eg
2
Department of Chest Diseases, Faculty of Medicine, Sohag University
AUTHOR
Mohammed
Al Sayed
alaa_abusedera@med.sohag.edu.eg
3
AUTHOR
Mohammed
Ali
4
AUTHOR
1- Hara AK, Johnson CD, Reed JE. Colorectal lesions: Evaluation by CT colonography. RadioGraphics 1997; 1:1157-1167.
1
2- Silva AC, Hara AK, Leighton JA, Heppell JP. CT Colonography with Intravenous Contrast Material: Varied Appearances of Colorectal Carcinoma. RadioGraphics 2005; 25:1321–1334.
2
3- Mang T, Maier A, Plank C, Mueller-Mang C, Herold C, Schima W. Pitfalls in Multi–Detector Row CT Colonography: A Systematic Approach. RadioGraphics 2007; 27:431–454
3
4- Taylor SA, Halligan S, Bartram CI. CT colonography: methods, pathology and pitfalls. Clin Radiol 2003;58:179–90.
4
5- Laghi A. Virtual colonoscopy: clinical application. Eur Radiol 2005;15(Suppl 4):D138–41.
5
6- Fletcher JG, Johnson CD, Krueger WR, et al. Contrast-enhanced CT colonography in recurrent colorectal carcinoma: feasibility of simultaneous evaluation for metastatic disease, local recurrence, and metachronous neoplasia in colorectal carcinoma. AJR Am J Roentgenol 2002;178:283–90.
6
7- Lefere P, Gryspeerdt S, Baekelandt M, Dewyspelaere J, van Holsbeeck B. Diverticular disease in CT colonography. Eur Radiol 2003;13(Suppl 4):L62–74.
7
8- Sosna J, Blachar A, Amitai M, et al. Colonic perforation at CT colonography: assessment of risk in a multicenter large cohort. Radiology 2006;239:457–63.
8
9- Royster AP, Fenlon HM, Clarke PD, Nunes DP, Ferrucci JT. CT colonoscopy of colorectal neoplasms: two-dimensional and three dimensional virtual-reality techniques with colonoscopic correlation. AJR Am J Roentgenol 1997;169:1237–42.
9
10- Rogalla P, Lembcke A, Ruckert JC, et al. Spasmolysis at CT colonography: butyl scopolamine versus glucagon. Radiology 2005;236:184–8.
10
11- Pickhardt PJ, Choi JR, Hwang I, et al. Computed tomographic virtual colonoscopy to screen for colorectal neoplasia in asymptomatic adults. N Engl J Med 2003;349:2191–200.
11
12- Yee J, Kumar NN, Hung RK, Akerkar GA, Kumar PR, Wall SD. Comparison of supine and prone scanning separately and in combination at CT colonography. Radiology 2003;226:653–61.
12
13- Barish MA, Soto JA, Ferrucci JT. Consensus on current clinical practice of virtual colonoscopy. AJR Am J Roentgenol 2005;184:786–92
13
14- Macari M, Bini EJ, Xue X, et al. Colorectal neoplasms: prospective comparison of thin-section low-dose multi-detector row CT colonography and conventional colonoscopy for detection.Radiology 2002;224:383–92.
14
15- Morrin MM, Farrell RJ, Kruskal JB, Reynolds K, McGee JB, Raptopoulos V. Utility of intravenously administered contrast material at CT colonography. Radiology 2000;217:765–71.
15
16- Dachman AH,Kuniyoshi JK, Boyle CM, et al. CTcolonography with three dimensional problem solving for detection of colonic polyps. AJR Am J Roentgenol 1998;171:989–95.
16
17- Fenlon HM, Clarke PD, Ferrucci JT. Virtual colonoscopy: imaging features with colonoscopic correlation. AJR Am J Roentgenol 1998;170:1303–9.
17
18- Laks S, Macari M, Bini EJ. Positional change in colon polyps at CT colonography. Radiology 2004;231:761–6.
18
19- Gluecker TM, Johnson CD, Wilson LA, et al. Extracolonic findings at CT colonography: evaluation of prevalence and cost in a screening population. Gastroenterology 2003;124:911–6.
19
ORIGINAL_ARTICLE
Virtual CT Colonography Versus Lower Endoscopy in Detection of Colorectal Lesions.
Colorectal cancer is the third most common cancer and the second leading cause of cancer-related death in Western countries. As with other malignancies, screening and early detection is fundamental for successful management of colorectal cancer. Computed tomographic (CT) colonography is a noninvasive, rapidly evolving technique that has been shown in some studies to be comparable with conventional colonoscopy for the screening of colorectal cancer. CT colonography is being increasingly applied as a routine screening method for the detection of colorectal cancer in last few years as it is more convenient and less invasive than colonoscopy. In addition, it has an upper hand in diagnosis of small lesions less than 10mm (Choi, et al., 2011). Patients and methods:This prospective double blind comparative study will be conducted on 23 patients with colorectal symptoms and signs as altered bowel habits, bleeding per rectum, abdominal pain, weight loss, unexplained fatigue and loss of appetite.An informed written consent was obtained from all patients and approval of the faculty research ethics committee was obtained. Results: Total of 108 colonic lesions were analyzed in 23 patient; Seven colonic masses were diagnosed in 6 patients, 41 polyps in 8 patients and 60 diverticulae in 5 patients. Six patients had incomplete colonoscopy. Of them, 2 patients had a large polypoidal mass that prevents further colonoscopic introduction. Using CT colonography we were able to evaluate those polypoidal masses. Moreover, we could complete the examination and evaluation of the proximal colon and one of them had a polypoidal sigmoid colon mass and showed another proximal annular mass. Four patients presented with colonic obstruction and good preparation to the proximal parts of the colon failed, So completing the colonoscopy was difficult. After undergoing CT colonography, 2 patients were normal and 2 patients had annular masses causing proximal obstruction and marked distension. ConclusionCT Colonography (Virtual Colonoscopy) is a reliable tool and more sensitive for detecting colonic mass lesions larger than 5 mm, polyps larger than 5 mm, strictures and diverticulosis. CTC is of value in evaluating the colonic segment lying proximal to colonic cancers including those with occlusive growths or strictures. Contrast-enhanced CTC is also useful in identifying extra-colonic findings.Virtual Colonoscopy is a good screening tools for malignant or premalignant lesions in patients presented with colorectal symptoms.
https://smj.journals.ekb.eg/article_34967_8d91495b905d0bb331818e509e1daddd.pdf
2018-01-01
53
64
10.21608/smj.2018.34967
Hossam
saro
hossam.salah@med.sohag.edu.eg
1
Faculty of Medicine- Sohag University.
AUTHOR
khaled
Alkhayat
khaled_mohamed@med.sohag.edu.eg
2
Department of Chest Diseases, Faculty of Medicine, Sohag University
AUTHOR
Mohammed
Al Sayed
alaa_abusedera@med.sohag.edu.eg
3
Faculty of Medicine- Sohag University
AUTHOR
Mohammed
Ali
4
Faclty of medicine-sohag university
AUTHOR
Wael
Barakat
5
faculty of medicine- sohag university
AUTHOR
1- Barish MA, Soto JA, Ferrucci JT. Consensus on current clinical practice of virtual colonoscopy. AJR Am J Roentgenol 2005;184:786–92
1
2- Brown G, Kirkham A, Williams GT, et al: High-resolution MRI of the anatomy important in total mesorectal excision of the rectum. AJR 2004; 182:431-439.
2
3- Burling D, Taylor SA, Halligan S, et al. Automated insufflation of carbon dioxide for MDCT colonography: distension and patient experience compared with manual insufflation. AJR Am J Roentgenol 2006;186:96 103.
3
4- Charanjeet Singh. colon tumours outlines, 2003-2011.
4
5- Charanjeet Singh. colon tumours outlines, 2003-2012.
5
6- Chen JS, Hsieh PS, Chiang JM, et al. Clinical outcome of signet ring cell carcinoma and mucinous adenocarcinoma of the colon. Chang Gung Med J 2010;33:51-7.
6
7- Dachman AH,Kuniyoshi JK, Boyle CM, et al. CTcolonography with three dimensional problem solving for detection of colonic polyps. AJR Am J Roentgenol 1998;171:989–95.
7
8- Edge SB, Byrd DR, Compton CC, et al. AJCC Cancer Staging Handbook, 7th edition. New York: Springer, 2010:173-206.
8
9- Fenlon HM, Clarke PD, Ferrucci JT. Virtual colonoscopy: imaging features with colonoscopic correlation. AJR Am J Roentgenol 1998;170:1303–9.
9
10- Fletcher JG, Johnson CD, Krueger WR, et al. Contrast-enhanced CT colonography in recurrent colorectal carcinoma: feasibility of simultaneous evaluation for metastatic disease, local recurrence, and metachronous neoplasia in colorectal carcinoma. AJR Am J Roentgenol 2002;178:283–90.
10
11 - Gluecker TM, Johnson CD, Wilson LA, et al. Extracolonic findings at CT colonography: evaluation of prevalence and cost in a screening population. Gastroenterology 2003;124:911–6.
11
12- Halligan S, Altman DG, Taylor SA, et al. CT colonography in the detection of colorectal polyps and cancer: systematic review, meta analysis, and proposed minimum data set for study level reporting. Radiology 2005;237:893–904.
12
13- Hamilton SR, Aaltonen LA: World Health Organization classification of tumours. Pathology and genetics, tumours of the digestive system, IARC Press, 2000.
13
14-Hamilton SR, Bosman FT, Boffetta P, et al. Carcinoma of the colon and rectum. In: WHO Classification of Tumours of the Digestive System. Bosman FT, Carneiro F, Hruban RH, Theise ND, eds. Lyon: IARC Press, 2010:134-46.
14
15-Iannaccone R, Laghi A, Catalano C, et al. Computed tomographic colonography without cathartic preparation for the detection of colorectal polyps. Gastroenterology 2004;127:1300–11.
15
16-Isaacson PG: Lymphoproliferative disorders of the gastrointestinal tract In Pathology of the gastrointestinal tract, second edition, Ming SC, Goldman H.
16
17-J.G. Fletcher, Fargol Booya, C. Daniel Johnson, David Ahlquist. Curr Opin Gastroenterol. 2005;21(1):90-98.
17
18-Juchems MS, Fleiter TR, Pauls S, Schmidt SA, Brambs HJ, Aschoff AJ. CT colonography: comparison of a colon dissection display versus 3D endoluminal view for the detection of polyps. Eur Radiol 2006;16:68–72.
18
19-Laghi A. Virtual colonoscopy: clinical application. Eur Radiol 2005;15(Suppl 4):D138–41.
19
20-Laks S, Macari M, Bini EJ. Positional change in colon polyps at CT colonography. Radiology 2004;231:761–6.
20
21- Lefere P, Gryspeerdt S, Baekelandt M, Dewyspelaere J, van Holsbeeck B. Diverticular disease in CT colonography. Eur Radiol 2003;13(Suppl 4):L62–74.
21
22-Leopoldo S, Lorena B, Cinzia A, et al. Two subtypes of mucinous adenocarcinoma of the colorectum: clinicopathological and genetic features. Ann Surg Oncol 2008;15:1429-39.
22
23-Macari M, Bini EJ, Jacobs SL, Lange N, Lui YW. Filling defects at CT colonography: pseudo- and diminutive lesions (the good), polyps (the bad), flat lesions, masses, and carcinomas (the ugly). Radiographics 2003;23:1073–91.
23
24-Macari M, Bini EJ, Xue X, et al. Colorectal neoplasms: prospective comparison of thin-section low-dose multi-detector row CT colonography and conventional colonoscopy for detection.Radiology 2002;224:383–92
24
25-Macari M, Bini EJ. CT colonography: where have we been and where are we going? Radiology 2005;237:819–33.
25
26-Macari M, Milano A, Lavelle M, Berman P, Megibow AJ. Comparison of time-efficient CT colonography with two- and three-dimensional colonic evaluation for detecting colorectal polyps. AJR Am J Roentgenol 2000;174:1543–9.
26
27-Makino T, Tsujinaka T, Mishima H, et al. Primary signet-ring cell carcinoma of the colon and rectum: report of eight cases and review of 154 Japanese cases. Hepatogastroenterology 2006;53:845-9.
27
28-Mang T, Maier A, Plank C, Mueller-Mang C, Herold C, Schima W. Pitfalls in Multi–Detector Row CT Colonography: A Systematic Approach. RadioGraphics 2007; 27:431–454.
28
29- Ming SC, Goldman H: Pathology of the gastrointestinal tract, second edition, Philadelphia, 1998, Williams and Wilkins.
29
30-Morrin MM, Farrell RJ, Kruskal JB, Reynolds K, McGee JB, Raptopoulos V. Utility of intravenously administered contrast material at CT colonography. Radiology 2000;217:765–71.
30
31- Neri E, Giusti P, Battolla L, et al. Colorectal cancer: role of CT colonography in preoperative evaluation after incomplete colonoscopy. Radiology, 2002;223:615–9.
31
32-Owen DA, Kelly JK: Atlas of gastrointestinal pathology, Philadelphia, 1994, Saunders, p170
32
33- PJ, Choi JR, Hwang I, et al. Computed tomographic virtual colonoscopy to screen for colorectal neoplasia in asymptomatic adults. N Engl J Med 2003;349:2191–200.
33
34-Pickhardt PJ. Translucency rendering in 3D endoluminal CTcolonography: a useful tool for increasing polyp specificity and decreasing interpretation time. AJR Am J Roentgenol 2004;183:429–36
34
35- BJ, Fujii T, Cairns A, et al. Flat and depressed colonic neoplasms: a prospective study of 1000 colonoscopies in the UK. Lancet 2000;355:1211–4.
35
36-Rockey DC, Paulson E, Niedzwiecki D, et al. Analysis of air contrast barium enema, computed tomographic colonography, and colonoscopy: prospective comparison. Lancet 2005;365:305–11.
36
37-Rogalla P, Lembcke A, Ruckert JC, et al. Spasmolysis at CT colonography: butyl scopolamine versus glucagon. Radiology 2005;236:184–8.
37
38-Royster AP, Fenlon HM, Clarke PD, Nunes DP, Ferrucci JT. CT colonoscopy of colorectal neoplasms: two-dimensional and three dimensional virtual-reality techniques with colonoscopic correlation. AJR Am J Roentgenol 1997;169:1237–42.
38
39- Sosna J, Blachar A, Amitai M, et al. Colonic perforation at CT colonography: assessment of risk in a multicenter large cohort. Radiology 2006;239:457–63.
39
40-Stoker J, Bartram CI, Halligan S: Imaging of the posterior pelvic floor. Eur Radiol 2002; 12:779-788.
40
41-Summers RM, Yao J, Pickhardt PJ, et al. Computed tomographic virtual colonoscopy computer-aided polyp detection in a screening population. Gastroenterology 2005;129:1832–44.
41
42-Svensson MH, Svensson E, Lasson A, Hellstrom M. Patient acceptance of CT colonography and conventional colonoscopy: prospective comparative study in patients with or suspected of having colorectal disease. Radiology 2002;222:337–45.
42
43-Taylor SA, Halligan S, Bartram CI. CT colonography: methods, pathology and pitfalls. Clin Radiol 2003;58:179–90.
43
44- Taylor SA, Halligan S, Goh V, Morley S, Atkin W, Bartram CI. Optimizing bowel preparation for multidetector row CT colonography: effect of Citramag and Picolax. Clin Radiol 2003;58:723–32.
44
45-Taylor SA, Halligan S, Saunders BP, et al. Use of multidetector-row CT colonography for detection of colorectal neoplasia in patients referred via the Department of Health “2-week-wait” initiative. Clin Radiol 2003;58:855–61.
45
46- Thirunavukarasu P, Sathaiah M, Singla S, et al. Medullary carcinoma of the large intestine: a population based analysis. Int J Oncol 2010;37:901 7.
46
47- Thomas Mang, Anno Graser, Wolfgang Schima, Andrea Maier: CT colonography: Techniques, indications, findings. European Journal of Radiology 61 (2007) 388–399.
47
48- van Gelder RE, Birnie E, Florie J, et al. CT colonography and colonoscopy: assessment of patient preference in a 5-week follow-up study. Radiology 2004;233:328–37.
48
49- Verhulst J, Ferdinande L, Demetter P, et al. Mucinous subtype as prognostic factor in colorectal cancer: a systematic review and meta analysis. J Clin Pathol 2012;65:381-8.
49
50- Vos FM, van Gelder RE, Serlie IW, et al. Three-dimensional display modes for CT colonography: conventional3Dvirtual colonoscopy versus unfolded cube projection. Radiology 2003;228:878–85.
50
51-Winawer SJ, Stewart ET, Zauber AG, et al. A comparison of colonoscopy and double-contrast barium enema for surveillance after polypectomy. National Polyp Study Work Group. N Engl J Med 2000;342:1766–72.
51
52-Yee J, Kumar NN, Hung RK, Akerkar GA, Kumar PR, Wall SD. Comparison of supine and prone scanning separately and in combination at CT colonography. Radiology 2003;226:653–61.
52
53- Yoshida H, Dachman AH. CAD techniques, challenges, and controversies in computed tomographic colonography. Abdom Imaging 2005;30:26–41.
53
54- Zalis ME, Barish MA, Choi JR, et al. CT colonography reporting and data system: a consensus proposal. Radiology 2005;236:3–9.
54
ORIGINAL_ARTICLE
Role of leptin and visfatin in infertility in obese and non obese women
Infertility considered a big health problem with increasing prevalence, having several causes, some of these causes refer to adipose tissue abnormalities. Many substances secreted from white adipose tissue like leptin ,visfatin may have a role in several cases in infertility in women Objective:to answer questions concerned with the relation between lepin ,visfatin and omen's infertility through analysis of data from previous studies. Thwe strategy of this systematic review will be based on raising some research questions that give an idea about the relationship between leptin and visfatin level and women infertility. لإhe research questions 1-Is there a relationship between obesity and infertility in women? 2-Is there a relationship between obesity and leptin and visfatin level ? 3- Is there a relationship between leptin and visfatin level and infertility in women ? 4-Is there a difference in leptin ,visfatin level between obese and non obese infertile women ? 5-How does leptin ,visfatin affect women's fertility?
https://smj.journals.ekb.eg/article_34992_02ad53dcd8adc2f0df3eee25f0c58c9d.pdf
2018-01-01
65
71
10.21608/smj.2018.34992
leptin
Visfatin
Obesity
Infertility
Hussein
Hussein
1
Faculty of medicine -sohag university
AUTHOR
Mahmoud
Abdel Fadeil
2
faculty of medicine -sohag university
AUTHOR
Abdou Saeed
Ait-allah
3
faculty of medicine -sohag universty
AUTHOR
1. Boivin, J., Bunting, L., Collins, J. A., & Nygren, K. G. (2007). International estimates of infertility prevalence and treatment-seeking: potential need and demand for infertility medical care. Human reproduction, 22(6), 1506-1512.
1
2.Saely, C. H., Geiger, K., & Drexel, H. (2012). Brown versus white adipose tissue: a mini-review. Gerontology, 58(1), 15-23.
2
3.Chan, J. L., Bullen, J., Stoyneva, V., DePaoli, A. M., Addy, C., & Mantzoros, C. S. (2005). Recombinant methionyl human leptin administration to achieve high physiologic or pharmacologic leptin levels does not alter circulating inflammatory marker levels in humans with leptin sufficiency or excess. The Journal of Clinical Endocrinology & Metabolism, 90(3), 1618-1624.
3
4-Wang, T., Zhang, X., Bheda, P., Revollo, J. R., Imai, S. I., & Wolberger, C. (2006). Structure of Nampt/PBEF/visfatin, a mammalian NAD+ biosynthetic enzyme. Nature structural & molecular biology, 13(7), 661.
4
5- Polotsky, A. J., Hailpern, S. M.,
5
Skurnick, J. H., Lo, J. C., Sternfeld, B., & Santoro, N. (2010). Association of adolescent obesity and lifetime nulliparity—The Study of Women's Health Across the Nation (SWAN). Fertility and sterility, 93(6), 2004-2011.
6
6-Bellver, J., Pellicer, A., García-Velasco, J. A., Ballesteros, A., Remohí, J., & Meseguer, M. (2013). Obesity reduces uterine receptivity: clinical experience from 9,587 first cycles of ovum donation with normal weight donors. Fertility and sterility, 100(4), 1050-1058.
7
7- Sim, K. A., Dezarnaulds, G. M., Denyer, G. S., Skilton, M. R., & Caterson, I. D. (2014). Weight loss improves reproductive outcomes in obese women undergoing fertility treatment: a randomized controlled trial. Clinical obesity, 4(2), 61-68.
8
8- Kort, J. D., Winget, C., Kim, S. H., & Lathi, R. B. (2014). A retrospective cohort study to evaluate the impact of meaningful weight loss on fertility outcomes in an overweight population with infertility. Fertility and sterility, 101(5), 1400-1403.
9
9- Esmaeilzadeh, S., Andarieh, M. G., Ghadimi, R., & Delavar, M. A. (2015). Body mass index and gonadotropin hormones (LH & FSH) associate with clinical symptoms among women with polycystic ovary syndrome. Global journal of health science, 7(2), 101.
10
10- McKinnon, C. J., Hatch, E. E., Rothman, K. J., Mikkelsen, E. M., Wesselink, A. K., Hahn, K. A., & Wise, L. A. (2016). Body mass index, physical activity and fecundability in a North American preconception cohort study. Fertility and sterility, 106(2), 451-459.
11
11-Zahorska-Markiewicz, B., Olszanecka-Glinianowicz, M., Janowska, J., Kocełak, P., Semik-Grabarczyk, E., Holecki, M., ... & Skorupa, A. (2007). Serum concentration of visfatin in obese women. Metabolism, 56(8), 1131-1134.
12
12- Samara, A., Pfister, M., Marie, B., & Visvikis‐Siest, S. (2008). Visfatin, low‐grade inflammation and body mass index (BMI). Clinical endocrinology, 69(4), 568-574.
13
13 Vardhana, P. A., Dicken, C., Tortoriello, D. V., Chu, M., Carmina, E., & Lobo, R.A. (2009). Increasing adiposity in normal ovulatory women affects adipocytokine expression in subcutaneous and visceral abdominal fat. International Journal of Gynecology & Obstetrics, 104(2), 121-124.
14
14- Kamińska, A., Kopczyńska, E., Bronisz, A., Żmudzińska, M., Bieliński, M., Borkowska, A., ... & Junik, R. (2010). An evaluation of visfatin levels in obese subjects. Endokrynologia Polska, 61(2), 169-173.
15
15- Reda, R., Shehab, A., Soliman, D., Gabr, A., & Abbass, A. (2011). Serum visfatin levels in a group of Egyptian obese individuals. The Egyptian journal of immunology, 18(1), 25-32.
16
16- Terra, X., Auguet, T., Quesada, I., Aguilar, C., Luna, A. M., Hernández, M., ... & Pellitero, S. (2012). Increased levels and adipose tissue expression of visfatin in morbidly obese women: the relationship with pro‐inflammatory cytokines. Clinical endocrinology, 77(5), 691-698.
17
17- Carmo Martins, M., Faleiro, L. L., & Fonseca, A. (2012). Relationship between leptin and body mass and metabolic syndrome in an adult population. Revista Portuguesa de Cardiologia (English Edition), 31(11), 711-719.
18
18- Derosa, G., Fogari, E., D’Angelo, A., Bianchi, L., Bonaventura, A., Romano, D., & Maffioli, P. (2013). Adipocytokine levels in obese and non-obese subjects: an observational study. Inflammation, 36(4), 914-920.
19
19- Bienertová-Vašků, J., Novák, J., Zlámal, F., Forejt, M., Havlenová, S., Jackowská, A., ... & Vašků, A. (2014). The prediction role of indexes of circulating adipokines for common anthropometric and nutritional characteristics of obesity in the obese Central European population. Eating behaviors, 15(2), 244-251.
20
20- Indulekha, K., Surendar, J., Anjana, R. M., Geetha, L., Gokulakrishnan, K., Pradeepa, R., & Mohan, V. (2015). Metabolic obesity, adipocytokines, and inflammatory markers in Asian Indians—CURES-124. Diabetes technology & therapeutics, 17(2), 134-141.
21
21- Luo, Q., Li, N., Abulikem, S., & Yao, X. (2016). 16-02 ASSOCIATION OF SERUM CONCENTRATIONS OF LEPTIN WITH OBESITY AMONG UYGUR POPULATION IN. Journal of hypertension, 34, e218.
22
22- Ersoy, C., Sadikoglu, G., Orhan, H., Guclu, M., Sarandol, E., Akgun, M. D., ... & Imamoglu, S. (2010). Body fat distribution has no effect on serum visfatin levels in healthy female subjects. Cytokine, 49(3), 275-278.
23
23- Miazgowski, T., Major-Goluch, A., & Safranow, K. (2012). Selected adipokines and metabolic profiles in normal-weight women with abdominal obesity. Pol Arch Med Wewn, 122(9), 406-412.
24
24- Saboori, S., Hosseinzadeh-Attar, M. J., Hosseini, M., Mirzaei, K., & Ahmadivand, Z. (2015). The comparison of serum vaspin and visfatin concentrations in obese and normal weight women. Diabetes & Metabolic Syndrome: Clinical Research & Reviews, 9(4), 320-323.
25
25- Demir, B., Guven, S., Guven, E. S. G., Atamer, Y., Gunalp, G. S., & Gul, T. (2007). Serum leptin level in women with unexplained infertility. Journal of reproductive immunology, 75(2), 145-149.
26
26- Shafi, R., & Afzal, M. N. (2008). Status of serum leptin levels in females with infertility. Saudi medical journal, 29(10), 1419-1422.
27
27- Farooq, R., Lutfullah, S., & Ahmed, M. (2014). Serum leptin levels in obese infertile men and women. Pakistan journal of pharmaceutical sciences, 27(1).
28
28-Kamyabi, Z., & Gholamalizade, T. (2015). A comparative study of serum and follicular fluid leptin concentrations among explained infertile, unexplained infertile and fertile women. International journal of fertility & sterility, 9(2), 150.
29
29- Nilgün Güdücü, Herman İşçi, Uzay Gِrmüş, Alin Başgül Yiğiter & Ilkkan Dünder. (2012 ).Serum visfatin levels in women with polycystic ovary syndrome. Gynecological Endocrinology, 28(8): 619–623.
30
30- Svendsen, P. F., Christiansen, M., Hedley, P. L., Nilas, L., Pedersen, S. B., & Madsbad, S. (2012). Adipose expression of adipocytokines in women with polycystic ovary syndrome. Fertility and sterility, 98(1), 235-241.
31
31- Farshchian, F., Tehrani, F. R., Amirrasouli, H., Pour, H. R., Hedayati, M., Kazerouni, F., & Soltani, A. (2014). Visfatin and resistin serum levels in normal-weight and obese women with polycystic ovary syndrome. International journal of endocrinology and metabolism, 12(3).
32
32- Gul, O. O., Cander, S., Gul, B., Açıkgoz, E., Sarandol, E., & Ersoy, C. (2015). Evaluation of insulin resistance and plasma levels for visfatin and resistin in obese and non-obese patients with polycystic ovary syndrome. European cytokine network, 26(4), 73-78.
33
33- Chou, S. H., Chamberland, J. P., Liu, X., Matarese, G., Gao, C., Stefanakis, R., ... & Mantzoros, C. S. (2011). Leptin is an effective treatment for hypothalamic amenorrhea. Proceedings of the National Academy of Sciences, 108(16), 6585-6590.
34
34-Zheng, S. H., Du, D. F., & Li, X. L. (2017). Leptin Levels in Women with Polycystic Ovary Syndrome: A Systematic Review and a Meta-Analysis. Reproductive Sciences, 24(5), 656-670.
35
35- Tao, Y., Zhang, Q., Huang, W., Zhu, H., Zhang, D., & Luo, W. (2011). The Peritoneal Leptin, MCP‐1 and TNF‐α in the Pathogenesis of Endometriosis‐Associated Infertility. American Journal of Reproductive Immunology, 65(4), 403-406. 36- Barcz, E., Milewski, Ł., Radomski, D., Dziunycz, P., Kamiński, P., Roszkowski, P. I., & Malejczyk, J. (2008). A relationship between increased peritoneal leptin levels and infertility in endometriosis. Gynecological Endocrinology, 24(9), 526-530.
36
37- Choi, Y. S., Oh, H. K., & Choi, J. H. (2013). Expression of adiponectin, leptin, and their receptors in ovarian endometrioma. Fertility and sterility, 100(1), 135-141.
37
38- Dayer, D., Nikbakht, R., & Elyaderani, M. K. (2013). Comparison of leptin concentrations between infertile women with polycystic ovary syndrome and fertile women. Iranian journal of reproductive medicine, 11(12), 1033.
38
39-Jalilian, N., Haghnazari, L., & Rasolinia, S. (2016). Leptin and body mass index in polycystic ovary syndrome. Indian journal of endocrinology and metabolism, 20(3), 324.
39
40- Behboudi-Gandevani, S., Tehrani, F. R., Yarandi, R. B., Noroozzadeh, M., Hedayati, M., & Azizi, F. (2017). The association between polycystic ovary syndrome, obesity, and the serum concentration of adipokines. Journal of Endocrinological Investigation, 1-8.
40
ORIGINAL_ARTICLE
Updates of Pulmonary Embolism
Pulmonary embolism (PE) is the third most common cause of cardiovascular death worldwide, behind myocardial infarction and stroke. Due to pulmonary bed obstruction, PE can result in acute right ventricular (RV) failure which is a life-threatening condition. Because most patients ultimately die within the first hours of presentation, early diagnosis is very important (1). Mortality due to pulmonary embolism varies greatly, depending on various factors including age, comorbid conditions, and stability on presentation. Patients with low-risk PE have a 1-year survival rate over 95%. In contrast, patients presenting with high risk PE and hemodynamic instability have an approximately 40% mortality rate within 90-days. In this review, we will discuss the basic pathophysiology of PE, risk factors for developing PE, and standard diagnostic testing modalities. We will also cover risk stratification of patients presenting with PE and the implications for treatment and disposition. While no exact epidemiological data are available, the incidence of PE is estimated to be approximately 60 to 70 per 100,000, and that of venous thrombosis approximately 124 per 100,000 of the general population (2). The European guidelines for the diagnosis and management of PE report annual incidence rates of venous thrombosis and PE of approximately 0.5 to 1.0 per 1000 inhabitants (3). However, the actual figures are likely to be substantially higher because silent PE can develop in up to 40% to 50% of patients with deep vein thrombosis (DVT) (3)
https://smj.journals.ekb.eg/article_35256_49ecfb347b337193925897adf5f53688.pdf
2018-01-01
73
80
10.21608/smj.2018.35256
Mohamed
Elsayed
mohamed_elsayed@med.sohag.edu.eg
1
Department of Internal Medicine. faculty of medicine.sohag University
AUTHOR
1. Bĕlohlávek J, Dytrych V, Linhart A. Pulmonary embolism, part I: Epidemiology, risk factors and risk stratification, pathophysiology, clinical presentation, diagnosis and nonthrombotic pulmonary embolism. Experimental & Clinical Cardiology. 2013;18(2):129-38.
1
2. Oger E. Incidence of venous thromboembolism: a community-based study in Western France. EPI-GETBP Study Group. Groupe d'Etude de la Thrombose de Bretagne Occidentale. Thrombosis and haemostasis. 2000;83(5):657-60.
2
3. Torbicki A, Perrier A, Konstantinides S, Agnelli G, Galie N, Pruszczyk P, et al. Guidelines on the diagnosis and management of acute pulmonary embolism: the Task Force for the Diagnosis and Management of Acute Pulmonary Embolism of the European Society of Cardiology (ESC). Eur Heart J. 2008;29(18):2276-315.
3
4. Riedel M. Acute pulmonary embolism 1: pathophysiology, clinical presentation, and diagnosis. Heart. 2001;85(2):229-40.
4
5. Meyer G, Vieillard-Baron A, Planquette B. Recent advances in the management of pulmonary embolism: focus on the critically ill patients. Annals of Intensive Care. 2016;6:19.
5
6. Aujesky D, Roy PM, Le Manach CP, Verschuren F, Meyer G, Obrosky DS, et al. Validation of a model to predict adverse outcomes in patients with pulmonary embolism. Eur Heart J. 2006;27(4):476-81.
6
7. Poort SR, Rosendaal FR, Reitsma PH, Bertina RM. A common genetic variation in the 3'-untranslated region of the prothrombin gene is associated with elevated plasma prothrombin levels and an increase in venous thrombosis. Blood. 1996;88(10):3698-703.
7
8. Ginsburg KS, Liang MH, Newcomer L, Goldhaber SZ, Schur PH, Hennekens CH, et al. Anticardiolipin antibodies and the risk for ischemic stroke and venous thrombosis. Annals of internal medicine. 1992;117(12):997-1002.
8
9. Goldhaber SZ, Grodstein F, Stampfer MJ, Manson JE, Colditz GA, Speizer FE, et al. A prospective study of risk factors for pulmonary embolism in women. Jama. 1997;277(8):642-5.
9
10. Sanchez O, Trinquart L, Caille V, Couturaud F, Pacouret G, Meneveau N, et al. Prognostic factors for pulmonary embolism: the prep study, a prospective multicenter cohort study. American journal of respiratory and critical care medicine. 2010;181(2):168-73.
10
11.Kabrhel C, Okechukwu I. Factors associated with clinical deterioration shortly after PE. 2014;69(9):835-42.
11
12. Carrier M, Righini M, Djurabi RK, Huisman MV, Perrier A, Wells PS, et al. VIDAS D-dimer in combination with clinical pre-test probability to rule out pulmonary embolism. A systematic review of management outcome studies. Thrombosis and haemostasis. 2009;101(5):886-92.
12
13. Ghignone M, Girling L, Prewitt RM. Volume expansion versus norepinephrine in treatment of a low cardiac output complicating an acute increase in right ventricular afterload in dogs. Anesthesiology. 1984;60(2):132-5.
13
14. Mercat A, Diehl JL, Meyer G, Teboul JL, Sors H. Hemodynamic effects of fluid loading in acute massive pulmonary embolism. Critical care medicine. 1999;27(3):540-4.
14
15. Konstantinides S, Torbicki A, Agnelli G, Danchin N, Fitzmaurice D, Galie N, et al. Downloaded from Schindler TH, Svitil P, Vonk Noordegraaf A, Zamorano JL, Zompatori M. 2014 ESC guidelines on the diagnosis and management of acute pulmonary embolism. Eur Heart J. 2014;35:3033-69.
15
ORIGINAL_ARTICLE
LIPID PROFILE INPATIENTS WITH RHEUMATOID ARTHRITIS: CORRELATION WITH DISEASE ACTIVITY
Objectives:To study changes in lipid profile in patients with rheumatoid arthritis (RA) and to evaluate the relation between lipid profile and disease severity of RA. Design: Cross-sectional study. Patients:Patients with rheumatoid arthritis (RA) according to 2010 ACR/EULAR classification criteria for RA (n = 150). Methods: Demographic data, arthritis history, medical and therapeutic history were evaluated. Disease activity was evaluated using DAS28 (ESR). Immunological investigations included RF, ESR, CRP, and anti-CCP.Lipid profile levels were measured. Results:Raised TG was found in 38 (25.3 %) of patients, raised TC was found in 69 (46 %) of patients and decreased HDL-C was detected in 85 (56.7 %) of the patients
https://smj.journals.ekb.eg/article_35373_d13809ceb776516d2b2ec93de9d7fb62.pdf
2018-01-01
83
87
10.21608/smj.2018.35373
Rheumatoid Arthritis
Lipid profile
DAS28
Ali
Kasem
1
Department of Internal Medicine- Faculty of Medicine- Sohag University
AUTHOR
Esam
Abo Al-Fadl
essam_mohamed@med.sohag.edu.eg
2
Department of Rheumatology, Rehabilitation and Physical medicine,Faculty of Medicine- Sohag University.
AUTHOR
Hanan
Mohammed Abo-Zeid
hanan_abozaid@med.sohag.edu.eg
3
Department of Rheumatology, Rehabilitation and Physical medicine - Faculty of Medicine- Sohag University.
AUTHOR
Ashraf
Abd El-Latif
ashraf_abdelwahab@med.sohag.edu.eg
4
Department of Dermatology, Venereology and Andrology- Faculty of Medicine- Sohag University.
AUTHOR
Ebtesam
Ali Fayez
ebtsamkhalaf@med.sohag.edu.eg
5
Department ofPhysical medicine,Rheumatology and Rehabilitation- Faculty of Medicine- Sohag University
AUTHOR
1. Smolen JS, Aletaha D and Mcinnes IB: Rheumatoid arthritis.Lancet. 2016; 388(10055): 2023-38.
1
2. Silman AJ and Pearson JE: Epidemiology and genetics of rheumatoid arthritis.Arthritis Res. 2002; 4 Suppl 3: S265-72.
2
3. Faden G, Viapiana O, Fischetti F, Faganello G, Gatti D: Cardiovascular risk stratification and management of patients with rheumatoid arthritis in clinical practice: the "EPIDAURO registry".Int J Cardiol. 2014; 172(2): 534-6.
3
4. Erum U, Ahsan T and Khowaja D: Lipid abnormalities in patients with Rheumatoid Arthritis.Pak J Med Sci. 2017; 33(1): 227-230.
4
5. Ferraz-Amaro I, Gonzalez-Juanatey C, Lopez-Mejias R, Riancho-Zarrabeitia L and Gonzalez-Gay MA: Metabolic syndrome in rheumatoid arthritis.Mediators Inflamm. 2013; 2013: 710928.
5
6. Charles-Schoeman C, Fleischmann R, Davignon J, Schwartz H, Turner SM: Potential mechanisms leading to the abnormal lipid profile in patients with rheumatoid arthritis versus healthy volunteers and reversal by tofacitinib.Arthritis Rheumatol. 2015; 67(3): 616-25.
6
7. Choy E and Sattar N: Interpreting lipid levels in the context of high-grade inflammatory states with a focus on rheumatoid arthritis: a challenge to conventional cardiovascular risk actions.Ann Rheum Dis. 2009; 68(4): 460-9.
7
8. Robertson J, Peters MJ, Mcinnes IB and Sattar N: Changes in lipid levels with inflammation and therapy in RA: a maturing paradigm.Nat Rev Rheumatol. 2013; 9(9): 513-23.
8
9. Myasoedova E, Crowson CS, Kremers HM, Roger VL, Fitz-Gibbon PD: Lipid paradox in rheumatoid arthritis: the impact of serum lipid measures and systemic inflammation on the risk of cardiovascular disease.Ann Rheum Dis. 2011; 70(3): 482-7.
9
10. Aletaha D, Neogi T, Silman AJ, Funovits J, Felson DT: 2010 rheumatoid arthritis classification criteria: an American College of Rheumatology/European League Against Rheumatism collaborative initiative.Ann Rheum Dis. 2010; 69(9): 1580-8.
10
11. Jung YO and Kim HA: Recent paradigm shifts in the diagnosis and treatment of rheumatoid arthritis.Korean J Intern Med. 2012; 27(4): 378-87.
11
12. Karvounaris SA, Sidiropoulos PI, Papadakis JA, Spanakis EK, Bertsias GK: Metabolic syndrome is common among middle-to-older aged Mediterranean patients with rheumatoid arthritis and correlates with disease activity: a retrospective, cross-sectional, controlled, study.Ann Rheum Dis. 2007; 66(1): 28-33.
12
13. Galarza-Delgado DA, Azpiri-Lopez JR, Colunga-Pedraza IJ, Cardenas-De La Garza JA, Vera-Pineda R: Prevalence of comorbidities in Mexican mestizo patients with rheumatoid arthritis.Rheumatol Int. 20
13
14. Van Breukelen-Van Der Stoep DF, Van Zeben D, Klop B, Van De Geijn GJ, Janssen HJ: Marked underdiagnosis and undertreatment of hypertension and hypercholesterolaemia in rheumatoid arthritis.Rheumatology (Oxford). 2016; 55(7): 1210-6.
14
15. Nisar A, Rasheed U, Aziz W and Farooqi AZ: Prevalence of dyslipidemias in autoimmune rheumatic diseases.J Coll Physicians Surg Pak. 2012; 22(4): 235-9.
15
16. Attar SM: Hyperlipidemia in rheumatoid arthritis patients in Saudi Arabia. Correlation with C-reactive protein levels and disease activity.Saudi Med J. 2015; 36(6): 685-91.
16
17. Sheng X, Murphy MJ, Macdonald TM and Wei L: Effectiveness of statins on total cholesterol and cardiovascular disease and all-cause mortality in osteoarthritis and rheumatoid arthritis.J Rheumatol. 2012; 39(1): 32-40.
17
18. Solomon DH, Reed GW, Kremer JM, Curtis JR, Farkouh ME: Disease activity in rheumatoid arthritis and the risk of cardiovascular events.Arthritis Rheumatol. 2015; 67(6): 1449-55.
18
ORIGINAL_ARTICLE
Radiological Parameters of Calcaneovalgus Deformity of the Foot
Background Calcaneo valgus deformity is postural deformity of infancy which is characterized by dramatic hyperdorsiflexion of the foot that appears to be plastered up against the anterior surface of the tibia. Planter flexion of the foot is frequently limited as a result of contracture of the anterior ankle and foot structures. Aim of the work:To asses radiological parameters of calcaenovalgus deformity of the foot in children. Patients and methods:The patients were children up to 5 years old. The participants were 7 males and 13 females. The affected foot were 10 right sided and 10 left sided. Results: The present study was designed to asses radiological parameters of calcaenovalgus deformity of the foot in children. Conclusion The radiological parameters of calcaenovalgus deformity of the foot in children varies widly accodrding it is vevtical talus or oblique talus deformity.
https://smj.journals.ekb.eg/article_36787_8fdfea6731eb2d3a8aaf117ed674c112.pdf
2018-01-01
89
94
10.21608/smj.2018.36787
Abodoma
Shabeb
1
Department of Orthopaedic and traumatoulogy , Faculty of Medicine, Sohag University.
AUTHOR
Mohamed
Kenawy
2
Department of Orthopaedic and traumatoulogy , Faculty of Medicine, Sohag University.
AUTHOR
Ahmed
Kassem
3
Department of Orthopaedic and traumatoulogy , Faculty of Medicine, Sohag University.
AUTHOR
Ashraf
Marzouk
4
Department of Orthopaedic and traumatoulogy , Faculty of Medicine, Sohag University.
AUTHOR
Hassan
Noamany
5
Department of Orthopaedic and traumatoulogy , Faculty of Medicine, Sohag University.
AUTHOR
1. Van de Perre S, Vanhoenacker FM, De Vuyst D, Parizel R. Imaging anatomy of the ankle. JBR-BTR : organe de la Societe royale belge de radiologie. 2004;87(6):310-4.
1
2. Hernandez-Diaz C, Saavedra MA, Navarro-Zarza JE, Canoso JJ, Villasenor-Ovies P, Vargas A, et al. Clinical anatomy of the ankle and foot. Reumatologia clinica. 2012;8 Suppl 2:46-52.
2
3. Golano P, Vega J, de Leeuw PA, Malagelada F, Manzanares MC, Gotzens V, et al. Anatomy of the ankle ligaments: a pictorial essay. Knee surgery, sports traumatology, arthroscopy : official journal of the ESSKA. 2010;18(5):557-69.
3
4. Attarian DE, McCrackin HJ, DeVito DP, McElhaney JH, Garrett WE, Jr. Biomechanical characteristics of human ankle ligaments. Foot & ankle. 1985;6(2):54-8.
4
5. Milner CE, Soames RW. Anatomy of the collateral ligaments of the human ankle joint. Foot & ankle international. 1998;19(11):757-60.
5
6. Campbell KJ, Michalski MP, Wilson KJ, Goldsmith MT, Wijdicks CA, LaPrade RF, et al. The ligament anatomy of the deltoid complex of the ankle: a qualitative and quantitative anatomical study. The Journal of bone and joint surgery American volume. 2014;96(8)e62.
6
ORIGINAL_ARTICLE
Prognostic Factors Of Extradural Heamatoma Evacuation
Objective: To assess the Prognostic Factors of Extradural Heamatoma Evacuation Methodology :This study was conducted on 50 patients with extradural heamatoma 14 females and 36males, the oldest was 63 years old and the youngest was 3 years old, with mean age of 38.48 years, the cause of trauma was road traffic accident in 23 patients of them and falling from high in 14 patients of them and assault in 11 patients and animal kick in 2 patients, according to the clinical presentation the most common was manifestation of increase intracranial tension as headache and vomiting in 38 cases, followed by Loss of consciousness in 28 patients and 19 cases have typical lucid interval followed by disturbed conscious level in 12 cases, then weakness of one sideof the body in 8 cases, then unilateral dilated pupil in 5 cases followed by fits in 2 cases, while 2 cases were neurologically free and one case has bilateral dilated fixed pupil,the volume of EDH was between 20-30cc in 27 patients and between30-40cc in 17 patients and between 40 -50cc in 5 patients and more than 50cc in one patient, the EDH located in temperoparietal region in 16 patients and purely in the temporal lobe in 13 patients and in the parietal lobe in 8 patients and frontoparietal in 6 patients and the frontal lobe in 3 patients and in the posterior fossa in 3 patients and biparietal in one patient ,we operate 2patients in the 1st hour and 14 in the 2nd and 14 in the 3rd and 10 in the 4th and 6 in the 5th and 4 cases after 5 hours. RESULT: We operate 50 patients 39 of them show full recovery and 7 patients show neurological deficit and 4 patients died and no one show vegetative state and from the 46 patients who recovered 6 patients develop superficial wound infection and one patients show recollection of EDH and reoperation. Conclusion: The EDH is more common in middle aged males .As regard the site of EDH we found that the site play minimal rule in the outcome of EDH and as the most common sites was temperoparietal and temporal so mostly the middle meningial artery is the most common source of EDH and the posterior fossa is the most dangerous site as one case of the 3 patient presented with posterior fossa EDH died (33.3%) followed by temporal lobe EDH as 2(6.5%) cases from the 15 case died. the size and time from the trauma to evacuation and clinical presentation of EDH thy are the major factors that affect EDH. The clinical presentation especially the conscious level is the main factor affecting theoutcome as all the 4 cases who died the GCS was less than 8 when they arrived.
https://smj.journals.ekb.eg/article_40569_5355d961a2ede642663612b996ec0dca.pdf
2018-01-01
95
103
10.21608/smj.2018.40569
Extradural Heamatoma
surgical evacuation
Prognostic factors
Ahmed
ELsayed
1
Department of Neurosurgery , Faculty of Medicine, Sohag University.
AUTHOR
Khaled
Fadle
khaled_ahmed@med.sohag.edu.eg
2
Department of Neurosurgery , Faculty of Medicine, Sohag University.
AUTHOR
Mohammed
AbdElaal
mohamed_abdelaal@med.sohag.edu.eg
3
Department of Neurosurgery , Faculty of Medicine, Sohag University.
AUTHOR
Roshdy
Elkhayat
4
Department of Neurosurgery , Faculty of Medicine, Assuit University.
AUTHOR
1. A Mishra, S Mohanty - –Contre-coup extradural haematoma: a short report. Neurology India, 2001
1
2. BT Andrews - 2003 - New York: Thieme, 2003 Intensive care in neurosurgery
2
3. Erşahin, Y., Mutluer, S. & Güzelbag, Extradural hematoma: analysis of 146 cases E. Child''s Nerv Syst (1993) Volume 9, Issue 2, pp 96–99
3
4. Gerlach R, Dittrich S, Schneider W, Ackermann H, Seifert V, Kieslich M (2009) unselected cases. PediatrEmerg Care 25:164–169
4
5. H.BinderaM.MajdandT.M.TiefenboeckaA.FochtmannbM.MichelaS.HajduaW.MauritzcJ.LeitgebaOrthopaedics & Traumatology: Surgery & Research October 2016, Pages 769-774
5
6. Noman Khaled, MZ Raihan, FH Chowdhury, ATM Ashadullah, MH Sarkar, SS Hossain (2008)Surgical management of traumatic extradural haematoma: Experiences with 610 patients and prospective analysis Thieme Medical and Scientific Publishers Private Ltd
6
7. Phoebe S.Y.CheungaJenny M.Y.LamabJanice H.H.YeungabColin A.GrahamabTimothy H.Rainerab Outcome of traumatic extradural haematoma in Hong Kong Volume 38, Issue 1, January 2007, Pages 76-80
7
8. Tallon JM, Ackroyd-Stolarz S, Karim SA, Clarke DB (2008) Can J Surg. 2008 Oct; 51(5): 339–345.
8
9. Taussky P, Widmer HR, Takala J, Fandino J (2008) Outcome after acute traumatic subdural and epidural haematoma in Switzerland: a single-centre experience. Swiss Med Wkly 138:281–285
9
10. uday, C., Uzan, M. & Hanci, M. (1994) Statistical analysis of the factors affecting the outcome of extradural haematomas: 115 CasesActa Neurochirurgica Volume 131, Issue 3–4, pp 203–206
10
ORIGINAL_ARTICLE
Sohag experience in treatment of Dorsolumbar fractures according to Thoracolumbar injury classification and severity score(TLICS)
Background:.The Thoracolumbar Injury Classification and Severity Score (TLICS) was developed to improve injury classification and guide surgical decision making, yet validation remains necessary. This study evaluates the functional ,clinical and radiological outcome of patients with thoracolumbar spine trauma (TLST) treated according to the TLICS. Aim of the work:To validate the efficacy of Thoracolumbar injury classification and severity score (TLICS) in orthopaedic emergency department at sohag university hospitals. Patients and methods:The TLICS was prospectively applied to a consecutive series of patients (30 cases) treated for TLST between October 2016 and October 2017. Patients with a TLICS score more than 4 points were surgically treated, whereas patients with a TLICS score of less than 4 points were conservatively managed.Those with a score of equal 4 ,group were managed conservatively and the other were operated.The primary outcome was the American Spinal Injury Association Impairment Scale (AIS)(1). Results:The decision taken according to TLICS either conservative if the final score 4. Conservative treatment in the form of rest and dorsolumbosacral brace .Operative in form of posterior fixation with or without decompression .Transpedicular fixation and decompression was needed in 10 cases (33.33%) because they were suffering from neurological insult.The mean age was 34years.There were a marked improvement in angle of kyphosis , vertebral height loss and Oswestry disability index .No patient had neurological worsening during the follow-up. Conclusion:.Thoracolumnar injury and severity score is valid and safe for management of thoracolumbar fractures and has good reliability.
https://smj.journals.ekb.eg/article_40591_03baba957681d134b76112dd944cc068.pdf
2018-01-01
105
109
10.21608/smj.2018.40591
Ahmed
Abdelrhman
1
Department of Orthpaedic and Traumatology , Faculty of Medicine, Sohag University.
AUTHOR
Ahmed
Shaker
ahmed_saleem@med.sohag.edu.eg
2
Department of Orthpaedic and Traumatology , Faculty of Medicine, Sohag University.
AUTHOR
Ahmed
Kassem
ahmedhamed@med.sohag.edu.eg
3
Department of Orthopedic Surgery,Faculty of Medicine,Sohag University Hospital, Egypt.
AUTHOR
Ashraf
Ahmed
ashraf_marzouk@med.sohag.edu.eg
4
Department of Orthpaedic and Traumatology , Faculty of Medicine, Sohag University.
AUTHOR
Mohamed
Abdel-Wanis
mohamed_abdelwanees@med.sohag.edu.eg
5
Department of Orthpaedic and Traumatology , Faculty of Medicine, Sohag University.
AUTHOR
1. Kirshblum, Steven C.; Burns, Stephen P.; Biering-Sorensen, Fin; Donovan, William; Graves, Daniel E.; Jha, Amitabh; Johansen, Mark; Jones, Linda; Krassioukov, Andrei; Mulcahey, M.J.; Schmidt-Read, Mary; Waring, William (2011). "International standards for neurological classification of spinal cord injury (Revised 2011)". The Journal of Spinal Cord Medicine. 34 (6): 535–546
1
2. Hu R, Mustard CA, Burns C. Epidemiology of incident spinal fracture in a complete population. Spine 1996;21:492.
2
3. Tran NT, Watson NA, Tender AF, et al. Mechanism of the burst fracture inthoracolumbar spine. Spine 1995; 20:1984 -8.
3
4. Bohlman HH. Treatment of fractures and dislocations of the thoracic and lumbar spine. J Bone Joint Surg Am 1985;67:165-9.
4
5.Keynan, Ory; Fisher, CG; Vaccaro, A; Fehlings, MG; Oner, FC; Dietz, J; Kwon, B;
5
Rampersaud, R; Bono, C; France, J; Dvorak, M (Mar 1, 2006). "Radiographic measurement parameters in thoracolumbar fractures: a systematic review and consensus statement of the spine trauma study group.". Spine 31 (5): E156–65. doi:10.1097/01.brs.0000201261.94907.0d. PMID 16508540. Retrieved 15 December 2012
6
6. Andrei F. Joaquim(2013), the spine journal, retrospective eavaluation of the validity of thoracolumbar injury and severity score. Volume 13|issue 12
7
7. George Sapkas1, Konstantinos Kateros2, Stamatios A. Papadakis(2010) Treatment of Unstable Thoracolumbar Burst Fractures by Indirect Reduction and Posterior Stabilization: Short-Segment Versus Long- Segment Stabilization The Open Orthopaedics Journal, 2010, 4, 7-13
8
8. Spiros G.Pneumaticos ,panagiotis K.Karaminos (2016) Evaluation of TLICS for thoracolumbar fractures .Eur spinr J.25:1123-1127 DOI 10.1007/500586-015-3889y.
9
ORIGINAL_ARTICLE
Measurement of Knowledge, attitudes and practices of parents on misuse of antibiotics in children with acute upper respiratory tract infections in Sohag district
Background: Upper respiratory tract infections (URTIs) are considered to be the most common reason for children’s visits to outpatient clinics. The emergence and spread of resistance related to the irrational use of antibiotics is a major global public health problem. Aim of the work: This study aimed to assess parents’ knowledge, attitude, and practice (KAP) regarding the use of antibiotics in URTIs in children. Methodology: A cross-sectional study wascarried out among parents(N=800) of children who were attending the maternal and child health center in Sohag city and the family medicine unit in Elmahamdaelbahria village in the period from 1st July 2016 till 31th May 2017 .Results:Our results revealed that females were about 62.6%, those not sharing in labor force were 55.9 %, and urban parents were about58.8%. The mean age of parents was 33 years old.There is a statistically highly significant difference between mother & father in mean scoresof knowledge, attitude, practice; they were lower in fathers. Also, there is statistically significant difference between parents with different ages in practice score. There are highly statistically significant differences between mothers who were sharing and not sharing in labor force in Attitude, Practice scores. Conclusion:Parents with loweducational level, rural residence, low income and with two children or less have lack of knowledge ,inappropriate beliefs andpractices so they are vulnerable for misusing antibiotics for their children.
https://smj.journals.ekb.eg/article_40606_7abd9f5ecbbf778d357a2fcdaa0d00a2.pdf
2018-01-01
111
119
10.21608/smj.2018.40606
eman
mohamed
eman_mohamed@med.sohag.edu.eg
1
Department of public health and community medicine , Faculty of medicine, Sohag University, sohag, egypt.
AUTHOR
ahmed
Hamed
ahmed_hamed@med.sohag.edu.eg
2
Department of public health and community medicine , Faculty of medicine, Sohag University, sohag, egypt.
AUTHOR
Fouad
Yousef
fouad_atya@med.sohag.edu.eg
3
Department of public health and community medicine , Faculty of medicine, Sohag University, sohag, egypt.
AUTHOR
Ayat
Ahmed
4
Department of public health and community medicine , Faculty of medicine, Sohag University, sohag, egypt.
AUTHOR
1- Kisuule F, Wright S, Barreto J, Zenilman J. Improving antibiotic utilization among hospitalists: a pilot academic detailing project with a public health approach. Journal of hospital medicine. 2008 Jan 1; 3 (1):64-70
1
2- Kotwani A, Wattal C, Katewa S, Joshi PC, Holloway K. Factors influencing primary care physicians to prescribe antibiotics in Delhi India. Family practice. 2010 Jul 26; 27 (6):684-90.
2
3- Finkelstein JA, Metlay JP, Davis RL, Rifas-Shiman SL, Dowell SF, Platt R. Antimicrobial use in defined populations of infants and young children.Archives of pediatrics & adolescent medicine. 2000 Apr 1; 154 (4):395-400.
3
4-Kardas P, Devine S, Golembesky A, Roberts C. A systematic review and meta-analysis of misuse of antibiotic therapies in the community. International journal of
4
antimicrobial agents. 2005 Aug 31; 26 (2):106-13.
5
5-Cully M. The politics of antibiotics: policy-makers and medical experts need to think globally if we are to prevent an antibiotic' tragedy of the commons'. Nature. 2014 May 1; 509 (7498 SI):516-8.
6
6-Albrich WC, Monnet DL, Harbarth S. Antibiotic selection pressure and resistance in Streptococcus pneumoniae and Streptococcus pyogenes.Emerging infectious diseases. 2004 Mar; 10 (3):514.
7
7- Sarahroodi S, Arzi A, Sawalha AF, Ashtarinezhad A. Antibiotics self-medication among southern iranian university students. IJP-International Journal of Pharmacology. 2010;6 (1):48-52.
8
8- Van De Sande-Bruinsma N, Grundmann H, Verloo D, Tiemersma E, Monen J, Goossens H, Ferech M. European Antimicrobial Resistance Surveillance System. Antimicrobial drug use and resistance in Europe.Emerging infectious diseases. 2008 Nov; 14(11):1722.
9
9-Al-Dossari K. Parental knowledge, attitude and practice on antibiotic use for upper respiratory tract infections in children. Majmaah Journal of Health Sciences. 2013 Apr; 1 (1):33-45
10
10-Saed HZ, Taha AA, Araj KF, Abahri IA, Sawalha AF, Sweileh WM, Awang R, Al-Jabi SW. Parental knowledge, attitudes and practices regarding antibiotic use for
11
acute upper respiratory tract infections in children: a cross-sectional study in Palestine. BMC pediatrics. 2015 Nov 11; 15 (1):176.
12
11-Bi P, Tong S, Parton KA.Family self-medication and antibiotics abuse for
13
children and juveniles in a Chinese city.Social science & medicine. 2000 May 16; 50 (10):1445-50.
14
12-Edwards DJ, Richman PB, Bradley K,.Parental use and misuse of antibiotics: are there differences in urban vs. suburban settings? Academic emergency medicine. 2002 Jan 1; 9 (1):22-6.
15
13-Mitsi G, Jelastopulu E, Basiaris H, Skoutelis A, Gogos C. Patterns of antibiotic use among adults and parents in the community: a questionnaire-based survey in a Greek urban population. International journal of antimicrobial agents. 2005 May 31; 25(5):439-43.
16
14-Islahudin F, TameziAM, Shah NM. Knowledge, attitudes and practices about antibiotic use among the general public in Malaysia. Southeast Asian Journal of Tropical Medicine and Public Health. 2014 Nov 1; 45(6):1474.
17
15- Chan GC, Tang SF. Parental knowledge, attitudes and antibiotic use for acute upper respiratory tract infection in children attending a primary healthcare clinic inMalaysia.Malaysian Family Physician. 2012 Mar 31; 2 (1):5.
18
ORIGINAL_ARTICLE
Risk Factors of Delayed Milestones Among Children Attending Sohag General Hospital
Developmental delay occurs when a child exhibits a significant delay in the acquisition of milestones or skills, in one or more domains of development (i.e., gross motor, fine motor, speech/language, cognitive, personal/social, or activities of daily living). Objectives: present study aims to investigate the most common risk factors of The delayed development in children under four years attending Sohag GeneralHospital. Subjects and methods: A case control study was conducted in Sohag General Hospital during the period from January 2015 to June 2016 on children attending Pediatric, Physiotherapy and phoniatric clinicsin Sohag General Hospital, Sohag Governorate. The sample size was 150 cases and 150 controls. One hundred and fifty children (aged 1.5 month to 48 months) diagnosed with developmental delay by a specialist or/and a developmental pediatrician were recruited as cases. Results: In the logistic regression model, the odds of developing delayed milestones is significantly higher among children with cyanosis (OR = 16.391), low birth weight (OR = 6.147), parental consanguinity (OR = 5.489), 1st birth order (OR = 4.048), urban residence (OR = 3.702) and history of neonatal jaundice (OR = 2.518). Conclusion: The urban children, first children and from few number of family members were more frequently at risk for developmental delay.
https://smj.journals.ekb.eg/article_40878_26e0dd85a57250661798cbd4b2312544.pdf
2018-01-01
121
136
10.21608/smj.2018.40878
developmental delay
risk factors
Sohag General Hospital
Ekram
Abdel khalek
1
Department of Public Health and Community Medicine , Faculty of Medicine, Assiut university.
AUTHOR
Sabra
Ahmed
2
Department of Public Health and Community Medicine , Faculty of Medicine,Assiut university.
AUTHOR
Ramadan
Ahmed
ramadan_mahmoud@med.sohag.edu.eg
3
Department of Pediatrics , Faculty of Medicine, Sohag university.
AUTHOR
Gamal
Soliman
4
Department of Public Health and Community Medicine , Al-Azhar Faculty of Medicine, Assiut branch.
AUTHOR
Accardo PJ, Whitman BY, Behr SK, Farrell A, Magenis E and Morrow-Gorton J (2003): Dictionary of developmenta disabilities terminology. 2nd edition. Brookes Publishing Co.
1
2. Tervo R (2003): Identifying patterns of developmental delay can help diagnose neurodevelopmental disorders. Pediatrics Perspective, 12 (3):1.
2
3. World Health Organization (2008): The global burden of disease: 2004 update. Geneva: World Health Organization Press.
3
4. El Meliegy E and Hossam El Sabbagh M (2004): Etiology of developmental delay in Egyptian children. Int. J. Ch. Neuropsychiatry, 1(1): 29-40.
4
5. Zhou WJ, Liang AM, Wang FZ, Cui WH, Wang XY, Liu QM, You H, He CY, Peng JR, Zhang YW, Yu C, Huang QH, Guo MM, Ji TY, Sang T, Yang YL, Zhu SN, Wang JM and Jiang YW (2013): Epidemiological study on developmental delay of 18-month-old children from four districts/counties in Beijing. Beijing Da Xue Xue Bao, 45(2):211-216.
5
Service Delivery. Chicago: University of Chicago Press.
6
6.Frankenburg WK, Dodds J, Archer P (1992): The DENVER II: A major revision and restandardization of the Denver Developmental Screening Test. Pediatrics, 89:91–97.
7
7- Abd El-Tawab Abd El-Ah (2004): Family socio-economic scale. Journal of Faculty of Education, Assiut University. 20(2).
8
8. Cornish AM, McMahon CA, Ungerer JA, Barnett B, Kowalenko N and Tennant C (2005): Postnatal depression and infant cognitive and motor development in the second postnatal year: The impact of depression chronicity and infant gender. Infant Behavior and Development, 28 (4): 407–417.
9
9. Hops H (1995): Age- and gender-specific effects of parental depression: A commentary. Developmental Psychology, 31 (3): 428–431.
10
10. Communicative skills in relation to gender, birth order, childcare and socioeconomic status in 18-month-old children. Scandinavian Journal of Psychology, 46 (6):485–491.
11
11. Salih SA, Hassan B(1998): Normal developmental milestones. Saudi Medical Journal. 19:244-248
12
12. Horwitz SM, Irwin JR, Briggs-Gowan MJ, Bosson Heenan JM, Mendoza J and Carter AS (2003): Language delay in a community cohort of young children. Journal of American Academy of Child and Adolescent Psychiatry, 42: 932–940.
13
13. Walker CK, Ashwood P, Hertz-Picciotto I (2015): JAMA Pediatr, 169(6):606-7.
14
14. Hoff E (2003): The specificity of environmental influence: Socioeconomic status affects early vocabulary development via maternal speech. Child Development, 74 (5):1368–1378.
15
15. Zubrick SR, Taylor KL, Rice ML and Slegers DW (2007): Late language emergence at 24 Months: An epidemiological study of prevalence, predictors, and covariates. Journal of Speech, Language and Hearing Research, 50: 1562–1592.
16
16. Berger SE and Nuzzo K (2008): Older siblings influence younger siblings’ motor development. Infant and Child Development, 17 (6): 607–615.
17
17. Bowlby J (1969): Attachment and loss : 1. Attachment. New York: Basic Books.
18
18 Belsky J (2001): Developmental risks (still) associated with early child care. Journal of Child Psychology and Psychiatry, 42: 845–859.
19
19. Thompson RA (2008): Early attachment and later development: Familiar questions, new answers. (Vol. Eds.), Handbook of attachment: Theory, research, and clinical applications (2nd ed.,). New York, NY: Guilford Press, 2: 348–365.
20
20. Nomaguchi KM (2006): Maternal employment, nonparental care, mother–child, interactions, and children’s outcomes during preschool years. Journal of Marriage and Family, 68 (5): 1341–1369.
21
21. Creasy RK, Resnik R and Iams J (Eds.) (2004): Maternal-fetal medicine (5th ed.). Philadelphia: Saunders.
22
22. Hultman CM, Sparen P and Cnattangius S (2002): Perinatal risk factors for infantile autism. Epidemiology, 13: 417–423.
23
23. Hultman CM, Sparen P and Cnattangius S (2002): Perinatal risk factors for infantile autism. Epidemiology, 13: 417–423.
24
24. Davis NM, Ford GW, Anderson PJ and Doyle LW (2007): Developmental coordination disorder at 8 years of age in a regional cohort of extremely-lowbirthweight or very preterm infants. Developmental Medicine & Child Neurology, 49: 325–330
25
25. Holsti L, Grunau RV and Whitfield MF (2002): Developmental coordination disorder in extremely low birth weight children at nine years. Journal of Developmental & Behavioral Pediatrics, 23: 9–15.
26
26. Ahlfors CE, Amin SB and Parker AE (2009): Unbound bilirubin predicts abnormal automated auditory brainstem response in a diverse newborn population. Journal of Perinatology, 29: 305–309.
27
27.Strauss RS and Dietz WH (1998): Growth and development of term children born with low birth weight: effects of genetic and environmental factors. Journal of Pediatrics, 133: 67-72.
28
28. Papaioannou A, Patelarou E, Chatzi L, Koutis A, Kafatos A and Kogevinas M (2008): Use of healthcare services and risk factors among pregnant women in Crete. International Journal of Gynaecology & Obstetrics, 103 (3): 253–255.
29
29. Dinas K, Mavromatidis G, Dovas D, Giannoulis C, Tantanasis T and Loufopoulos A (2008): Current caesarean delivery rates and indications in a major public hospital in northern Greece. The Australian and New Zealand Journal of Obstetrics and Gynaecology, 48 (2): 142–146.
30
30.Mathews TJ and MacDorman MF (2010): Infant mortality statistics from the 2006 period linked birth/infant death data set. Nat Vital Stat Rep, 58:1-31.
31
31.Salt A and Redshaw M (2006): Neurodevelopmental follow-up after preterm birth: Follow up after two years. Early Human Development, 82 (3): 185–197.
32
32. Bhutta AT, Cleves MA, Casey P, Cradock MM and Anand KJ (2002): Cognitive and behavioral outcomes of school-aged children who were born preterm: A meta-analysis. JAMA: The Journal of the American Medical Association, 288 (6): 728–737.
33
33. Del Bono E and Ermisch J (2009): Birth weight and the dynamics of early cognitive and behavioral development. IZA Discussion, 4270.
34
34.Bittles AH (2001): Consanguinity and its relevance to clinical genetics. Clin Genet, 60: 89–98.
35
ORIGINAL_ARTICLE
Fixation of pilon Fracture & Comminuted distal tibial fracture with Triangular External fixator
Back ground : patients with pilon fractures and distal comminuted fractures, These fractures give the surgeon a great challenge In methods of fixation starting from External fixator up to platting and Illizarov But our method of fixation which Is Triangular External fixator acheive a great success.
https://smj.journals.ekb.eg/article_40889_f6cbd89fc3e596906696d9e9e663b8ed.pdf
2018-01-01
137
141
10.21608/smj.2018.40889
Shazly
Musa
shazli_mousa@med.sohag.edu.eg
1
Department of Orthpaedic and Traumatology , Faculty of Medicine, Sohag University.
AUTHOR
Ahmed
Eldosoky
ahmed_eldesouky@med.sohag.edu.eg
2
Department of Orthpaedic and Traumatology , Faculty of Medicine, Sohag University.
AUTHOR
Mostafa
Ibrahim
mostafaismail@med.sohag.edu.eg
3
Department of Orthpaedic and Traumatology , Faculty of Medicine, Sohag University.
AUTHOR
Mohamed
Ahmed
mohamed_mohamed2@med.sohag.edu.eg
4
Department of Orthpaedic and Traumatology , Faculty of Medicine, Sohag University.
AUTHOR
Hasan
Ahmed
5
Department of Orthpaedic and Traumatology , Faculty of Medicine, Sohag University.
AUTHOR
Teeny S, Wiss DA. Open reduction and internal fixation of tibial plafond fractures. ClinOrthop. 1993;292:108-17.
1
Ovaida DN, Beals RK. Fractures of the tibial plafond. J Bone Joint Surg. 1986;68-A:453-551.
2
Bourne RB. Pilon fractures of the distal tibia. ClinOrthop. 1989;240:42-6.
3
Wyrsch B, McFerran M, McAndrew M. Operative treatment of fractures of the tibial plafond. A randomized prospective study. J Bone Joint Surg. 1996;78-A:1646-57.
4
Barbieri R, Schenk R, Koval K. Hybrid external fixation in the treatment of tibial plafond fractures. ClinOrthop. 1996;332:16-22.
5
Marsh JL, Bonar S, Nepola JV. Use of an articulated external fixator for fractures of the tibial plafond. J Bone Joint Surg. 1995;77-A:1498-509.
6
Bone L, Stegemann P, McNamara K. External fixation of severely comminuted and open tibialpilonfracures. ClinOrthop. 1993;292:101-7.
7
Marsh JL, Weigel DP, Dirschl DR. Tibial plafond fractures: how do these ankles function over time? J Bone Joint Surg. 2003;85-A:287-95.
8
Tornetta P, Weiner L, Bergman M. Pilon fractures: treatment with combined internal and external fixation. J Orthop Trauma. 1993;7:489-96.
9
Haidukewych GJ. Temporary external fixation for the management of complex intra-and periarticular fractures of the lower extremity. J Orthop Trauma. 2002;11:678-85.
10
Patterson MJ, Cole DJ. Two-staged delayed open reduction and internal fixation of severe pilon fractures. J Orthop Trauma. 1999;2:85-91.
11
Sirkin M, Sanders R, DiPasquale T, Herscovici D. A staged protocol for soft tissue management in the treatment of complex pilon fractures. J Orthop Trauma. 1999;2:78-84.
12
Koval KJ, Clapper MF, Brumback RJ. Complications of reamed intramedullary nailing of the tibia. J Orthop Trauma. 1991;5:184-9.
13
Robinson CM, McLauchlan GJ, McLean IP, Court-Brown CM. Distal metaphyseal fractures of the tibia with minimal involvement of the ankle. Classification and treatment by locked intramedullary nailing. J Bone Joint Surg Br. 1995;77:781-7.
14
Mazur JM, Schwartz E, Sheldon RS. Ankle arthrodesis: Long-term follow-up with gait analysis. J Bone Joint Surg. 1979;61-A:964-75.
15
Ruedi TP, Allgower M. The operative treatment of intraarticular fractures of the lower end of the tibia. ClinOrthop. 1979;138:105-10.
16
Etter G, Ganz R. Long-term results of tibial plafond fractures treated with open reduction and internal fixation. Arch Orthop Trauma Surg. 1991;110:277-83.
17
Mcferran M, Smith S, Boulas HJ. Complications encountered in the treatment of pilon fractures. J Orthop Trauma. 1992; 6:195-200.
18
Marsh JL, Mueling V, Dirschl DR, Hurwitz S, Brown TD, Nepola J. Tibial plafond fracture: Articulated external fixation with and without motion similar, J Orthop Trauma. 2006;20(8):536-41.
19
Okcu G, Aktuglu K. Intra-articular fractures of the tibial plafond a comparison of the results using articulated and ring external fixators. J Bone Joint Surg. 2004;86-B:868-75.
20
Kapukaya A, Subasi M, Arslan H. Management of comminuted closed tibial plafond fractures using circular external fixators. ActaOrthop Belg. 2005;71:582-9.
21
Antoci V, Voor MJ, Seligson D, Roberts CS. Biomechanics of external fixation of distal tibial extra-articular fractures: is spanning the ankle with a foot plate desirable? J Orthop Trauma. 2004;18(10):665-73.
22
Pugh KJ, Wolinsky PR, McAndrew PM, Johnson KD. Tibialpilon fractures: a comparison of treatment methods. J Trauma. 1999;47:937-42.
23
Leung KL, Kwok HY, Pun TS, Chow SP. Open reduction and Ilizarov external fixation in the treatment of distal tibial fractures Injury. 2004;35:278-83.
24
Varsalona R, Liu GT. Fibular fixation in distal tibial metaphyseal fractures. Strat Traum Limb Recon. 2006;1:42-50.
25
ORIGINAL_ARTICLE
The Use of Interleukin-22 as a Novel Marker of Disease Activity in Female Patients with Rheumatoid Arthritis
Rheumatoid arthritis (RA) is a systemic autoimmune disease characterized by progressively destructive joint inflammation and destruction of articular cartilage, bone and synovial hyperplasia. Cytokines play a fundamental role in the processes that cause inflammation, articular destruction and extra-articular manifestations associated with RA.The preferential production of interleukin22 (IL22) by T cells suggests that elevated levels of this cytokine exist in chronic, T cell-mediated diseases, such as psoriasis and RA and that IL-22 plays an important role in the pathogenesis of these disorders. Objective: To study the role of IL-22 in RA. Methods:IL-22 serum levelswere measuredin55 female patients with RA, 28 of them on medical treatment and the other 27 were newly diagnosed patients and in 18 healthy controls. Patients are assessed for clinical and laboratory variables. Correlations of IL-22 serum levels with disease activity markers as disease activity score for 28 joints (DAS28), serological markers, bone erosions were assessed. Results: IL-22 levels were increased in patients with RA compared with controls (mean 34.6 pg/ml and 3.2pg/ml, respectively; P < 0.001). Levels of IL-22 correlated positively with DAS28 score (P <0.001). C-reactive protein (CRP) correlated positivity with high levels of IL-22 in RA patients (mean 53.8 pg/ml; P < 0.001) and rheumatoid factor (RF) correlated positivity with high levels of IL-22 in RA patients (mean 46.1 pg/ml;P < 0.001). The presence of bone erosions was associated with high IL-22 levels (P = 0.008). Conclusion:IL-22 is elevated in the serum of patients with RA.Elevated serum IL-22allows discrimination between patients with different clinical and laboratory measures and indicates thepotential of IL-22 as an additional tool for assessment of activity in RA, particularly in patients with RFantibodies. IL-22 is associated with bone destructive disease.
https://smj.journals.ekb.eg/article_40904_ea5fc0d13248fbc4ea9078a3fa85ecb5.pdf
2018-01-01
143
153
10.21608/smj.2018.40904
Interleukin-22
Rheumatoid Arthritis
disease activity
Disease activity score 28
Laila
Yousef
lailamohamed@med.sohag.edu.eg
1
Department of Clinical and Chemical pathology, Faculty of Medicine, Sohag University.
AUTHOR
Sahar
Aboalftoh
sahr_mahran@med.sohag.edu.eg
2
Department of Clinical and Chemical pathology, Faculty of Medicine, Sohag University.
AUTHOR
Tamer
Abdel-Latef
tamer_soliman@med.sohag.edu.eg
3
Department of Clinical and Chemical pathology, Sohag Faculty of Medicine, Sohag University.
AUTHOR
Khalid
Ali
4
Department of Clinical and Chemical pathology, Faculty of Medicine, Sohag University.
AUTHOR
1. Feldmann M., Brennan F.M., Maini R.N. (1996): Role of cytokines in rheumatoid arthritis. Annu. Rev. Immunol. 14, 397–440.
1
2. Tian J., Yong J., Dang H., Kaufman D.L. (2011):Oral gaba treatment downregulates inflammatory responses in amouse model of rheumatoid arthritis. Autoimmunity 44, 465–470.
2
3. Sakaguchi S., Benham H., Cope A.P., Thomas R. (2012):T-cell receptor signaling and the pathogenesis ofautoimmune arthritis: Insights from mouse and man. Immunol. Cell. Biol. 90, 277–287.
3
4. Choy E.H. and Panayi G.S. (2001):Cytokine pathways and joint inflammation in rheumatoid arthritis. Engl. J. Med.344, 907–916.
4
5. Linsley P.S. and Nadler S.G. (2009):The clinical utility of inhibiting cd28-mediated costimulation. Immunol. Rev. 229, 307–321.
5
6. Sprent J. and Surh C.D. (2011):Normal t cell homeostasis: The conversion of naive cells into memory-phenotype cells.Nat. Immunol. 12, 478–484.
6
7. Devergne O., Hummel M., Koeppen H., Le Beau M.M., Nathanson E.C., Kieff E., Birkenbach M. (1996):A novelinterleukin-12 p40-related protein induced by latent epstein-barr virus infection in b lymphocytes. J. Virol. 70, 1143–1153.
7
8. Wolk K. and Sabat R. (2006):Interleukin-22: A novel T- and NK-cell derived cytokine that regulates the biology of tissue cells. Cytokine Growth Factor Rev;17:367-80..
8
9.Zenewicz L.A. and Flavell R.A. (2011):Recent advances in IL-22 biology. Int Immunol. 23:159-63.
9
10. Xie M.H., Aggarwal S, Ho WH, Foster J, Zhang Z, Stinson J, et al. (2000):Interleukin (IL)-22, a novel human cytokine that signals through the interferon receptor-related proteins CRF2-4 and IL-22R. J Biol Chem 275:31335-9.
10
11.Kotenko S.V., Izotova L.S., Mirochnitchenko O.V., Esterova E., Dickensheets H, Donnelly RP, et al. (2001):Identification of the functional interleukin-22 (IL-22) receptor complex: The IL-10R2 chainIL-10R-beta) is a common chain of both the IL-10 and IL-22IL-10-related T cell-derived inducible factor, IL-TIF) receptor complexes. J Biol Chem 276:2725 32.
11
12. Liang S.C., Tan X.Y., Luxenberg D.P., Karim R., Dunussi-Joannopoulos K., Collins M., et al. (2006):Interleukin (IL)-22 and IL-17 are coexpressed by Th17 cells and cooperatively enhance expression of antimicrobial peptides. J Exp Med 203:2271-9.
12
13. Andoh A., Zhang Z., Inatomi O., Fujino S., Deguchi Y., Araki Y., et al. (2005):Interleukin-22, a member of the IL-10 subfamily, induces inflammatory responses in colonic subepithelial myofibroblasts. Gastroenterology 129:969-84.
13
14. Ikeuchi H., Kuroiwa T., Hiramatsu N., Kaneko Y., Hiromura K., Ueki K., et al. (2005):Expression of interleukin-22 in rheumatoid arthritis: Potential role as a proinflammatory cytokine. Arthritis Rheum 52:1037-46.
14
15. Leipe J., Schramm M.A., Grunke M., Baeuerle M., Dechant C., Nigg A.P., et al. (2011):Interleukin 22 serum levels are associated with radiographic progression in rheumatoid arthritis. Ann Rheum Dis 70:1453-7.
15
16. Shen H., Goodall J.C. and Hill Gaston J.S. (2009):Frequency and phenotype of peripheral blood Th17 cells in ankylosing spondylitis and rheumatoid arthritis. Arthritis Rheum 60:1647-56.
16
17. Shen H., Goodall J.C. and Gaston J.S. (2010):Frequency and phenotype of T helper 17 cells in peripheral blood and synovial fluid of patients with reactive arthritis. J Rheumatol;37:2096-9.
17
18. Wolk K., Kunz S., Witte E., Friedrich M., Asadullah K. and Sabat R. (2004):IL-22 increases the innate immunity of tissues. Immunity 21:241-54.
18
19. Lavoie T.N., Stewart C.M., Berg K.M., Li Y., Nguyen C.Q. (2011):Expression of interleukin-22 in Sjogren’s syndrome: Significant correlation with disease parameters. Scand J Immunol 74:377-82.
19
20. Cascao R., Moura R.A., Perpetuo I., Canhao H., Vieira-Sousa E., Mourao A.F., et al. (2010):Identification of a cytokine network sustaining neutrophil and Th17 activation in untreated early rheumatoid arthritis. Arthritis Res Ther 12:R196.
20
21. Aletaha D., Neogi T., Silman A.J. et al. (2010): Rheumatoid arthritis classification criteria: An American Colleague of Rheumatology/European League against Rheumatism Collaborative initiative. Arthritis and Rheumatism, 62, 2569-2581
21
22. Prevoo M.L., van’t Hof M.A., Kuper H.H., van Leeuwen M.A., van de Putte L.B., and van Riel P.L :(1995).Modified disease activity scores that include twenty-eight-joint counts. Development and validation in a prospective longitudinal study of patients with rheumatoid arthritis. Arthritis Rheum; 38:44-8.
22
23.Westergren (1991): Studies of the suspension stability of blood in pulmonary tuberculosis. Acta Medica; 54: 247.
23
24.Fisher C.L., Nakamura R. and Amr J. (1976): laboratory medicine immunology. Immunol; 20 (6) 12 – 15.
24
25.Heller G., Jacobson S., Koloday M. et al., (1954): The determination of rheumatoid factor. Immunol; 6 (1): 46 – 50.
25
26.Coenen D., Verschueren P., Westhovens R. and Bossuyt X. (2007): Technical and diagnostic performance of 6 assays for the measurement of citrullinated protein/peptide antibodies in the diagnosis of rheumatoid arthritis. Clin Chem; 53(3):498-504.
26
27. Larsen A. (1995): How to apply Larsen Score in evaluating radiographs of rheumatoid arthritis in long term studies? J Rheumatol. 22: 1974-1975.
27
28. Piccoli A.K., Alegretti A.P., Schneider L., Schmidt P.L. and Xavier R.M. (2011):Expression of complement regulatory proteins CD55, CD59, CD35, and CD46 in rheumatoid arthritis. Rev Bras Reumatol; 51(5):497-510
28
29. Liu F.L., Chen C.H., Chu S.J., Chen J.H., Lai J.H. Sytwu H.K. and Chang D.M. (2007): Interleukin (IL)-23 p19 expression induced by IL-1beta in human fibroblast-like synoviocytes with rheumatoid arthritis via active nuclear factor-kappaB and AP-1 dependent pathway. Rheumatology (Oxford). 46: 1266–1273.
29
30.Wolk K., Witte E., Witte K., Warszawska K. and Sabat R. (2010): Biology of interleukin-22, Semin Immunopathol 32:17–31.
30
31. Rocha Jr L.F., Duarte A.L., Dantas A.T., Mariz H.A., Pitta I.D., Galdino S.L., et al. (2012): Increased serum interleukin 22 in patients with rheumatoid arthritis and correlation with disease activity. Journal of Rheumatology; 39; 1320-1325.
31
32. Egila. S., Osama S., Emtethal A.S. and Shimaa H.M. (2014): Serum IL-22 in rheumatoid arthritis patients; Page 81 – 96
32
33. Zhang L., J. M. Li, X.G. Liu, et al. (2011): Elevated Th22 cells correlated with Th17 cells in patients with rheumatoid arthritis. J. Clin. Immunol. 31: 606–614.
33
34. Pan Hai-Feng, Xiang-Pei Li, Song Guo Zheng and Dong-Qing Y (2013): Emerging role of interleukin-22 in autoimmune diseases Cytokine & Growth Factor Reviews. 24: 51–57.
34
ORIGINAL_ARTICLE
Efficacy of microneedling in treatment of acne scars
Introduction: Microneedling is a relatively new minimally invasive procedure involving superficial and controlled puncturing of the skin by rolling with miniature fine needles.Traditionally used as a collagen induction therapy for skin rejuvenation and facial scars specially acne scars. Aim of the work: Evaluation of efficacy of microneedling in treatment of acne scars. Patients and Methods: Ten patients with post acne atrophic facial scars attending the outpatient clinic of Dermatology in Sohag University Hospitals between June2014 to September 2017 were offered six sessions of microneedling at an interval of 1 month.They were evaluated monthly and one month after completion of sessions for both efficacy and safety of the procedure. Results: The mean ± SD of the patients' age in the study population were26.900±5.952years old.eight females and two males with mean acne scars duration ± SD 8.500±6.311 years, 60% of patients had psychological distress from their acne scars. At the end of study duration Out of the ten patients 7(70%) achieved one grade reduction in their Goodman and Baron qualitative grading score while 4 patients (40% ) achieved reduction in their quantitative ECCA " Echella d'e valuation Clinique des cicatrices d'acne" score with 8.55% improvement in the ECCA score. The mean ECCA score value of V scar started to decrease earlier than U scar , but M scar was fixed up to end of sessions. 50% of patients had good satisfaction, 30% of them had very good satisfaction and only 10% had excellent satisfaction. All treated patients , had adverse events of temporary erythema, edema, bleeding, or a serous ooze resolving with crusting or scabbing following each session of microneedling but in 1 patient (10%) aggravation of acne occurred, bacterial infection not occurred in any of our patients. Conclusion: Multiple minimally invasive sessions of skin microneedling is an effective treatment for post-acne atrophic scars with the advantage of being a relatively risk-free, in-office procedure with minimal patient recovery time.
https://smj.journals.ekb.eg/article_40927_ee7186859ff97ffb497e2689da1bac36.pdf
2018-01-01
155
162
10.21608/smj.2018.40927
Acne
scar
Microneedling
ESSAMELDIN
NADA
essameldin_nada@med.sohag.edu.eg
1
Department of Dermatology , Venereology and Andrology, Faculty of Medicine , sohag university.
AUTHOR
Ramadan
Abdo
ramadan_saleh@med.sohag.edu.eg
2
Department , of Dermatology, Venereology and Andrology , Faculty of Medicine- , Sohag University.
AUTHOR
Rasha
Mohhmed
rashaismail@med.sohag.edu.eg
3
Department of Dermatology, Faculty of Medicine, Sohag University.
AUTHOR
Mohammed
Mostafa
4
Department of Dermatology, Faculty of Medicine, Sohag University.
AUTHOR
1. Admani S, Barrio VR. Evaluation and treatment of acne from infancy to preadolescence. Dermatologic therapy. 2013;26(6):462-6.
1
2. Fabbrocini G, Annunziata MC, D'Arco V, De Vita V, Lodi G, Mauriello MC, et al. Acne scars: pathogenesis, classification and treatment. Dermatology research and practice. 2010;2010:893080.
2
3. Cunliffe WJ, Gould DJ. Prevalence of facial acne vulgaris in late adolescence and in adults. British medical journal. 1979;1(6171):1109-10
3
4. Midwood KS, Williams LV, Schwarzbauer JE. Tissue repair and the dynamics of the extracellular matrix. The international journal of biochemistry & cell biology. 2004;36(6):1031-7.
4
5. Kravvas G, Veitch D, Al-Niaimi F. The increasing relevance of biofilms in common dermatological conditions. The Journal of dermatological treatment. 2017:1-6.
5
6. Fernandes D. Minimally invasive percutaneous collagen induction. Oral and maxillofacial surgery clinics of North America. 2005;17(1):51-63, vi.
6
7. Doddaballapur S. Microneedling with dermaroller. Journal of cutaneous and aesthetic surgery. 2009;2(2):110-1.
7
8 . Bariya SH, Gohel MC, Mehta TA, Sharma OP. Microneedles: an emerging transdermal drug delivery system. The Journal of pharmacy and pharmacology. 2012;64(1):11-29.
8
9. Fabbrocini G, Fardella N, Monfrecola A, Proietti I, Innocenzi D. Acne scarring treatment using skin needling. Clinical and experimental dermatology. 2009;34(8):874-9.
9
10. Goodman GJ, Baron JA. Postacne scarring: a qualitative global scarring grading system. Dermatologic surgery : official publication for American Society for Dermatologic Surgery [et al]. 2006;32(12):1458-66.
10
11. Dreno B, Khammari A, Orain N, Noray C, Merial-Kieny C, Mery S, et al. ECCA grading scale: an original validated acne scar grading scale for clinical practice in dermatology. Dermatology. 2007;214(1):46-51.
11
12. Leheta T, El Tawdy A, Abdel Hay R, Farid S. Percutaneous collagen induction versus full-concentration trichloroacetic acid in the treatment of atrophic acne scars. Dermatologic surgery : official publication for American Society for Dermatologic Surgery [et al]. 2011;37(2):207-16.
12
13. Sharad J. Combination of microneedling and glycolic acid peels for the treatment of acne scars in dark skin. Journal of cosmetic dermatology. 2011;10(4):317-23.
13
14. Gadkari R, Nayak C. A split-face comparative study to evaluate efficacy of combined subcision and dermaroller against combined subcision and cryoroller in treatment of acne scars. Journal of cosmetic dermatology. 2014;13(1):38-43.
14
15. Leheta TM, Abdel Hay RM, El Garem YF. Deep peeling using phenol versus percutaneous collagen induction combined with trichloroacetic acid 20% in atrophic post-acne scars; a randomized controlled trial. The Journal of dermatological treatment. 2014;25(2):130-6.
15
16. El-Domyati M, Barakat M, Awad S, Medhat W, El-Fakahany H, Farag H. Microneedling Therapy for Atrophic Acne Scars: An Objective Evaluation. The Journal of clinical and aesthetic dermatology. 2015;8(7):36-42
16
17. Majid I. Microneedling therapy in atrophic facial scars: an objective assessment. Journal of cutaneous and aesthetic surgery. 2009;2(1):26-30.
17
18. Chawla S. Split Face Comparative Study of Microneedling with PRP Versus Microneedling with Vitamin C in Treating Atrophic Post Acne Scars. Journal of cutaneous and aesthetic surgery. 2014;7(4):209-12.
18
19. Dogra S, Yadav S, Sarangal R. Microneedling for acne scars in Asian skin type: an effective low cost treatment modality. Journal of cosmetic dermatology. 2014;13(3):180-7.
19
20. Nofal E, Helmy A, Nofal A, Alakad R, Nasr M. Platelet-rich plasma versus CROSS technique with 100% trichloroacetic acid versus combined skin needling and platelet rich plasma in the treatment of atrophic acne scars: a comparative study. Dermatologic surgery : official publication for American Society for Dermatologic Surgery [et al]. 2014;40(8):864-73.
20
21. Asif M, Kanodia S, Singh K. Combined autologous platelet-rich plasma with microneedling verses microneedling with distilled water in the treatment of atrophic acne scars: a concurrent split-face study. Journal of cosmetic dermatology. 2016;15(4):434-43.
21
22. Fabbrocini G, De Vita V, Di Costanzo L, Pastore F, Mauriello MC, Ambra M, et al. Skin needling in the treatment of the aging neck. Skinmed. 2011;9(6):347-51.
22
23. Singh A, Yadav S. Microneedling: Advances and widening horizons. Indian dermatology online journal. 2016;7(4):244-54.
23
24. Harris AG, Naidoo C, Murrell DF. Skin needling as a treatment for acne scarring: An up-to-date review of the literature. International journal of women's dermatology. 2015;1(2):77-81.
24
ORIGINAL_ARTICLE
Efficacy of microneedling with topical vitamin C in treatment of acne scars
Introduction: Acne scars are largely preventable complications of acne. 95% of the scars occur over the face thus impacting the quality of life. Correction of scars is the priority for acne patients. There is no single treatment modality that has been shown to be universally effective. Microneedling is a relatively new minimally invasive procedure used as a collagen induction therapy for skin rejuvenation and facial scars. Aim of the work: Evaluation of efficacy of microneedling with topical vitamin C in treatment of acne scars. Patients and Methods: Ten patients with post acne atrophic facial scars attending the outpatient clinic of Dermatology in Sohag University Hospitals between June 2014 to September 2017 were offered six microneedling sessions plus topical vit. C (during the session of microneedling and daily topical application in between sessions) microneedling sessions were four weeks apart. They were evaluated monthly and one month after completion of sessions for both efficacy and safety of the procedure. Results: The mean ± SD of the patients' age in the study population were 28.900 ±5.384yers old nine females and one males with mean acne scars duration ± SD 11.900±5.506 years, 90%% of patients had psychological distress from their acne scars. At the end of study duration Out of the ten patients 6(60%) achieved one grade reduction in their Goodman and Baron qualitative grading score and 2 (20%) achieved two grade reduction. According to the quantitative ECCA " Echella d'e valuation Clinique des cicatrices d'acne" score 80% 0f patients achieved reduction in their score with 27.5% improvement in the ECCA score. The mean ECCA score value of V scar started to decrease earlier than both U scar, and M scar. 40% of patients had excellent satisfaction and 60% had very good satisfaction. All treated patients, had adverse events of temporary erythema, edema, bleeding, or a serous ooze resolving with crusting or scabbing following each session of microneedling, bacterial infection not occurred in any of our patients. Conclusion: Multiple minimally invasive sessions of skin microneedling with topical vitamin C during sessions and daily application is an effective treatment for post-acne atrophic scars with the advantage of being a relatively risk-free, in-office procedure with minimal patient recovery time.
https://smj.journals.ekb.eg/article_40958_c9563750652df58d20d3cf739449999c.pdf
2018-01-01
163
170
10.21608/smj.2018.40958
Microneedling
Vitamen C
acne scar
ESSAMELDIN
NADA
essameldin_nada@med.sohag.edu.eg
1
DERMATOLOGY, Venereology and Andrology, Faculty of Medicine , sohag university
AUTHOR
Ramadan
Abdo
ramadan_saleh@med.sohag.edu.eg
2
Department , of Dermatology, Venereology and Andrology , Faculty of Medicine- , Sohag University
AUTHOR
Mohammed
Mostafa
3
Department of Dermatology, Faculty of Medicine, Sohag University.
AUTHOR
Rasha
Mohhmed
rashaismail@med.sohag.edu.eg
4
Department of Dermatology, Faculty of Medicine, Sohag University.
AUTHOR
1. Admani S, Barrio VR. Evaluation and treatment of acne from infancy to preadolescence. Dermatologic therapy. 2013;26(6):462-6.
1
2. Fabbrocini G, Annunziata MC, D'Arco V, De Vita V, Lodi G, Mauriello MC, et al. Acne scars: pathogenesis, classification and treatment. Dermatology research and practice. 2010;2010:893080.
2
3. Layton AM, Henderson CA, Cunliffe WJ. A clinical evaluation of acne scarring and its incidence. Clinical and experimental dermatology. 1994;19(4):303-8.
3
4. Cunliffe WJ, Gould DJ. Prevalence of facial acne vulgaris in late adolescence and in adults. British medical journal. 1979;1(6171):1109-10.
4
5. Midwood KS, Williams LV, Schwarzbauer JE. Tissue repair and the dynamics of the extracellular matrix. The international journal of biochemistry & cell biology. 2004;36(6):1031-7.
5
6. Kravvas G, Veitch D, Al-Niaimi F. The increasing relevance of biofilms in common dermatological conditions. The Journal of dermatological treatment. 2017:1-6.
6
7. Fernandes D. Minimally invasive percutaneous collagen induction. Oral and maxillofacial surgery clinics of North America. 2005;17(1):51-63, vi.
7
8. Doddaballapur S. Microneedling with dermaroller. Journal of cutaneous and aesthetic surgery. 2009;2(2):110-11
8
9. Bariya SH, Gohel MC, Mehta TA, Sharma OP. Microneedles: an emerging transdermal drug delivery system. The Journal of pharmacy and pharmacology. 2012;64(1):11-29.
9
10. Fabbrocini G, Fardella N, Monfrecola A, Proietti I, Innocenzi D. Acne scarring treatment using skin needling. Clinical and experimental dermatology. 2009;34(8):874-9.
10
11. Oresajo C, Stephens T, Hino PD, Law RM, Yatskayer M, Foltis P, et al. Protective effects of a topical antioxidant mixture containing vitamin C, ferulic acid, and phloretin against ultraviolet-induced photodamage in human skin. Journal of cosmetic dermatology. 2008;7(4):290-7.
11
12. Chen L, Hu JY, Wang SQ. The role of antioxidants in photoprotection: a critical review. Journal of the American Academy of Dermatology. 2012;67(5):1013-24.
12
13. Sauermann K, Jaspers S, Koop U, Wenck H. Topically applied vitamin C increases the density of dermal papillae in aged human skin. BMC dermatology. 2004;4(1):13.
13
14. Goodman GJ, Baron JA. Postacne scarring: a qualitative global scarring grading system. Dermatologic surgery : official publication for American Society for Dermatologic Surgery [et al]. 2006;32(12):1458-66.
14
15. Dreno B, Khammari A, Orain N, Noray C, Merial-Kieny C, Mery S, et al. ECCA grading scale: an original validated acne scar grading scale for clinical practice in dermatology. Dermatology. 2007;214(1):46-51.
15
16. Leheta T, El Tawdy A, Abdel Hay R, Farid S. Percutaneous collagen induction versus full-concentration trichloroacetic acid in the treatment of atrophic acne scars. Dermatologic surgery : official publication for American Society for Dermatologic Surgery [et al]. 2011;37(2):207-16.
16
17. Sharad J. Combination of microneedling and glycolic acid peels for the treatment of acne scars in dark skin. Journal of cosmetic dermatology. 2011;10(4):317-23
17
18. El-Domyati M, Barakat M, Awad S, Medhat W, El-Fakahany H, Farag H. Microneedling Therapy for Atrophic Acne Scars: An Objective Evaluation. The Journal of clinical and aesthetic dermatology. 2015;8(7):36-42.
18
19. Gadkari R, Nayak C. A split-face comparative study to evaluate efficacy of combined subcision and dermaroller against combined subcision and cryoroller in treatment of acne scars. Journal of cosmetic dermatology. 2014;13(1):38-43.
19
20. Leheta TM, Abdel Hay RM, El Garem YF. Deep peeling using phenol versus percutaneous collagen induction combined with trichloroacetic acid 20% in atrophic post-acne scars; a randomized controlled trial. The Journal of dermatological treatment. 2014;25(2):130-6.
20
21. Majid I. Microneedling therapy in atrophic facial scars: an objective assessment. Journal of cutaneous and aesthetic surgery. 2009;2(1):26-30.
21
22. Chawla S. Split Face Comparative Study of Microneedling with PRP Versus Microneedling with Vitamin C in Treating Atrophic Post Acne Scars. Journal of cutaneous and aesthetic surgery. 2014;7(4):209-12.
22
23. Dogra S, Yadav S, Sarangal R. Microneedling for acne scars in Asian skin type: an effective low cost treatment modality. Journal of cosmetic dermatology. 2014;13(3):180-7.
23
24. Nofal E, Helmy A, Nofal A, Alakad R, Nasr M. Platelet-rich plasma versus CROSS technique with 100% trichloroacetic acid versus combined skin needling and platelet rich plasma in the treatment of atrophic acne scars: a comparative study. Dermatologic surgery: official publication for American Society for Dermatologic Surgery [et al]. 2014;40(8):864-73.
24
25. Pinnell SR, Yang H, Omar M, Monteiro-Riviere N, DeBuys HV, Walker LC, et al. Topical L-ascorbic acid: percutaneous absorption studies. Dermatologic surgery : official publication for American Society for Dermatologic Surgery [et al]. 2001;27(2):137-42.
25
26. Matsuda S, Shibayama H, Hisama M, Ohtsuki M, Iwaki M. Inhibitory effects of a novel ascorbic derivative, disodium isostearyl 2-O-L-ascorbyl phosphate on melanogenesis. Chemical & pharmaceutical bulletin. 2008;56(3):292-7.
26
27. Fabbrocini G, De Vita V, Di Costanzo L, Pastore F, Mauriello MC, Ambra M, et al. Skin needling in the treatment of the aging neck. Skinmed. 2011;9(6):347-51.
27
28. Alam M, Han S, Pongprutthipan M, Disphanurat W, Kakar R, Nodzenski M, et al. Efficacy of a needling device for the treatment of acne scars: a randomized clinical trial. JAMA dermatology. 2014;150(8):844-9.
28
ORIGINAL_ARTICLE
Association of CA 15-3 and CEA with Clinicopathological Parameters In Patients With Metastatic Breast Cancer
Background. Breast cancer is the most common cancer and the leading cause of cancer death for women, a third of women are diagnosed with breast cancer at a late stage when the disease has a poor prognosis. Serum tumor markers have been widely used as noninvasive tools for measuring treatment response, early diagnosis of recurrence and predicting prognosis. In breast cancer, the most widely used serum tumor markers are cancer antigen 15-3 (CA 15-3) and carcinoembryonic antigen (CEA). The aim of this study was to investigate the association of serum CA15-3 and CEA levels with clinicopathological parameters in patients diagnosed with metastatic breast cancer (MBC). Patients and methods. This retrospective study was conducted on 50 patients who had used to predict response to chemotherapy in patients with metastatic breast cancer. The concentration of serum CA15-3 and CEA levels were measured using chemiluminescent enzyme immunoassays (ABBOTT ARCHITECT). The upper limits of normal for CA15-3 and CEA were 31.3 U/ml and 5 ng/ml, respectively. Result. Of the 50 patients, elevated CA 15-3 and CEA levels at initial diagnosis of recurrence were identified in 37 (74%) and 32 (64%) patients, respectively. Elevated CA 15-3 and CEA levels were significantly associated with breast cancer molecular subtypes (P=0.005 and P=0.008, respectively). Elevated CA 15-3 level was correlated with bone metastasis (P=0.047). Conclusion. CA 15-3 and CEA level elevation at initial diagnosis of recurrence were found to be associated with breast cancer molecular subtype; these serum tumor markers are frequently increased in the HER2-enriched and triple negative (TN) molecular subtypes of breast cancer.
https://smj.journals.ekb.eg/article_40972_af30ed9a4047aea0926efd346abb54c6.pdf
2018-01-01
173
178
10.21608/smj.2017.40972
Zeinab
Mahmoud
zainbdiab@med.sohag.edu.eg
1
Department of clinical and chemical pathology, Sohag Faculty of Medicine, Sohag University.
AUTHOR
Sahar
Abd Elwahed
sahr_mahran@med.sohag.edu.eg
2
Department of Clinical and Chemical pathology, Faculty of Medicine, Sohag University.
AUTHOR
Doaa
El Badry
3
Department of Clinical Pathology, Faculty of medicine, Sohag university.
AUTHOR
Ahmed
Mohammed
ahmed_ahmed3@med.sohag.edu.eg
4
Department of clinical pathology, Faculty of medicine, Sohag university.
AUTHOR
1- Garcia M et al (2007). Global Cancer Facts & Figures. Atlanta, GA: American Cancer Society.
1
2- Sayer HG, Kath R, Kliche KO and Höffken K (2002): Premenopausal breast cancer: chemotherapy and endocrine therapy. Drugs 62: 202-520;38.
2
3- De Bono JS, Tolcher AW and Rowinsky EK (2003): The future of cytotoxic therapy: selective cytotoxicity based on biology is the key. Breast Cancer Res 5: 154-159
3
4- Yonemori K, Katsumata N, Noda A, et al (2008): Development and verification of a prediction model using serum tumor markers to predict the response to chemotherapy of patients with metastatic or recurrent breast cancer. J Cancer Res Clin Oncol 134: 1199 -1206.
4
5- Lumachi F, Basso S, Brandes A, Pagano D and Ermani M (2004)
5
470, Pages 51–55 Relationship Between Tumor Markers CEA and CA 15-3, TNM Staging, Estrogen Receptor Rate and MIB-1 Index in Patients with pT1-2 Breast Cancer.
6
6- Hosseni S.M, Ramjoo S, Arvandi S.H and Barat T (2015). CEA and CA 15-3 Serum Level in Metastatic Breast Cancer and Its Correlation with Distant Metastasis. Biomedical & Pharmacology Journal; Vol. 8 :721-727
7
7- Shao Y, Sun X, He Y, Liu C, Liu H.
8
(2015) Elevated Levels of Serum Tumor
9
Markers CEA andCA15-3 Are Prognostic Parameters for Different Molecular Subtypes of Breast Cancer. PLoS ONE 10(7).
10
8- Wu S.G, He Z.Y, Zhou J, Sun J.Y, Li F.Y, Lin Q, Guo L and Lin H.X(2014)
11
Serum levels of CEA and CA15-3 in different molecular subtypes and prognostic value in Chinese breast cancer. The Breast; 23: 88- 93.
12
9-Geng Biao, Man-Man, Liang Xiao-, et al. (2015) Molecular and Clinical Oncology 3: 232-236.
13
10-Weigang Wang, Xiaoqin Xu, Baoguo Tian, et al (2017) The diagnostic value of serum tumor markers CEA, CA19-9, CA125, CA15-3, and TPS in metastatic breast cancer Clinica Chimica Acta Volume.
14
ORIGINAL_ARTICLE
Comparative Prospective Study Between Platlete Rich Plasma and Steroid Injection in Treatment of Chronic Planter Fasciitis
Purpose:Compare the results of injection of steroid and PRP in cases of chronic plantar fasciitis
INTRODUCTION: plantar fasciitis can be a difficult condition to treat. results of platelet rich plasma (PRP) injection have been promising. We compared PRP to cortisone injection in the treatment of chronic plantar fasciitis resistant to conservative management.
METHODS:38 heels (20 heels in the steroid group and 18heels in the PRP group) with plantar fasciitis failed conservative treatment were included to receive either PRP or Steroid injection. All patients were assessed by Visual Analogue Score (VAS) for pain, at 2 weeks 1 month and 3months post injection .
RESULTS:Our study included 38 patients; 20 in the steroid arm and 18 had PRP injections. The average age of the steroid injection group was 43.1±9.7 years and in the PRP was 43.1±8.4 years (P= 0.698).
The starting average pain scores were 8.6 for both groups (P= 0.712). Then our patients were followed up clinically at 2 weeks, 1 month and 3 months following the injections. There was statistically significant lower VAS scores for the steroid injection group at all follow up visits (P< 0.001 in all follow ups). The average pain scores were 4.9 and 6.7 at 2 weeks follow up for the steroid injection versus the PRP respectively, it was 2 and 4.2 at 1 month and last 0.6 and 1.2 after 3 months respectively.
CONCLUSIONS:PurposThe purpose of this study was to assess the safety and preliminary clinical results of platelet-rich plasma (PRP) injections for treating chronic plantar fasciitisMethods
Fourteen consecutive patients with chronic plantar fasciitis receiving three injections of PRP into the plantar fascia were assessed 12 months after the procedure. The modified Roles and Maudsley score and a visual analogue scale (VAS) for pain were used to evaluate the clinical results.
Results
According to criteria of the Roles and Maudsley score, at 12 months of follow-up, results were rated as excellent in nine (64.3 %), good in two (14.3 %), acceptable in two (14.3 %) and poor in one (7.1 %) patient. VAS for pain was significantly decreased from 7.1 ± 1.1 before treatment to 1.9 ± 1.5 at the last follow-up (p < 0.01).
Conclusions
In this single-centre, uncontrolled, prospective, preliminary study, results indicate that treating chronic plantar fasciitis with PRP injections is safe and has the potential to reduce pain.
This study demonstrates that both steroid and PRP injections are highly effective in treatment of chronic plantar fasciitis but improvement in pain was more rapid with steroid injection. This study recommends for follow up for a longer period than three months to compare long term benefits of steroids and PRP.
https://smj.journals.ekb.eg/article_40981_9510ae00e330c04990a4c523005d975b.pdf
2018-01-01
181
186
10.21608/smj.2018.40981
Wael
salama
waeladel@med.sohag.edu.eg
1
Department of Orthopedics and Traumatology, Faculty of medicine, Sohag university, Egypt
AUTHOR
Mostafa
Ibrahim
mostafaismail@med.sohag.edu.eg
2
Department of Orthpaedic and Traumatology , Faculty of Medicine, Sohag University.
AUTHOR
Abdel Rahman
Abo takia
3
Department of Orthopedics and Traumatology, Faculty of medicine, Sohag university, Egypt
AUTHOR
Abdel Rahman
El sheikh
4
Department of Orthopedics and Traumatology, Faculty of medicine, Sohag university, Egypt.
AUTHOR
1. Dunn JE, Link CL, Felson DT et al. Prevalence of foot and ankle conditions ina multiethnic community sample of older adults. Am J Epidemiol 2004; 159:491–498.
1
2. Riddle DL, Schappert SM. Volume of ambulatory care visits and patterns ofcare for patients diagnosed with plantar fasciitis: a national study of medicaldoctors. Foot Ankle Int 2004; 25: 303–310.
2
3. Riddle DL, Pulisic M, Pidcoe P, Johnson RE. Risk factors for plantar fasciitis: amatched case-control study. J Bone Joint Surg Am 2003; 85: 872–877.
3
4. Gill LH. Plantar fasciitis: diagnosis and conservative management. J Am AcadOrthopSurg 1997; 5: 109–117
4
5. Hicks JH. The mechanics of the foot. II. The plantar aponeurosis and the arch.J Anat 1954; 88: 25–30.
5
6. Woolnough J. Tennis heel. Med J Aust 1954; 2: 857.
6
7. Lemont H, Ammirati KM, Usen N. Plantar fasciitis: a degenerative process(fasciosis) without inflammation. J Am Podiatr Med Assoc 2003; 93: 234–237.
7
8. Schon LC, Glennon TP, Baxter DE. Heel pain syndrome: electrodiagnosticsupport for nerve entrapment. Foot Ankle 1993; 14: 129–135.
8
9. Tanz SS. Heel pain. ClinOrthopRelat Res 1963; 28: 169–178.
9
10. Shmokler RL, Bravo AA, Lynch FR, Newman LM. A new use of instrumentation in fluoroscopy controlled heel spur surgery. J Am Podiatr Med Assoc 1988; 78:194–197.
10
11. Chimutengwende-Gordon M, O’Donnell P, Singh D. Magnetic resonance imagingin plantar heel pain. Foot Ankle Int 2010; 31: 865–870.
11
12. Donley BG, Moore T, Sferra J et al. The efficacy of oral nonsteroidal anti-inflammatory medication (NSAID) in the treatment of plantar fasciitis: arandomized, prospective, placebo-controlled study. Foot Ankle Int 2007; 2820–23
12
13. Crawford F, Atkins D, Young P, Edwards J. Steroid injection for heelpain: evidence of short-term effectiveness. A randomized controlled trial.Rheumatology 1999; 38: 974–977.
13
14. Acevedo JI, Beskin JL. Complications of plantar fascia rupture associated withcorticosteroid injection. Foot Ankle Int 1998; 19: 91–97.
14
15. Leach R, Jones R, Silva T. Rupture of the plantar fascia in athletes. Bone JointSurg Am 1978; 60: 537–539.
15
16. DiGiovanni BF, Nawoczenski DA, Lintal ME et al. Tissue-specific plantar fasciastretchingexercise enhances outcomes in patients with chronic heel pain. Aprospective, randomized study. J Bone Joint Surg Am 2003; 85: 1,270–1,277.
16
17. DiGiovanni BF, Nawoczenski DA, Malay DP et al. Plantar fascia-specificstretching exercise improves outcomes in patients with chronic plantar fasciitis.A prospective clinical trial with two-year follow-up. J Bone Joint Surg Am 2006;88: 1,775–1,778.
17
18. Wolgin M, Cook C, Graham C, Mauldin D. Conservative treatment of plantarheel pain: long-term follow-up. Foot Ankle Int 1994; 15: 97–102.
18
19. Snook GA, Chrisman OD. The management of subcalcaneal pain. ClinOrthopRelat Res 1972; 82: 163–168.
19
20. Furey JG. Plantar fasciitis. The painful heel syndrome. J Bone Joint Surg Am
20
1975; 57: 672–673.
21
21. Babcock MS, Foster L, Pasquina P, Jabbari B. Treatment of pain attributed toplantar fasciitis with botulinum toxin a: a short-term, randomized, placebocontrolled,double-blind study. Am J Phys Med Rehabil 2005; 84: 649–654.
22
22. Ogden JA, Alvarez RG, Levitt RL et al. Electrohydraulic high-energy shockwavetreatment for chronic plantar fasciitis. J Bone Joint Surg Am 2004; 86:2,216–2,228.
23
23. Hammer DS, Rupp S, Kreutz A et al. Extracorporeal shockwave therapy (ESWT)
24
in patients with chronic proximal plantar fasciitis. Foot Ankle Int 2002; 23:309–313.
25
24. Wang CJ, Chen HS, Huang TW. Shockwave therapy for patients with plantarfasciitis: a one-year follow-up study. Foot Ankle Int 2002; 23: 204–207.
26
25. Gerdesmeyer L, Frey C, Vester J et al. Radial extracorporeal shock wave therapyis safe and effective in the treatment of chronic recalcitrant plantar fasciitis:results of a confirmatory randomized placebo-controlled multicenter study. AmJ Sports Med 2008; 36: 2,100–2,109.
27
26. Anderson RB, Foster MD. Operative treatment of subcalcaneal pain. Foot Ankle1989; 9: 317–323.
28
27. Murphy GA, Pneumaticos SG, Kamaric E et al. Biomechanical consequences ofsequential plantar fascia release. Foot Ankle Int 1998; 19: 149–152.
29
28. Baxter DE, Pfeffer GB. Treatment of chronic heel pain by surgical release ofthe first branch of the lateral plantar nerve. ClinOrthopRelat Res 1992; 279:229–236.
30
29. Barrett SL, Day SV, Pignetti TT, Egly BR. Endoscopic heel anatomy: analysis of200 fresh frozen specimens. J Foot Ankle Surg 1995; 34: 51–56
31
30. Marafkَ C. Endoscopic partial plantar fasciotomy as a treatment alternative inplantar fasciitis. ActaChirOrthopTraumatolCech 2007; 74: 406–409.
32
31. Hogan KA, Webb D, Shereff M. Endoscopic plantar fascia release. Foot Ankle
33
ORIGINAL_ARTICLE
Assessment of Hemodialysis Adequacy in patients with Chronic Kidney Disease in the Hemodialysis Unit at Sohag University Hospital
introduction evaluation of HD adequacy in patients with ESRD who were being maintained on regular HD in a trial to identify the prevalence and causes of inadequate HD among the patients and the impact of HD adequacy on other parameters. design and setting:prospective study, at sohag university hospital in egypt. METHODS All patients in this study were subjected to laboratory investigations including blood urea nitrogen (BUN) (before dialysis and after dialysis), serum albumin, and hemoglobin (Hb) level. • URR = (1 - [postdialysis BUN ÷ predialysis BUN]) Kt/V was calculated using the second-generation Daugirdas formula • Single-pool Kt/V = −In (R −0.008 × t) + (4 −3.5 × R)×UF/W, R is the ratio of postdialysis to predialysis BUN; t is the length of a dialysis session in hours; UF is the ultrafiltration volume in liters; and W is the patient’s postdialysis weight in kilograms. RESULTS The results shown that 69,64% of patients had adequate HD (KT\V >1,2),and only 30,36% of patients had indequate HD (KT\V>1,2). CONCLUSION A significant percentage(69,64%) of patients in the HD unit of Sohag University hospital had adequate HD. HD adequacy was influenced by several factors such as duration and frequency of the dialysis session.
https://smj.journals.ekb.eg/article_41088_9147014111f5014f3ad1520416dad7d9.pdf
2018-01-01
187
191
10.21608/smj.2018.41088
Lotfy
Abo Dahab
loutfy_abodahab@med.sohag.edu.eg
1
Department of Internal Medicine, Faculty of Medicine, Sohag University.
AUTHOR
Eman
Sabet
eman_thabet@med.sohag.edu.eg
2
Department of Internal medicine ; Faculty of medicine; Sohag University.
AUTHOR
Emad
Mohammed
emad_youssif@med.sohag.edu.eg
3
Department of Internal Medicine, Faculty of Medicine, Sohag University.
AUTHOR
Abdallah
abdel-Naiem
4
Department of Internal medicine ; Faculty of medicine; Sohag University.
AUTHOR
1. Krame r A, Ste l V, Zoccal i C, Hea f J, Ansel l D, Grönhagen-Riska C, et al. ERA-EDTA Registry An update on renal replacement therapy in Europe: ERA-EDTA Registry data from 1997 to 2006. Nephrol Dial Transplant 2009; 24:3557 –66.
1
2.Vanholde r R, Davenpor t A, Hannedouch e T, Kooma n J, Kribbe n A, Lameire N, et al., Dialysis Advisory Group of American Society of Nephrology Reimbursement of dialysis: a comparison of seven countries. J Am Soc Nephrol 2012; 23:129 1–8
2
3. Aghigh i M, Heidary Rouch i A, Zamyad i M, et al.: Dialysis in Iran. Iran J Kidney Dis 2008; 2:1 1-5
3
4. Hall YN, Jolly SE, Abrass CK, et al.. Regional differences in dialysis care and mortality among American Indians and Alaska Natives. J Am Soc Nephrol 2011; 22:2287 –95.
4
5. Gotch FA, Sargent JA. A mechanistic analysis of the National
5
Cooperative Dialysis Study (NCDS). Kidney Int 1985; 28:526 –34.
6
6. Plantinga LC, Fink NE, Jaar BG, et al.: Frequency of sit-down patient care rounds, attainment of clinical performance targets, hospitalization, and mortality in hemodialysis patients. J Am Soc Nephrol 15 : 3144 –3153, 2004.
7
ORIGINAL_ARTICLE
The Relationship of Serum 25-Hydroxyvitamin D Levels with Disease Activity in Upper Egyptian Patients with Rheumatoid Arthritis
Aim of the work: To assess the serum 25-hydroxyvitamin D concentrations [25(OH)D] and their relationship with parameters of disease activity in upper Egyptian patients with rheumatoid arthritis (RA). Patients and methods: A case-control study was made on 34 patients with RA and 34 healthy control subjects. The following values were assessed for each patient: erythrocyte sedimentation rate (ESR), C reactive protein (CRP), rheumatoid factor (RF), anti-cyclic citrullinated peptide antibodies (Anti-CCP), visual analogue scale of pain (VAS), disease activity score 28 (DAS28), and serum 25-hydroxyvitamin D concentrations. Results: Patients with RA had mild to moderate (DAS28 ˂ 5.1) disease activity. The mean serum level of 25(OH)D in patients with RA (24.35±5.66 ng/ml) was significantly lower (P˂ 0.001) than controls (42.46±11.33 ng/ml). Serum 25(OH)D levels did not show correlation with disease duration, ESR, CRP, VASor DAS28 in patients with RA.Serum 25(OH)D levels were significantly correlated with age in RA patients (P˂ 0.01).Serum 25(OH)D levels had no relation to RF or anti-CCP positivity. Conclusion: Although serum 25(OH)D levels were lower in RA patients of upper Egypt, there was no correlation with disease activity parameters, therefore, serum 25(OH)D concentrations cannot be used to reflect disease activity.
https://smj.journals.ekb.eg/article_41100_b999f141bfb8da4a345af3ed20484e7d.pdf
2018-01-01
192
198
10.21608/smj.2018.41100
disease activity
Rheumatoid Arthritis
Vitamin D
Abdullah
Ahmed
abdalah_radwan@med.sohag.edu.eg
1
Department of Rheumatology and Rehabilitation, Faculty of Medicine, Sohag University, Egypt.
AUTHOR
Ahmed
Allam
ahmed_farag@med.sohag.edu.eg
2
Department of Clinical Pathology, Faculty of Medicine, Sohag University, Egypt.
AUTHOR
1. Jeffery LE, Raza K, Hewison M. Vitamin D in rheumatoid arthritis-towards clinical application. Nature reviews Rheumatology. 2016;12(4):201-10.
1
2. Chaudhari K, Rizvi S, Syed BA. Rheumatoid arthritis: current and future trends. Nature reviews Drug discovery. 2016;15(5):305-6.
2
3. Hall AC, Juckett MB. The role of vitamin D in hematologic disease and stem cell transplantation. Nutrients. 2013;5(6):2206-21.
3
4. Gulko PS, Winchester RJ. Rheumatoid arthritis. . In: Samter’s Immunologic Diseases Austen KF, Frank MM, Atkinson JP, Cantor H (eds) Lippincott, Williams & Wilkins, Baltimore, MD. 2001:427-63.
4
5. Lin J, Liu J, Davies ML, Chen W. Serum Vitamin D Level and Rheumatoid Arthritis Disease Activity: Review and Meta-Analysis. PLoS One. 2016;11(1):e0146351.
5
6. Braun-Moscovici Y, Toledano K, Markovits D, Rozin A, Nahir AM, Balbir-Gurman A. Vitamin D level: is it related to disease activity in inflammatory joint disease? Rheumatology international. 2011;31(4):493-9.
6
7. Craig SM, Yu F, Curtis JR, Alarcon GS, Conn DL, Jonas B, et al. Vitamin D status and its associations with disease activity and severity in African Americans with recent-onset rheumatoid arthritis. The Journal of rheumatology. 2010;37(2):275-81.
7
8. Hong Q, Xu J, Xu S, Lian L, Zhang M, Ding C. Associations between serum 25-hydroxyvitamin D and disease activity, inflammatory cytokines and bone loss in patients with rheumatoid arthritis. Rheumatology. 2014;53(11):1994-2001.
8
9. Kostoglou-Athanassiou I, Athanassiou P, Lyraki A, Raftakis I, Antoniadis C. Vitamin D and rheumatoid arthritis. Therapeutic advances in endocrinology and metabolism. 2012;3(6):181-7.
9
10. Racovan M, Walitt B, Collins CE, Pettinger M, Parks CG, Shikany JM, et al. Calcium and vitamin D supplementation and incident rheumatoid arthritis: the Women's Health Initiative Calcium plus Vitamin D trial. Rheumatology international. 2012;32(12):3823-30.
10
11. Rossini M, Maddali Bongi S, La Montagna G, Minisola G, Malavolta N, Bernini L, et al. Vitamin D deficiency in rheumatoid arthritis: prevalence, determinants and associations with disease activity and disability. Arthritis research & therapy. 2010;12(6):R216.
11
12. Sahebari M, Mirfeizi Z, Rezaieyazdi Z, Rafatpanah H, Goshyeshi L. 25(OH) vitamin D serum values and rheumatoid arthritis disease activity (DA S28 ESR). Caspian journal of internal medicine. 2014;5(3):148-55.
12
13. Turhanoglu AD, Guler H, Yonden Z, Aslan F, Mansuroglu A, Ozer C. The relationship between vitamin D and disease activity and functional health status in rheumatoid arthritis. Rheumatology international. 2011;31(7):911-4.
13
14. Aletaha D, Neogi T, Silman AJ, Funovits J, Felson DT, Bingham CO, 3rd, et al. 2010 rheumatoid arthritis classification criteria: an American College of Rheumatology/European League Against Rheumatism collaborative initiative. Annals of the rheumatic diseases. 2010;69(9):1580-8.
14
15. Mallya RK, Mace BE. The assessment of disease activity in rheumatoid arthritis using a multivariate analysis. Rheumatology and rehabilitation. 1981;20(1):14-7.
15
16. Prevoo ML, van 't Hof MA, Kuper HH, van Leeuwen MA, van de Putte LB, van Riel PL. Modified disease activity scores that include twenty-eight-joint counts. Development and validation in a prospective longitudinal study of patients with rheumatoid arthritis. Arthritis Rheum. 1995;38(1):44-8.
16
17. Szodoray P, Nakken B, Gaal J, Jonsson R, Szegedi A, Zold E, et al. The complex role of vitamin D in autoimmune diseases. Scandinavian journal of immunology. 2008;68(3):261-9.
17
18. Gatenby P, Lucas R, Swaminathan A. Vitamin D deficiency and risk for rheumatic diseases: an update. Current opinion in rheumatology. 2013;25(2):184-91.
18
19. Haque UJ, Bartlett SJ. Relationships among vitamin D, disease activity, pain and disability in rheumatoid arthritis. Clinical and experimental rheumatology. 2010;28(5):745-7.
19
20. Dong H, Xu L, Bi L. [An investigation on vitamin D levels in peripheral blood in rheumatoid arthritis]. Wei sheng yan jiu = Journal of hygiene research. 2012;41(2):313-5.
20
21. Gheita TA, Sayed S, Gheita HA, Kenawy SA. Vitamin D status in rheumatoid arthritis patients: relation to clinical manifestations, disease activity, quality of life and fibromyalgia syndrome. International journal of rheumatic diseases. 2016;19(3):294-9.
21
22. Attar SM. Vitamin D deficiency in rheumatoid arthritis. Prevalence and association with disease activity in Western Saudi Arabia. Saudi medical journal. 2012;33(5):520-5.
22
23. Pakchotanon R, Chaiamnuay S, Narongroeknawin P, Asavatanabodee P. The association between serum vitamin D Level and disease activity in Thai rheumatoid arthritis patients. International journal of rheumatic diseases. 2016;19(4):355-61.
23
24. Matsumoto Y, Sugioka Y, Tada M, Okano T, Mamoto K, Inui K, et al. Relationships between serum 25-hydroxycalciferol, vitamin D intake and disease activity in patients with rheumatoid arthritis--TOMORROW study. Modern rheumatology / the Japan Rheumatism Association. 2015;25(2):246-50.
24
25. Cutolo M, Pizzorni C, Sulli A. Vitamin D endocrine system involvement in autoimmune rheumatic diseases. Autoimmunity reviews. 2011;11(2):84-7.
25
26. Cantorna MT, Hayes CE, DeLuca HF. 1,25-Dihydroxycholecalciferol inhibits the progression of arthritis in murine models of human arthritis. The Journal of nutrition. 1998;128(1):68-72.
26
27. Moghimi J, Sadeghi A, Malek M, Ghorbani R. Relationship between disease activity and serum levels of vitamin D and parathyroid hormone in rheumatoid arthritis. Endocrine regulations. 2012;46(2):61-6.
27
ORIGINAL_ARTICLE
Expansion in Head and Neck at Sohag University Hospital
Background: Tissue expansion is widely used in the head and neck, it have many advantages as the expanded tissue have the same color and texture of the treated area of the skin. Objectives:The aim of this work is to evaluate the expander utilization in head and neck reconstruction regarding indications and complications.Patients and methods: This is a prospective study included 30patients (18 female and 12 male), their age ranged from 3 to 36 years with mean value of 16 years,all patients were evaluated and managed in the plastic surgery department at Sohag university hospital. Results: the most cases of tissue expander used for scalp reconstruction followed by neck and nose reconstruction, young aged mostly treated with tissue expander than old aged and female more than male. Conclusion:The use of expanders provides the surgeon with a very reliable, simple method of reconstruction, the most common indications of expander uses were the post burn lesion alopecia of the scalp, post burn scar of the face, congenital melanocytic nevus of the forehead, haemangioma of the nose and congenital lymphatic malformations of the neck. The most common complications were expander exposure, wound dehiscent and serosa.
https://smj.journals.ekb.eg/article_41306_70847c2841d3bd111fb449e3d5d971d5.pdf
2018-01-01
199
206
10.21608/smj.2018.41306
tissue expander
Scalp
Reconstruction
Gamal
Elsayed
gamal_elsayed@med.sohag.edu.eg
1
Department of Plastic Surgery Faculty of Medicine University of Sohag
AUTHOR
Esam
Bahgat
2
Department of plastic surgery, Faculty of medicine, Sohag University.
AUTHOR
Tarek
Abulezz
tabulezz@med.sohag.edu.eg
3
Department of plastic surgery, Faculty of medicine, Sohag University.
AUTHOR
Hossam
Abd El Hameed
hossam_abdelhameed@med.sohag.edu.eg
4
Department of General surgery, Faculty of medicine, Sohag University.
AUTHOR
1- Bakhshaeekia, A. 2013. Ten-year experience in face and neck unit reconstruction using tissue expanders. Burns, 39(3): 522-527.
1
2- Egeland, B. M., & Cederna, P. S. 2008. A minimally invasive approach to the placement of tissue expanders. Paper presented at the Seminars in plastic surgery.
2
3- Turko, A., Fuzaylov, G., Savchyn, V., & Driscoll, D. 2013. Immediate and early tissue expander placement for acute closure of scalp wounds. Annals of plastic surgery, 71(2): 160-165.
3
4- Yeşilada, A. K., Akçal, A., Dağdelen, D., Sucu, D. Ö., Kılınç, L., & Tatlıdede, H. S. 2013. The feasibility of tissue expansion in reconstruction of congenital and aquired deformities of pediatric patients. International journal of burns and trauma, 3(3): 144.
4
5- Eisenmann-Klein, M., & Neuhann-Lorenz, C. 2010. Innovations in Plastic and Aesthetic Surgery: Springer Berlin Heidelberg.
5
6- Yeong, E.-K., Chen, K.-W., & Chan, Z.-H. 2011. Risk factors of tissue-expansion failure in burn-scar reconstruction. Journal of Plastic, Reconstructive & Aesthetic Surgery, 64(12): 1635-1640.
6
7- Almeida, M. 2000. Expanded shoulder flap in burn sequela. Acta chirurgiae plasticae, 43(3): 86-90.
7
8- Motamed, S., Niazi, F., Atarian, S., & Motamed, A. 2008. Post-burn head and neck reconstruction using tissue expanders. Burns, 34(6): 878-884.
8
9- Hudson, D. A., & Grob, M. 2005. Optimising results with tissue expansion: 10 simple rules for successful tissue expander insertion. Burns, 31(1): 1-4
9
10- Bozkurt, A., Groger, A., O’dey, D., Vogeler, F., Piatkowski, A., Fuchs, P. C., & Pallua, N. 2008. Retrospective analysis of tissue expansion in reconstructive burn surgery: evaluation of complication rates. Burns, 34(8): 1113-1118.
10
11- Antonyshyn, O., Gruss, J. S., Mackinnon, S., & Zuker, R. 1988. Complications of soft tissue expansion. British journal of plastic surgery, 41(3): 239-250.
11
12- Baker, S. R., & Swanson, N. A. 1990. Tissue expansion of the head and neck: indications, technique, and complications. Archives of Otolaryngology–Head & Neck Surgery, 116(10): 1147-1153.
12
13- Wieslander, J. B. 1991. Tissue expansion in the head and neck: a 6-year review. Scandinavian journal of plastic and reconstructive surgery and hand surgery, 25(1): 47-56.
13
ORIGINAL_ARTICLE
Use of mesenchymal stem cells in an experimental model of metabolic syndrome complicated with cardiomyopathy
Obesity is a major global health issue. Most obese patients develop metabolic syndrome, a cluster of clinical features characterized by hypertension, insulin resistance and dyslipidemia this pre-diabetic condition has recognized as an independent risk factor for cardiovascular diseases, particularly hypertension, atherosclerosis and diabetic cardiomyopathy. MSC can differentiate into many mesenchymal cells as cardiomyocytes. The application of MSCs in the treatment of DC in recent years offers promising results. Stem cell therapy has emerged as a promising strategy for the treatment of dead myocardium, directly or indirectly, and seems to offer functional benefits to patients.Recently, a substantial number of clinical trials have proven that stem cell therapy is safe. Infusion of bone marrow-derived stem cells (BMCs) represents the greatest number of clinical studies for MI. This review highlights the use of mesenchymal stem cells in metabolic syndrome and diabetic cardiomyopathy
https://smj.journals.ekb.eg/article_41313_cebb07da3eb655ffea368190944dac04.pdf
2018-01-01
207
211
10.21608/smj.2018.41313
Nagwa
Ahmad
nagwa_ahmed@med.sohag.edu.eg
1
Department of Biochemistry, Faculty of Medicine, Sohag University.
AUTHOR
Esam
Abdel Raheem
essam_abdelmawgoud@med.sohag.edu.eg
2
Department of Biochemistry, Faculty of Medicine, Sohag University.
AUTHOR
Hanan
Fouad
3
Department of Biochemistry, Faculty of Medicine, Cairo University.
AUTHOR
Tahia
Saleem
4
Department of Biochemistry, Faculty of Medicine, Assuit University.
AUTHOR
of the National Cholesterol Education Program (NCEP) expert panel on detection, evaluation, and treatment of high blood cholesterol in adults (adult treatment panel III) The Journal of the American Medical Association. 2001;285(19):2486–2497.
1
Alberti K. G., Eckel R. H., Grundy S. M., et al. Harmonizing the metabolic syndrome: a joint interim statement of the international diabetes federation task force on epidemiology and prevention; National heart, lung, and blood institute; American heart association; World heart federation; International atherosclerosis society; And international association for the study of obesity. Circulation. 2009;120(16):1640–1645.
2
Haffner S., Taegtmeyer H. Epidemic obesity and the metabolic syndrome. Circulation. 2003;108(13):1541–1545.
3
Silva D, Souza B, Azevedo C, Vasconcelos J, Carvalho R, Soares M, and Santos R. Intramyocardial transplantation of cardiac mesenchymal stem cells reduces myocarditis in a model of chronic Chagas disease cardiomyopathy. Stem Cell Research & Therapy. 2014, 5:81.
4
Secchiero P, Candido R, Corallini F, Zacchigna S, Toffoli B, Rimondi E, et al. Systemic tumor necrosis factor-related apoptosis-inducing ligand delivery shows antiatherosclerotic activity in apolipoprotein E-null diabetic mice. Circulation. 2006, 114:1522–30.
5
Poornima IG, Parikh P, Shannon RP. Diabetic cardiomyopathy: the search for a unifying hypothesis. Circ Res. 2006, 98:596–605.
6
Yoon YS, Uchida S, Masuo O, Cejna M, Park JS, Gwon HC, et al. Progressive attenuation of myocardial vascular endothelial growth factor expression is a seminal event in diabetic cardiomyopathy: restoration of microvascular homeostasis and recovery of cardiac function in diabetic cardiomyopathy afte
7
replenishment of local vascular endothelial growth factor. Circulation. 2005, 111:2073–85.
8
Dominici M, Le Blanc K, Mueller I, Slaper-Cortenbach I, Marini F, Krause D, et al. Minimal criteria for defining multipotent mesenchymal stromal cells.The International Society for Cellular Therapy position statement. Cytotherapy. 2006, 8:315–7.
9
Pittenger MF, Mackay AM, Beck SC, Jaiswal RK, Douglas R, Mosca JD, et al. Multilineage potential of adult human mesenchymal stem cells. Science. 1999, 284:143–7.
10
Tirino V, Paino F, d’Aquino R, Desiderio V, De Rosa A, Papaccio G. Methods for the identification, characterization and banking of human DPSCs: current strategies and perspectives. Stem Cell Rev. 2011, 7:608–15.
11
Volarevic V, Arsenijevic N, Lukic ML, Stojkovic M. Concise review: mesenchymal stem cell treatment of the complications of diabetes mellitus. Stem Cells. 2011, 29:5–10.
12
Davey GC, Patil SB, Loughlin AO and Brien TO. Mesenchymal stem cell-based treatment for microvascular and secondary complications of Diabetes mellitus. Frontiers in endocrinology. 2014, 5:1-15.
13
Haidar Ym and Cosman Bc (2011): Obesity epidemiology. Clin Colon Rectal Surg; 24(4): 205-210.
14
Bonora E., Kieciil S.,Willem J., et al .(2003):metabolic syndrome; epidemiology and more extensive phenotypic description. Cross- sectional data from the Bruned, Study. Int J., Obes Related Metab disord 27,1283-1289.
15
Obunai K, Ianis, and Dangas Gd (2007): Cardiovascular morbidity and mortality of metabolic syndrome . Med Clin North Am 91, 1169-1184.
16
Rubler S., Dlugash J., Yuceoglu Yz., et al. (1972): New type of cardiomyopathy associated with diabetic glomerulosclerosis. Am J Cardiol 30, 595-602
17
Asghar O., Al-Sunni A., Khavandi K., et al. (2009): Diabetic cardiomyopathy. Clin Sci (Lond) 116, 741-760.
18
Boudina S and Abel ED. (2010): Diabetic cardiomyopathy causes and effects. Rev Endocr Metab Disord., 11:31-39
19
Miki T., Yuda S., Kouzu H., et al. (2013): Diabetic cardiomyopathy: pathophysiology and clinical features. Heart Fail Rev 18, 149-166
20
Bernardi S., Severini Gm., Zauli G., et al. (2012): Cell-based therapies for diabetic complications. Exp Diabetes Res 2012, 872504.
21
Jones Da, Choudry F, And Mathur A (2012): Cell therapy in cardiovascular disease: the national society journals present selected research that has driven recent advances in clinical cardiology. Heart 98, 1626-1631.
22
ANKRUM J, and KARP JM (2010): Mesenchymal stem cell therapy: Two steps forward, one step back. Trends Mol Med 16, 203-209.
23
Haffner S., Taegtmeyer H. (2003): Epidemic obesity and the metabolic syndrome. Circulation.;108(13):1541–1545.
24
AlbertiK. G., Eckel R. H., Grundy S. M., et al. (2009): Harmonizing the metabolic syndrome: a joint interim statement of the international diabetes federation task force on epidemiology and prevention; National heart, lung, and blood institute; American heart association; World heart federation; International atherosclerosis society; And international association for the study of obesity. Circulation.; 120(16): 1640–1645.
25
Silva D., Souza B., Azevedo C., et al. (2014): Intramyocardial transplantation of cardiac mesenchymal stem cells reduces myocarditis in a model of chronic Chagas disease cardiomyopathy. Stem Cell Research & Therapy., 5:81.
26
Secchiero P., Candido R., Corallini F., et al. (2006): Systemic tumor necrosis factor-related apoptosis-inducing ligand delivery shows antiatherosclerotic activity in apolipoprotein E-null diabetic mice. Circulation., 114:1522–30.
27
Poornima IG, Parikh P, Shannon RP. (2006): Diabetic cardiomyopathy: the search for a unifying hypothesis. Circ Res., 98:596–605.
28
YoonYS., Uchida S., Masuo O., et al. (2005): Progressive attenuation of myocardial vascular endothelial growth factor expression is a seminal event in diabetic cardiomyopathy. Circulation., 111:2073–85
29
ORIGINAL_ARTICLE
Comparing the Performance of Tissue Doppler versus Left Atrial Strain in Predicting Left Ventricular End Diastolic Pressure in Patients with Different Left Ventricular Ejection Fractions
Background:Early trans-mitral inflow velocity and mitral annular tissue Doppler imaging (E/Em ratio) is widely applied to noninvasively estimate left ventricular (LV) filling pressures. However, E/Em ratio has a significant gray zone among patients with severely impaired ejection fraction. Speckle tracking echocardiography (STE) was recently proposed as an alternative surrogate to estimate LV filling pressures. This study aimed at assessing performance of tissue Doppler parameters and left atrial global longitudinal strain as non-invasive surrogates for LV filling pressures and comparing accuracy of these two parameters across different striae of LVEF. Methods: A total of 96 patients with sinus rhythm and different ejection fraction who divided into four groups of 24 patients each according to their EF(>55%, 45–54%, 30–44%, and <30%), had an invasive measurement of the LV pressure. Both medial and lateral E/Em ratio were measured in all subjects by 2D Tissue Doppler, peak atrial longitudinal strain (PALS) and Peak atrial contraction strain (PACS) were obtained by averaging all segments measured in the 4-chamber. Results: Significant Correlation between global PALS and invasive LVEDP in all groups (r = 0.70 P < 0.000), While Lateral E/E’ shows significant correlation only in two groups; preserved and mildly impaired EF (r=0.42 P=0.023, r=0.439 p-0.032; respectively) Conclusion:In patients with preserved or mildly reduced LV ejection fraction, global PALS and Lateral E/E’ ratio presented good correlations with LVEDP. In patients with moderate or severe reduction of EF, E/E’ ratio correlated poorly with invasively measured LV filling pressures. Global PALS provided an overall better estimation of LV filling pressures.
https://smj.journals.ekb.eg/article_41318_bd5d489f8bde850e7fe8c714b9510ede.pdf
2018-01-01
213
221
10.21608/smj.2018.41318
Aliaa
Mahfouz
1
Department of Cardiovascular Medicine, Aswan University, Aswan, Egypt.
AUTHOR
Mohammed
Salama
2
Department of Cardiovascular Medicine, Aswan University, Aswan, Egypt.
AUTHOR
Ramadan
Mohamed
3
Department of Cardiovascular Medicine, Aswan University, Aswan, Egypt.
AUTHOR
Mohamed
Saleh
4
Department of Cardiovascular Medicine, Aswan University, Aswan, Egypt.
AUTHOR
1. Go, A. S. et al. Heart disease and stroke statistics-2013 update: A Report from the American Heart Association. Circulation127, (2013).
1
2. Gottdiener, J. S., Kitzman, D. W., Aurigemma, G. P., Arnold, A. M. & Manolio, T. A. Left atrial volume, geometry, and function in systolic and diastolic heart failure of persons > or =65 years of age (the cardiovascular health study). AJC97, 83–89 (2006).
2
3. Schober, K. E., Luis Fuentes, V. & Bonagura, J. D. Comparison between invasive hemodynamic measurements and noninvasive assessment of left ventricular diastolic function by use of Doppler echocardiography in healthy anesthetized cats. Am. J. Vet. Res.64, 93–103 (2003).
3
4. Bruch, C., Grude, M., Müller, J., Breithardt, G. & Wichter, T. Usefulness of tissue Doppler imaging for estimation of left ventricular filling pressures in patients with systolic and diastolic heart failure. Am. J. Cardiol.95, 892–895 (2005).
4
5. Mullens, W., Borowski, A. G., Curtin, R. J., Thomas, J. D. & Tang, W. H. Tissue Doppler imaging in the estimation of intracardiac filling pressure in decompensated patients With advanced systolic heart failure. Circulation119, 62–70 (2009).
5
6. Cameli, M. et al. Left atrial longitudinal strain by speckle tracking echocardiography correlates well with left ventricular filling pressures in patients with heart failure. Cardiovasc Ultrasound8, 14 (2010).
6
7. Cameli, M. et al. Correlation of Left Atrial Strain and Doppler Measurements with Invasive Measurement of Left Ventricular End-Diastolic Pressure in Patients Stratified for Different Values of Ejection Fraction. Echocardiography33, 398–405 (2016).
7
8. LANG, R. et al. Recommendations for chamber quantification☆. Eur. J. Echocardiogr.7, 79–108 (2006).
8
9. De Oliveira, R. K. F. et al. Usefulness of pulmonary capillary wedge pressure as a correlate of left ventricular filling pressures in pulmonary arterial hypertension. J. Hear. Lung Transplant.33, 157–162 (2014).
9
10. Easby, D. & Dalrymple, P. Monitoring arterial, central venous and pulmonary capillary wedge pressure. Anaesthesia and Intensive Care Medicine10, 38–44 (2009).
10
11. Sharkey, S. W. Beyond the wedge: Clinical physiology and the Swan-Ganz catheter. The American Journal of Medicine83, 111–122 (1987).
11
12. Kuroda, T. et al. Prediction of prognosis of patients with idiopathic dilated cardiomyopathy: a comparison of echocardiography with cardiac catheterization. Jpn. J. Med.28, 180–8 (1989).
12
13. Ommen, S. R. et al. Clinical utility of Doppler echocardiography and tissue Doppler imaging in the estimation of left ventricular filling pressures: A comparative simultaneous Doppler-catheterization study. Circulation102, 1788–1794 (2000).
13
14. Prasad, A. et al. The Effects of Aging and Physical Activity on Doppler Measures of Diastolic Function. Am. J. Cardiol.99, 1629–1636 (2007).
14
15. Grossman, William; Baim, D. in Cardiac Catheterization, Angiography, and Intervention 1–17 (2014).
15
16. Mentz, R. J. et al. Clinical characteristics and outcomes of hospitalized heart failure patients with systolic dysfunction and chronic obstructive pulmonary disease: Findings from OPTIMIZE-HF. Eur. J. Heart Fail.14, 395–403 (2012).
16
17. Mann, D. L. & Bristow, M. R. Mechanisms and models in heart failure: The biomechanical model and beyond. Circulation111, 2837–2849 (2005).
17
18. Kusunose, K. et al. Independent association of left atrial function with exercise capacity in patients with preserved ejection fraction. Heart98, 1311–7 (2012).
18
19. Galderisi, M. et al. European multicentre validation study of the accuracy of E/e’ ratio in estimating invasive left ventricular filling pressure: EURO-FILLING study. Eur. Hear. J. - Cardiovasc. Imaging15, 810–816 (2014)
19
20. Lang, C. C. & Struthers, A. D. Targeting the renin-angiotensin-aldosterone system in heart failure. Nat. Rev. Cardiol.10, 125–34 (2013).
20
21. McMurray, J. J. V et al. ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure 2012. Eur. Heart J.33, 1787–1847 (2012).
21
ORIGINAL_ARTICLE
Closed Reduction and Percutaneous Screws Fixation in Tibial Plateau Fractures
Purpose:To evaluate treatment outcomes of closedreduction and percutaneous screw fixation for tibialplateau fractures. Methods:18 men and 4 women aged 21 to 64 (mean, 38.1) years underwent closed reduction and percutaneous screw fixation for closed tibial plateaufractures. According to theSchatzker classification, patients were classifiedinto type I (n=6), type III (n=10), type IV (n=4), andtype V (n=2). Closed reduction was achieved usingmanual ligamentotaxis with traction in extensionunder image intensifier control. Reduction was fixedpercutaneously with cancellous screws (6.5 mm) andwashers. Functional outcome (pain, walking capacity,extension lag, range of motion, stability and return to daily activity) wasevaluated using the Modified Hospital for Special Surgery Score. A total score of 55 to 60 was considered as excellent, 45 to 54 as good, 35 to 44 as fair, and Results:Patients were followed up for a mean of 8 (range, 6–12) months. The mean length of hospitalstay was 2 (range, 1–3) days. All the fracture unitedradiographically after a mean of 3 (range, 2.5–3.5)months. Respectively in Schatzker types-I, -III, -IV, and-V fractures, outcomes were excellent in 4, 1, 1, and 0 patients, good in 2, 6, 2, and 0 patients, fair in 0, 3, 0, and 1 patients, and poor in 0, 0, 1, and 1 patients. Outcome was satisfactory (good-to-excellent) in 100%, 70%, 75%, and 0% of the respective fracture typesof patients. The mean Modified-HSS score was 46.2 for all patients; it was 53.3 for type I, 40.3 for typeIII, 45 for type IV, and 36 for type V fractures. One patient had metal failure due to early weight bearing at 5 weeks. No patient had infection or wound dehiscence. Conclusion:Closed reduction and percutaneous screw fixation for tibial plateau fractures is minimally invasive. It reduces the length of hospitalstay and costs, enables early mobilization with minimal instrumentation, and achieves satisfactory outcomes.
https://smj.journals.ekb.eg/article_41657_8b3cdab8ef79d2cf47af2099e8f0bf2d.pdf
2018-01-01
223
227
10.21608/smj.2018.41657
Omar
Abdelkareem
1
Department of orthopedics and traumatology, Sohag University, Egypt.
AUTHOR
Anis
Shiha
anies_sheha@med.sohag.edu.eg
2
Department of orthopedics and traumatology, Sohag University, Egypt.
AUTHOR
Hussam Eldin
Elazab
hossameldin_azab@med.sohag.edu.eg
3
Department of orthopedics and traumatology, Sohag University, Egypt.
AUTHOR
Mohamed
Ali
4
Department of orthopedics and traumatology, Sohag University, Egypt.
AUTHOR
Hohl M. Articular fractures of the proximal tibial. In: Evarts CM, editor. Surgery of the musculoskeletal system. New York: Churchill-Livingstone; 1993:3471–97.
1
Schatzker J. Fracture of the tibial plateau. In: Schatzker J, Tile M, editors. The rationale of operative fracture care. Berlin: Springer-Verlag; 1987:279–95.
2
Stevens DG, Beharry R, McKee MD, Waddall JP, Schemitsch EH. The long-term functional outcome of operatively treated tibial plateau fractures. J Orthop Trauma 2001;15:312–20.
3
Sangwan SS, Siwach RC, Singh R, Mittal R. Minimal invasive osteosynthesis: a biological approach in treatment of tibial plateau fractures. Indian J Orthop 2002;36:246–50.
4
Shete K, Sancheti P, Kamdar R. Role of Esmarch bandage and percuteneous cannulated cancellous screws in tibial condylar fracture. Indian J Orthop 2006;40:173–6.
5
Weigel DP, Marsh JL. High-energy fractures of the tibial plateau. Knee function after longer follow-up. J Bone Joint Surg Am 2002;84:1541–51.
6
De Mourgues G, Chaix D. Treatment of fracture of the tibial plateau [in French]. Rev Chir Orthop Reparatrice Appar Mot 1964;50:103–22.
7
Apley AG. Fractures of the tibial plateau. Orthop Clin North Am 1979;10:61–74.
8
Mathur H, Acharya S, Nijhawan VK, Mandal SP. Operative results of closed tibial plateau fractures. Indian J Orthop 2005;39:108–12.
9
Lobenhoffer P, Schulze M, Gerich T, Lattermann C, Tscherne H. Closed reduction/percutaneous fixation of tibial plateau fractures: arthroscopic versus fluoroscopic control of reduction. J Orthop Trauma 1999;13:426–31.
10
Mast J, Jakob R, Ganz R. Reduction with distraction. In: Mast J, Jakob R, Ganz R, editors. Planning and reduction technique in fracture surgery. Berlin: Springer-Verlag; 1989:130–42.
11
Koval KJ, Sanders R, Borrelli J, Helfet D, DiPasquale T, Mast JW. Indirect reduction and percutaneous screw fixation of displaced tibial plateau fractures. J Orthop Trauma 1992;6:340–6.
12
Keogh P, Kelly C, Cashman WF, McGuinness AJ, O’Rourke SK. Percutaneous screw fixation of tibial plateau fractures. Injury 1992;23:387–9.
13
ORIGINAL_ARTICLE
Prevalence of gyrA and parE mutations in clinical isolates of Streptococcus pneumoniae with decreased susceptibilities to different Fluoroquinolones
Introduction: Streptococcus pneumoniae is a major Gram-positive pathogen responsible for pneumonia, bactermia, otitis media, and meningitis leading to considerable morbidity and mortality among children and elderly individuals. The primary goals of antibiotic treatment of respiratory tract infections are clinical efficacy of treatment, pathogen eradication, and prevention of resistance development. Resistance to fluoroquinolones in S. pneumoniae arises in a stepwise fashion and results from alterations in the target binding site due to the acquisition of spontaneous mutations in the quinolone resistance-determining regions (QRDRs) of the topoisomerase IV and DNA gyrase genes. Although mutations usually occur in the QRDRs of parC and gyrA, a role for mutations in the parE subunit in low-level resistance has been reported. Aim of the work: The aim of this study was to determine the prevalence of fluoroquinolone resistance Streptococcus pneumoniae (FQRSP) and to examine the genetic relatedness of pneumococcal isolates with parE and gyrA genes mutations in different specimens in Sohag University Hospital. Patients and Methods: This study was prospectively conducted over a period of 24 months between October 2015 and September 2017, at Sohag university hospital. During the study period, 78 patients hospitalized for a syndrome consistent with a diagnosis of community acquired pneumonia (CAP ) included in this study with a mean age of 34.5 years (range, 2 to 67), 60% of whom were males. A CAP syndrome was defined as a newly recognized pulmonary infiltrate together with 2 of the following findings: subjective fever or documented temperature 37.4 °C, increased cough, sputum production, or shortness of breath, pleuritic chest pain, confusion, rales, leukocytosis, (according to age) (1). Patients who had taken antibiotic treatment within 3 days prior to initial visit were excluded from this study. Results: Our study illustrate the role of mutation in the gyrA&parE genes and the effect of mutations in the both genes in fluoroquinolone resistance among S. pneumoniae isolates. Conclusion: The present study provide an opportunity to view the predominant mutations conferring reduced susceptibility to FQs in clinical pneumococcal isolates. There is a strong relationship between these mutations and decrese susceptibility to the most fameous FQs to some extent, although this varies between strains and for each drug.
https://smj.journals.ekb.eg/article_41679_9e04a14890c2922fbe60fb891a0eca5d.pdf
2018-01-01
229
241
10.21608/smj.2018.41679
gyrA
ParE
Streptococcus pneumonia
Fluoroquinolones
Laila
Yousef
lailamohamed@med.sohag.edu.eg
1
Department of Clinical and Chemical pathology, Faculty of Medicine, Sohag University.
AUTHOR
Ghada
Ismael
2
Department of Clinical Pathology, Faculty of Medicine, Ain Shams University.
AUTHOR
Ashraf
Mohammed
ashraf_abdallah@med.sohag.edu.eg
3
Department of Clinical Pathology, Faculty of Medicine, Sohag University.
AUTHOR
Mohamed
Mahmoud
4
Department of Clinical Pathology, Faculty of Medicine, Sohag University.
AUTHOR
1. Mandell LA, Wunderink RG, Anzueto A, Bartlett JG, Campbell GD, Dean NC, et al. Infectious Diseases Society of America/American Thoracic fluoroquinolones, such as sparfloxacin or gatifloxacin(25, 26), but are rarely reported for clinical isolates. This may reflect the relatively recent use of newer fluoroquinolones that select for gyrA mutations first. Also, isolates with a single mutation in gyrA may be overlooked if the MIC of the fluoroquinolone agent(s) used to screen for resistance is unchanged or only modestlyincreased. although this varies between strains and for eachdrug. in (QRDRs) in S. pneumonia isolates and resistance toFluoroquinlones. The maintenance of such surveillance is valuable in the preparation of future therapy guidelines and could lead to new therapeutic strategies for FQ-resistant S.Pneumoniae. Society consensus guidelines on the management of community-acquired pneumonia in adults. Clinical infectious diseases: anofficialpublication of the Infectious Diseases Society of America. 2007;44 Suppl 2:S27-72.
1
2. Patel SN, McGeer A,Melano R, Tyrrell GJ, Green K, Pillai DR, et al. Susceptibility of Streptococcus pneumoniae to fluoroquinolones in Canada. Antimicrobial agents and chemotherapy.2011;55(8):3703-8.
2
3. Morrissey I, Farrell DJ, Bakker S, Buckridge S, Felmingham D. Molecular characterization and antimicrobial susceptibility of fluoroquinolone-resistant or - susceptible Streptococcus pneumoniae from Hong Kong. Antimicrobial agents and chemotherapy.2003;47(4):1433-5.
3
4. de la Campa AG, Balsalobre L, Ardanuy C, Fenoll A, Perez-Trallero E, Linares J, et al. Fluoroquinolone resistance in penicillin-resistant Streptococcus pneumoniae clones, Spain. Emerging infectious diseases. 2004;10(10):1751-9.
4
5. Fisher LM, Gould KA, Pan XS, Patel S, Heaton VJ. Analysis of dual active fluoroquinolones in Streptococcus pneumoniae. The Journal of antimicrobial chemotherapy. 2003;52(2):312-3; author reply3-4.
5
6. Andersson MI, MacGowan AP. Development of the quinolones. The Journal of antimicrobial chemotherapy. 2003;51 Suppl 1:1-11.
6
7. Collins MD, Hutson RA, Hoyles L, Falsen E, Nikolaitchouk N, Foster G. Streptococcus ovis sp. nov., isolated from sheep. International journal of systematic and evolutionary microbiology. 2001;51(Pt3):1147-50.
7
8. Zhanel GG, Palatnick L, Nichol KA, Bellyou T, Low DE, Hoban DJ. Antimicrobial resistance in respiratory tract Streptococcus pneumoniae isolates: results of the Canadian Respiratory Organism Susceptibility Study, 1997 to 2002. Antimicrobial agents a chemotherapy. 2003;47(6):1867-74.
8
9. Tettelin H, Nelson KE, Paulsen IT, Eisen JA, Read TD, Peterson S, et al. Complete genome sequence of a virulent isolate of Streptococcus pneumoniae. Science. 2001;293(5529):498-506.
9
10. Hoskins J, Alborn WE, Jr., Arnold J, Blaszczak LC, Burgett S, DeHoff BS, et al. Genome of the bacterium Streptococcus pneumoniae strain R6. Journal of bacteriology. 2001;183(19):5709-17.
10
11. Kargar M, MoeinJahromi F, Doosti A, Handali S. Molecular Investigation of Quinolone Resistance of Quinolone Resistance-Determining Region in Streptococcus pneumoniae Strains Isolated from Iran Using Polymerase Chain Reaction- Restriction Fragment Length Polymorphism Method. Osong public health and research perspectives. 2014;5(5):245-50.
11
12. Bast DJ, Low DE, Duncan CL, Kilburn L, Mandell LA, Davidson RJ, et al. Fluoroquinoloneresistance in clinical isolates of Streptococcus pneumoniae: contributions of type II topoisomerase mutations and efflux to levels of resistance. Antimicrobial agents and chemotherapy. 2000;44(11):3049-54.
12
13. Broskey J, Coleman K, Gwynn MN, McCloskey L, Traini C, Voelker L, et al. Efflux and target mutations as quinolone resistance mechanisms in clinical isolates of Streptococcus pneumoniae. The Journal of antimicrobial chemotherapy. 2000;45 Suppl1:95-9.
13
14. Brueggemann AB, Coffman SL, Rhomberg P, Huynh H, Almer L, Nilius A, et al. Fluoroquinolone resistance in Streptococcus pneumoniae in United States since 1994-1995. Antimicrobial agents and chemotherapy.2002;46(3):680-8.
14
15. Korzheva N, Davies TA, Goldschmidt R. Novel Ser79Leu and Ser81Ile substitutions in thequinolone
15
resistance-determining regions of ParC topoisomerase IV and GyrA DNA gyrasesubunits fromb recent fluoroquinolone-resistant Streptococcuspneumoniaeclinical isolates.Antimicrobial agents and chemotherapy.2005;49(6):2479-86.
16
16. Davies TA, Evangelista A, Pfleger S, Bush K, Sahm DF, Goldschmidt R. Prevalence of single mutations in topoisomerase type II genes among levofloxacin-susceptible clinical strains of Streptococcus pneumoniae isolated in the United States in 1992 to 1996 and 1999 to 2000. Antimicrobial agents and chemotherapy.2002;46(1):119-24.
17
17. Lim S, Bast D, McGeer A, de Azavedo J, Low DE. Antimicrobial susceptibility breakpoints and first-step parC mutations in Streptococcus pneumoniae: redefining fluoroquinolone resistance. Emerging infectious diseases.2003;9(7):833-7.
18
18. Patel SN, Melano R, McGeer A, Green K, Low DE. Characterization of the quinolone resistant determining regions in clinical isolates of pneumococci collected in Canada. Annals of clinical microbiology and antimicrobials.2010;9:3.
19
19. Kawamura-Sato K, Hasegawa T, Torii K, Ito H, Ohta M. Prevalence of Ile-460-Val/ParE substitution in clinical Streptococcus pneumoniae isolates that were less susceptible to fluoroquinolones. Current microbiology.2005;51(1):27-30. Credito K, Kosowska-Shick K, McGhee P, Pankuch GA, Appelbaum PC. Comparative study of the mutant prevention concentrations of moxifloxacin, levofloxacin, and gemifloxacin against pneumococci. Antimicrobial agents and chemotherapy.2010;54(2):673-7.
20
20. Ip M, Chau SS, Chi F, Qi A, Lai RW. Rapid screening of fluoroquinolone resistance determinants in Streptococcus pneumoniae by PCR-restriction fragment length polymorphism and single- strandn conformational polymorphism. Journal of clinical microbiology.2006;44(3):970-5.
21
21. Sierra JM, Cabeza JG, Ruiz Chaler M, Montero T, Hernandez J, Mensa J, et al. The selection of resistance to and the mutagenicity of different fluoroquinolones in Staphylococcus aureus and Streptococcus pneumoniae. Clinical microbiology and infection : the official publication of the European Society of Clinical Microbiology and Infectious Diseases.2005;11(9):750-8.
22
22. Brino L, Urzhumtsev A, Mousli M, Bronner C, Mitschler A, Oudet P, et al. Dimerization of Escherichia coli DNA-gyrase B provides a structural mechanism for activating the ATPase catalytic center. The Journal of biological chemistry. 2000;275(13):9468-75.
23
23. Fass D, Bogden CE, Berger JM. Quaternary changes in topoisomerase II may direct orthogonal movement of two DNA strands. Nature structural biology.1999;6(4):322-6.
24
24. Fukuda H, HiramatsuK. Primary targets of fluoroquinolones in Streptococcuspneumoniae. Antimicrobialagents and chemotherapy.1999;43(2):41
25
25. Streptococcus pneumoniae by sparfloxacin: selective targeting of gyrase or topoisomerase IV by quinolones. Antimicrobial agents and chemotherapy. 1997;41(2):471-4.
26
ORIGINAL_ARTICLE
Comparative study between Tramadol and Midazolam as an admixture to bupivacaine inUltrasound guided supraclavicular brachial plexus block.
Background:This is a prospective, randomized, double blind study to evaluate the postoperative analgesia following ultrasound guided supraclavicular brachial plexus block with Tramadol or Midazolam as an admixture to bupivacaine in upper extremity surgery. Patientsand methods:Total 60 patients of ASA I and II undergoing upper extremity surgery under ultrasound guided brachial plexus block with Bupivacaine were randomly divided in to two groups; one group received Tramadol (1mg/kg) and the other group received midazolam (0.05mg/kg) as an admixture to Bupivacaine. The duration of postoperative analgesia was recorded in both groups using pain VAS score. Results: The mean duration of postoperative analgesia in the Midazolam group was 650±47.49 minutes while in the tramadol group it was 508±30.44 minutes. Conclusion: We concluded that midazolamwith local anaesthetic prolongs postoperative analgesiasignificantly than Tramadol (P<0.0001) when used as admixture to local anaesthetic inUltrasound guided brachialplexus block in upper extremity surgery.
https://smj.journals.ekb.eg/article_41680_b089ee6a7dfd61843671a085c944b8a8.pdf
2018-01-01
243
250
10.21608/smj.2018.41680
Analgesia
brachial plexus
Ultrasound
midazolam
tramadol
Mostafa
Abdelzaher
1
Department of Anesthesiology, Sohag University, Egypt.
AUTHOR
Hamza
Mahmoud
hamza_aboalam@med.sohag.edu.eg
2
Department of Anesthesia, Faculty of Medicine,Sohag University.
AUTHOR
Ahmed
Abd El-Mabood
ahmed_abdelmaboud@med.sohag.edu.eg
3
Department of Anesthesia, Faculty of Medicine,Sohag University.
AUTHOR
Khaled
Hassan
khaled_hassan@med.sohag.edu.eg
4
Department of Anesthesiology, Sohag University, Egypt.
AUTHOR
AnandLK,JindalR(2009). Regional anaesthesia for upper extremity in orthopaedics :areviewarticle.PunjabJ,Orthopaedics 11:1-8.
1
GebhardRE,Al-SamsamT,GregerJ,etal.Distal nerve block at the wrist for outpatient carpal tunnel surgery offer intraoperative cardiovascular stability and reduce discharge time.AnesthAnalg 2002;95:351.
2
Vermeylenk,Engelens,SermusL,SoetensF,Van de veldeM.supraclavicular brachial plexus blocks;review and current practice .ActaAnaesthesiolBelg 2012,63;15-21.
3
Duma A, Urbanek B, Sitzwohl C, Kreiger A, Zimpfer M, Kapral S. Clonidine as an adjuvant to local anaesthetic axillary brachial plexus block: A randomized, controlled study. Br J Anaesth. 2005;94:112–6.
4
RobauxS.,Blunt C.,VielF.e, Cuvillon P., Girad F. and Bouaziz H.(2004) Tramadol added to bupivacaine for axillary brachial plexus block improve postoperative analgesia.
5
Gear, R.W., Miaskowski, C. and Gorden, N.C. (1999) The The Mu receptors tramadol Produces Gender and Dose DependentAnalgesia and Antianalgesia in Patients with Postoperative Pain. Pain, 83, 339-345.
6
De Tran QH, Clemente A, Doan J, Finlayson RJ (2007). (8): 54. Canadian Journal of Anesthesia. review of approaches and techniques"662–74.
7
wakhlo ,Woolf CJ: Recent advances in the pathophysiology of acute pain. Br J Anaesth 2006; 63:139-146.
8
ORIGINAL_ARTICLE
Prevalence of Fluoroquinolone-Resistant Clinical Isolates of Escherichia Coli in Urinary Tract Infection
Introduction: The commonest bacterial agent involved in causation of UTIs is Escherichia coli. The emergence of FQ resistant uropathogenic E. coli is of great concern. Aim of the work: to study resistance towards urinary E. coli with various generations of fluoroquinolones. Patients & Methods:: our study was carried out in the Clinical Pathology Department, Sohag University Hospital during the period from June 2016 to May 2017. Our study included 140 participants. Isolates from the specimens were obtained and identified using; Gram staining, colony characteristics on different culture medias. VITEC 2 Compact 15 identification kits were be used to confirm the identification of the isolates Results: E.coli was isolated from 100 patients (71%) of all patients complaining of UTI with positive urinary culture (study or case group). By studying prevalence of Antibiotic resistance of E.coli isolates reveals that fluoroquinolones show sensitivities of 42-46%. Also Nitrofurantoin has the highest sensitivity of 87%. This is followed by meropenem (67%). Ampicillin shows sensitivity in only 6% of cases. Regarding drug sensitivity in out & inpatients, we find that all generations of fluoroquinolones show highly significant resistance ratios among inpatients compared to outpatients. Meropenem show resistance more in inpatients than outpatients, with significant difference, Ampicillin and Nitrofuratoin show non-significant difference. Conclusion: our study show an increased fluoroquinolone resistance among uropathogenic E. coli isolates mainly in hospital admitted patients.
https://smj.journals.ekb.eg/article_41769_57d877911adb22fef942a56f2ac65404.pdf
2018-01-01
253
262
10.21608/smj.2018.41769
Urinary tract infection (UTI)
Escherichia coli and fluoroquinolone resistant E.coli
Laila
Yousef
lailamohamed@med.sohag.edu.eg
1
Department of Clinical and Chemical pathology, Faculty of Medicine, Sohag University.
AUTHOR
Ashraf
Mohammed
ashraf_abdallah@med.sohag.edu.eg
2
Department of Clinical Pathology, Faculty of Medicine, Sohag University.
AUTHOR
Ahmed
Mohamed
ahmed_ibrahim@med.sohag.edu.eg
3
Department of Clinical Pathology, Faculty of Medicine, Sohag University.
AUTHOR
Doha
Ali
4
Department of Clinical and chemical pathology, Sohag Faculty of Medicine, Sohag University.
AUTHOR
1. Akram M, Shahid M, Khan AU. Etiology and antibiotic resistance patterns of community-acquired urinary tract infections in J N M C Hospital Aligarh, India. Annals of clinical microbiology and antimicrobials. 2007;6:4.
1
2. Ramakrishnan K, &, Scheid DC. Diagnosis and management of acute pyelonephritis in adults. . Am Fam Physician, . 2005;71(5):933-42..
2
3. Foxman B. Urinary tract infection syndromes: occurrence, recurrence, bacteriology, risk factors, and disease burden. Infectious disease clinics of North America. 2014;28(1):1-13.
3
4. Gururaju T, Sarojamma V, &, Ramakrishna V. Prevalence and Fluoroquinolone Resistance Pattern in Escherichia coli Isolates of Urinary Tract Infection (UTI) Patients. . Journal of Krishna Institute of Medical Sciences (JKIMSU), . 2015;4(2).
4
5. Laupland KB, Ross T, Pitout JD, Church DL, Gregson DB. Community-onset urinary tract infections: a population-based assessment. Infection. 2007;35(3):150-3.
5
6. Emody L, Kerenyi M, Nagy G. Virulence factors of uropathogenic Escherichia coli. International journal of antimicrobial agents. 2003;22 Suppl 2:29-33.
6
7. Talan DA, Takhar SS, Krishnadasan A, Abrahamian FM, Mower WR, Moran GJ, et al. Fluoroquinolone-Resistant and Extended-Spectrum beta-Lactamase-Producing Escherichia coli Infections in Patients with Pyelonephritis, United States(1). Emerging infectious diseases. 2016;22(9).
7
8. Somashekara SC, Deepalaxmi S, Jagannath N, Ramesh B, Laveesh MR, Govindadas D. Retrospective analysis of antibiotic resistance pattern to urinary pathogens in a Tertiary Care Hospital in South India. Journal of basic and clinical pharmacy. 2014;5(4):105-8.
8
9. Bader MS, Hawboldt J, Brooks A. Management of complicated urinary tract infections in the era of antimicrobial resistance. Postgraduate medicine. 2010;122(6):7-15.
9
10. Hwang TJ, Hooper DC. Association between fluoroquinolone resistance and resistance to other antimicrobial agents among Escherichia coli urinary isolates in the outpatient setting: a national crosssectional study. . J Antimicrob Chemother 2014;69(6): :1720-2.
10
11. Betitra Y, Teresa V, Miguel V, Abdelaziz T. Determinants of quinolone resistance in Escherichia coli causing community-acquired urinary tract infection in Bejaia, Algeria. Asian Pacific journal of tropical medicine. 2014;7(6):462-7.
11
12. Landry E, Sulz L, Bell A, Rathgeber L, Balogh H. Urinary Tract Infections: Leading Initiatives in Selecting Empiric Outpatient Treatment (UTILISE). The Canadian journal of hospital pharmacy. 2014;67(2):116-25.
12
13. Livermore DM, Hope R, Reynolds R, Blackburn R, Johnson AP, &, et al. Declining cephalosporin and fluoroquinolone non-susceptibility among bloodstream Enterobacteriaceae from the UK: links to prescribing change?. . Journal of Antimicrobial Chemotherapy. 2013;68(11): :2667-74.
13
14. Singh R, Swick MC, Ledesma KR, Yang Z, Hu M, Zechiedrich L, et al. Temporal interplay between efflux pumps and target mutations in development of antibiotic resistance in Escherichia coli. Antimicrobial agents and chemotherapy, . 2012;56(4): :1680-5.
14
15. Ronald AR, Nicolle LE, Stamm E, Krieger J, Warren J, Schaeffer A, et al. Urinary tract infection in adults: research priorities and strategies. International journal of antimicrobial agents. 2001;17(4):343-8.
15
16. Ronald A. The etiology of urinary tract infection: traditional and emerging pathogens. The American journal of medicine. 2002;113 Suppl 1A:14S-9S.
16
17. Fagan M, Lindbaek M, Grude N, Reiso H, Romoren M, Skaare D, et al. Antibiotic resistance patterns of bacteria causing urinary tract infections in the elderly living in nursing homes versus the elderly living at home: an observational study. BMC geriatrics. 2015;15:98.
17
18. Grude N, Tveten Y, Kristiansen BE. Urinary tract infections in Norway: bacterial etiology and susceptibility. A retrospective study of clinical isolates. Clinical microbiology and infection : the official publication of the European Society of Clinical Microbiology and Infectious Diseases. 2001;7(10):543-7.
18
19. Naber KG, Schito G, Botto H, Palou J, Mazzei T. Surveillance study in Europe and Brazil on clinical aspects and Antimicrobial Resistance Epidemiology in Females with Cystitis (ARESC): implications for empiric therapy. European urology. 2008;54(5):1164-75.
19
20. Niranjan V, Malini A. Antimicrobial resistance pattern in Escherichia coli causing urinary tract infection among inpatients. . Indian J Med Res 2014;139:945-48.
20
21. Saha S, Nayak S, Bhattacharyya I, Saha S, Mandal AK, Chakraborty S, et al. Understanding the patterns of antibiotic susceptibility of bacteria causing urinary tract infection in West Bengal, India. Frontiers in microbiology. 2014;5:463.
21
22. Mehta M, Dutta P, Gupta V. Antimicrobial susceptibility pattern of blood isolates from a teaching hospital in north India. Japanese journal of infectious diseases. 2005;58(3):174-6.
22
23. Alonso Sanz M, Abad Be´cquer M. Fenotipos de Resistencia en aislamientos urinarios de Escherichia coli en la comunidad: implicaciones terape´uticas. . Med Clin (Barc) 2003;120:361–4.
23
24. Kahlmeter G, Eco.Sens. An international survey of the antimicrobial susceptibility of pathogens from uncomplicated urinary tract infections: the ECO.SENS Project. J Antimicrob Chemother. 2003;51(1):69-76.
24
25. Hasan AS, Nair D, Kaur J, Baweja G, Deb M, Aggarwal P. Resistance patterns of urinary isolates in a tertiary Indian hospital. Journal of Ayub Medical College, Abbottabad : JAMC. 2007;19(1):39-41.
25
26. Forbes B, Sahm D, and, Weissfeld AS. Infections of the Urinary tract, In; Baileys and Scott s (11thedt.) Diagnostic Microbiology St. Louis, Missouri, . Mosby. 2002:927-238.
26
27. Boyd LB, Atmar RL, Randall GL, Hamill RJ, Steffen D, L. Z. Increased fluoroquinolone resistance with time in Escherichia coli from >17,000 patients at a large county hospital as a function of culture site, age, sex and location. BMC Infectious Diseases 2008;8.
27
28. Oteo J, Aracil B, Hoyo JF, Perianes J, Gomez-Garces JL, Alos JI. Do the quinolones still constitute valid empirical therapy for community-acquired urinary tract infections in Spain? Clinical microbiology and infection : the official publication of the European Society of Clinical Microbiology and Infectious Diseases. 1999;5(10):654-6.
28
29. Goettsch W, van Pelt W, Nagelkerke N, Hendrix MG, Buiting AG, Petit PL, et al. Increasing resistance to fluoroquinolones in escherichia coli from urinary tract infections in the netherlands. J Antimicrob Chemother. 2000;46(2):223-8.
29
30. Karlowsky JA, Kelly LJ, Thornsberry C, Jones ME, Sahm DF. Trends in antimicrobial resistance among urinary tract infection isolates of Escherichia coli from female outpatients in the United States. Antimicrobial agents and chemotherapy. 2002;46(8):2540-5.
30
31. Moreno E, Teresa P, Johnson R, A A. Quinolone, fluoroquinolone resistance in relation to virulence determinants and phylogenetic background among uropathogenic Escherichia coli. J Antimicrob Agents Chemother 2006;57(2)::204 –11.
31
32. Huang E, Stafford R. National patterns in the treatment of urinary tract infections in women by ambulatory care physicians. . Arch Intern Med 2002;162:41–7.
32
ORIGINAL_ARTICLE
Comparison of Fixation of supracondylar humeral fractures in children by lateral cross-wiring technique versus traditional lateral pinning
Introduction The currently accepted treatment for displaced supracondylar humeral fractures in children is closed reduction and fixation with percutaneous Kirschner wires. The aim of this study was to study the results of a cross-wiring technique, achieved solely from the lateral side, in an effort to reduce the risk of ulnar nerve injury. Conclusion there was no significant difference between lateral cross-wiring technique and traditional lateral pinning as regard postoperative clinical results and radiological results. Introduction Supracondylar fractures of the humerus in children accounts for 60% of all fractures around the elbow. (1) It represents 4 - 6.5% of all paediatric fractures. In treatment of non-displaced Type I fractures simple immobilization with a posterior splint applied at 60-90o of elbow flexion is preferred. (2) Currently, the treatment of choice for type II fractures is operative reduction and pinning rather than cast. (3) Most cases of type III fractures require operative reduction and pinning. The results of type III fractures treated with closed reduction and cast immobilization are not as good as the results of pinning. (4) There are various options for the pattern of K-wire fixation of displaced supracondylar fractures. Studies found the greatest resistance to rotation occurred with medial-lateral cross pinning. (5) The second most stable pattern was fixation utilizing three lateral diverging pins. The least stable was fixation with two lateral pins, which cross at the fracture site. While medial-lateral cross pinning has the greatest resistance; the disadvantage is the risk of ulnar nerve injury. (6) Lateral pinning is recommended (7) to avoid iatrogenic ulnar nerve injury that can occur with medial lateral cross pinning. Although iatrogenic ulnar nerve injuries usually resolve, several permanent iatrogenic ulnar nerve injuries have been described. (8) Closed reduction and lateral cross-wiring technique with ascending and descending K-wires is an effective method to treat type II and III supracondylar fractures in children. Regardless of stability, this method can be used to avoid iatrogenic ulnar nerve injuries. (9) Aim of the work The aim of this work is to assess clinical results of fixation of supracondylar humeral fractures by lateral cross-pinning versus traditional lateral pinning in children.
https://smj.journals.ekb.eg/article_41770_b98ef9df22483eb1d2ca2e322a6ef06d.pdf
2018-01-01
265
271
10.21608/smj.2018.41770
Abdelrahman
Sadek
1
Department of Orthopedic, Faculty of Medicine, Sohag University.
AUTHOR
Mostafa
Elsayed
mostafaismail@med.sohag.edu.eg
2
Department of Orthpaedic and Traumatology , Faculty of Medicine, Sohag University.
AUTHOR
Hussam Eldin
Elazab
hossameldin_azab@med.sohag.edu.eg
3
Department of orthopedics and traumatology, Sohag University, Egypt.
AUTHOR
Hassan
Abdel Rahman
hassan_abdelrahman@med.sohag.edu.eg
4
Department of Orthopedic, Faculty of Medicine, Sohag University.
AUTHOR
1. Noaman HH, M.D. Microsurgical reconstruction of brachial artery injuries in displased supracondylar fracture humerus in children. Microsurgery. 2006, 26, pp. 498-505.
1
2. J., Charnley. Closed Treatment of Common Fractures. Edinburgh: Churchill Livingstone. 1961, pp. 105-115.
2
3. Battaglia TC, Armstrong DG, Schwend RM. Factors affecting forearm compartment pressures in children with supracondylar fractures of the humerus. J Pediatr Orthop. 2002, 22 (4), pp. 431-439.
3
4. Cramer KE, Devito DP, Green NE. Comparison of closed reduction and percutaneous pinning versus open reduction and percutaneous pinning in displaced supracondylar fractures of the humerus in children. J Orthop Trauma. 1992, 6(4), pp. 407-412.
4
5. Zionts LE, McKellop HA, Hathaway. Torsional strength of pin configurations used to fix supracondylar fractures of the humerus in children. J Bone Joint Surg Am. 1994, 76, pp. 253–256.
5
6. Lyons JP, Ashley E, Hoffer MM. Ulnar nerve palsies after percutaneous cross-pinning of supracondylar fractures in children’s elbows. J Pediatr Orthop. 1998, 18, pp. 43–45.
6
7. Ariño VL, Lluch EE, Ramirez AM, et al. Percutaneous fixation of supracondylar fractures of the humerus in children. J Bone Joint Surg Am. 1977, 59(7), pp. 914-916.
7
8. Ramachandran M, Birch R, Eastwood DM. Clinical outcome of nerve injuries associated with supracondylar fractures of the humerus in children. The experience of a specialist referral centre. J Bone Joint Surg Br. 2006, 88(1), pp. 90-94.
8
9. Oliver Eberhardt, Francisco Fernandez, Thomas Ilchmann & Klaus Parsch. Cross pinning of supracondylar fractures from a lateral approach. Stabilization achieved with safety. J Child Orthop. 2007, 1, pp. 127–133.
9
10. Flynn, J.C. and Zink, W.P.: In: MacEwen GD, Kasser JR,Heinrich SD, eds. Pediatric fractures. A practical approach to assessment and treatment. Baltimore: Williams and Wilkins. 1993, pp. 133-164.
10
11. Brauer CA, Lee BM, Bae DS, Waters PM, Kocher MS.A. systematic review of medial and lateral entry pinning versus lateral entry pinning for supracondylar fractures of the humerus. J Pediatr Orthop. 2008, Vol. 2, 27, pp. 181-186.
11
12. Eberhardt O, Fernandez F, Ilchmann T, Parsch K. Cross pinning of supracondylar fractures from a lateral approach. Stabilization achieved with safety. J Child Orthop. 2007, 1, pp. 127-133.
12
13. Gangadharan S, Rathinam B, Madhuri V. Radial nerve safety in Dorgan's lateral cross-pinning of the supracondylar. J Pediatr Orthop B. 2014, 6, pp. 579-583.
13
14. Queally JM, Paramanathan N, Walsh JC, Moran CJ, Shannon FJ, D'Souza LG. Dorgan's lateral cross-wiring of supracondylar fractures of the humerus in children: A retrospective review. j. injury. 2010, 6.
14
15. Shannon FJ, Mohan P, Chacko J, D’Souza LG. Dorgan’s percutaneous lateral cross wiring of supracondylar fractures of the humerus in children. J Pediatr Orthop. 2004, 24, pp. 376-379.
15
16. Lee SS, Mahar AT, Miesen D, Newton PO. Displaced pediatric supracondylar humerus fractures: biomechanical analysis of percutaneous pinning techniques. J Pediatr Orthop. 2002, 22, pp. 440–443.
16
17. Sudeep Vaidya, Achyut Rajbhandari, Nabees Pradhan, Suman Shrestha. Percutenious Fixation Of Displaced Supracondylar Fracture In Children Comparing Lateral With Medial And Lateral Pin. J Pediatr Orthop. 2009, 13, pp. 521-555.
17
18. El-Adl WA, El-Said MA, Boghdady GW, Ali AM. Results of treatment of displaced supracondylar humeral fractures in children by percutaneous lateral cross-wiring technique. Strategies Trauma Limb Reconstr. 2008, Vol. 3, pp. 1–7.
18
19. Brown IC, Zinar DM. Traumatic and iatrogenic neurological complications after supracondylar fractures of the humerus in children. J Pediatr Orthop. 1995, 15, pp. 440–443.
19
20. Queally JM, Paramanathan N, Walsh JC, Cathal J Moran CJ, Fintan J, et al. Dorgan’s lateral cross-wiring of supracondylar fractures of the humerus in children: a retrospective review. Injury. 2010, 41, pp. 568–571.
20
21. Flynn JC, Matthews JG, Benoit RL. Blind pinning of displaced supracondylar fractures of the humerus in children. Sixteen years' experience with long-term follow-up. J Bone Joint Surg Am. 1974, Vol. 2, 56, pp. 263-272.
21
ORIGINAL_ARTICLE
Value of High Sensitive CRP in Hyperglycemic Patients with Acute Coronary Syndrome
BACKGROUND: Hyperglycemia on admission in patients with acute coronary syndromes is common, and it is a powerful predicator of increased risk of in hospital complications in patients with and without diabetes mellitus, high sensitivity c- reactive protein (hs- CRP) is a cardiovascular risk marker in patients with acute coronary syndrome. OBJECTIVES: 1. To determine the levels of high-sensitivity C-reactive protein (hs-CRP) in subjects of acute coronary syndrome with admission hyperglycemia whatever diabetic or not. 2. To determine the levels of high-sensitivity C-reactive protein (hs-CRP) in subjects of acute coronary syndrome without admission hyperglycemia. 3. To compare the results of the above two groups and assess the prognostic value of admission glucose and hs -CRP levels in hyperglycemic patients with acute coronary syndromes. DESIGN AND SETTING: Prospective study, at Sohag university hospital in Egypt. METHODS: We measured the blood glucose, hs -CRP, cardiac enzymes and HBAIC levels at admission in 100 consecutive patients with ACS. Glucose was categorized as ≤11.1mmol=200 mg/dl. hs -CRP negative 3 mg, HBAIC ≤ 6.5% or ≥ 6.5). RESULTS: In our study reveals a statistically significant relation between levels of admission glucose and left ventricular function (LV failure, pulmonary edema and cardiogenic shock) or arrhythmias in hyperglycemic patients with ACS (P< 0.0001). Also there is a significant relation between level of hs- CRP and LVF and type of myocardial infarction in-hospital complications. Also there is insignificant relation between HBAIC levels and left ventricular function in ACS at admission. CONCLUSION: We conclude that elevated admission glucose appears a more important in predicting in-hospital and short term complications particularly left ventricular failure and cardiogenic shock in patients with acute coronary syndromes. Also the increased levels of hs- CRP are a predictor for severity and extent of myocardial damage and left ventricular function especially in STEMI. The synergistic effect of associated both stress hyperglycaemia and hs- CRP is a strong predictor for poor ACS outcome.
https://smj.journals.ekb.eg/article_41790_531d1e8793f308dadec21157c5eb0775.pdf
2018-01-01
273
280
10.21608/smj.2018.41790
High-sensitivity C-reactive protein level
hyperglycemia
Inflammatory marker
Atherosclerosis
Acute Coronary Syndrome
Alaa
Said
1
Department of Internal Medicine, Sohag university Hospital.
AUTHOR
Omar
Mohammed
omar_salim@med.sohag.edu.eg
2
Department Internal Medicine, Sohag university Hospital.
AUTHOR
Yasser
Kamal
yasser_kamal@med.sohag.edu.eg
3
Department of Internal medicine , Faculty of Medicine, Sohag University.
AUTHOR
Adel
El Sayed
adel_elsayed@med.sohag.edu.eg
4
Department Internal Medicine , Sohag university Hospital.
AUTHOR
1. Ridker PM, Rifai N, Rose L, Buring JE, Cook NR. Comparison of C-reactive protein and low-density lipoprotein cholesterol levels in the prediction of first cardiovascular events. N Engl J Med. 2002;347(20):1557-65.
1
2. Clearfield MB. C-reactive protein: a new risk assessment tool for cardiovascular disease. J Am Osteopath Assoc. 2005;105(9):409-16 .
2
3. Pfützner A, Forst T. High-sensitivity C-reactive protein as cardio vascular risk marker in patients with diabetes mellitus. Diabetes Technol Ther. 2006;8(1):28- 36.
3
4. Ritchie SA, Connell JM. The link between abdominal obesity, metabolic syndrome and cardiovascular disease. Nutr MetabCardiovasc Dis.2007;17(4):319-26.
4
5. Rasoul S,Ottevanger JP, Bilo HJ, Timmer JR,Van’t Hof Aw,ambrink JH,Dikkeschei LD, Hoorntje Jc, de Boer MJ and Zijistra F. Neth J Med.2007 Mar; 65 (3): 95-100.
5
6. Foo K, S Cooper,C Knight , A Suliman, K Ranjadayalan and A DTimmis. Single Serum glucose measurement predicts adverse outcomes across the whole range of acute coronary syndromes. Heart 2003; May; 89(5):512-516.
6
7. Hadjads S, Coisne D, Mavco G, Ragot S, Duengler F, Sosner P, Torremocha F,Herpin D andMarechaudR.Prognostic value of admission plasma glucose and HbA inacute myocardial infarction. Diabetes Med.2004; 21:305-310.
7
8. Isihara M, Inoue I, Kawagoe T, Shimatani Y. Kurisu S, Nishioka K. Umemura T, Nikamura S, andYoshida M.Impact of acute hyperglycemia on left ventricular function after reperfusion therapy in patients with first anterior myocardial infarction. Am Heart J. 2003; 164:674-678.
8
9. Rasoul S,Ottevanger JP, Bilo HJ, Timmer JR,Van’t Hof Aw, Dambrink JH, DikkescheiLD, Hoorntje Jc, de Boer MJ and Zijistra F.Glucose Dysregulation in non diabetic patients with St-elevation myocardial Infarction : Acute and chronic glucose dysregulation in STEMI. Neth J Med.2007 Mar; 65 (3): 95-100.
9
10.Timmer, JP, Ottervanger, H.S.G, Bilo, J.H.E Dambrink, K, Miedema, J.C.A and Zigilstra F.Prognositc value of admission glucose and glycosylated haemoglobin levels inacute coronary syndromes. J Med 2006;99:237-243.
10
11. Malmberg K, Rydn L, Wadel H, Birkeland K, Bootsma A, Dickstink, Efendic S, Fisher M, Hamsten A.Herlitz J, Hildebrandt P, Macleod K, Laakso M, Torppederson C, and Valdenstrom A; DIEAMI Z Investigators. Intense Metabolic Control by means an insulin in patients with diabetes mellitus and acute myocardial infarction (DIGAMI Z): Effects on mortality and morbidity. Eur Heart J 2005; 26:650-61.
11
12.Kausik K, Christopher P, Canon, David A., Buros J, Rifai N, Carolyn H, Mc Cabe, C. Gibson M andBraunwald E. Synergestic relationship between hyperglycemia and inflammation with respect to clinical outcomes in Non-ST elevation acute coronary syndromes; Analysis from OPUS – TIMI 16 and TACTICS – TIMI 18. European Heart Journal 2007 28(7):806-813.
12
13.Timmer JR, Bilo HJG, Ottervanger JP, Dambrink JHE, Miedema K, Hoorntje JCA, Zijlstra F.Dysglycemia in suspected acute coronary syndromes. Eur J Intern Med2005; 16:29 9. Tenerz A, Nilsson G, Forberg R, Ohrvik J, Malmberg K, Berne C, Leppert J. Basal glucometabolic status has an impact on long-term prognosis following an acute myocardial infarction in non-diabetic patients. J Intern Med 2003; 254:494–503.
13
14.Gresele P, Guglielmini G, De Angelis M, Ciferri S, Ciofetta M, Falcinelli E, Lalli C, Ciabattoni G, Davi G, Bolli GB.Acute, short-term hyperglycemia enhances shear stress-induced platelet activation in patients with type II diabetes mellitus. J Am Coll Cardiol 2003; 41:1013–20.
14
15.Lind L, Fugmann A, Branth S, Vessby B, Millgard J, Berne C, Lithell H.The impairment in endothelial function induced by non-esterified fatty acids can be reversed by insulin. Clin Sci (Lond) 2000; 99:169–74.
15
16.Marfella R, Siniscalchi M, Esposito K, Sellitto A, De Fanis U, Romano C,Portoghese M, Siciliano S, Nappo F, Sasso FC, Mininni N, Cacciapuoti F, Lucivero G, Giunta R, Verza M, Giugliano D. Effects of stress hyperglycemia on acute myocardialinfarction: role of inflammatory immune process infunctional cardiac outcome. Diabetes Care 2003; 26:3129–35.
16
17.Esposito K, Nappo F, Marfella R, Giugliano G, Giugliano F, Ciotola M, Quagliaro L, Ceriello A, Giugliano D. Inflammatory cytokine concentrations are acutely increased by hyperglycemia in humans: role of oxidative stress. Circulation 2002; 106:2067–72
17
(18. Duarte ER, Pellanda LC, Portal VL. Perfil inflamatório, metabólico e lipídico na síndrome isquêmica aguda: relação com eventos intra e pós-hospitalares. Arq Bras Cardiol. 2005;84(2):122-9.
18
(19. Zebrack JS, Anderson JL, Maycock CA, Horne BD, Bair TL, Muhlestein JB. Usefulness of high–sensitivity C reactive protein in predicting long term risk of death or acute myocardial infarction in patients with unstable or stable angina pectoris or acute myocardial infarction. Am J Cardiol 2002;89:145 :9.
19
(20.Cusack MR, Marber MS, Lambiase PD, Bucknall CA, Redwood SR. Systemic inflammation in unstable angina is the result of myocardial necrosis. J Am Coll Cardiol 2002;39:1917-23.
20
(21.Rubins HB, Robins SJ, Collins D, Fye CL, Anderson JW, Elam MB, et al. Gemfibrozil for the secondary prevention of coronary heartdisease in men with low levels of high-density lipoprotein cholesterol. Veterans Affairs high-density lipoprotein cholesterol intervention trial study group. N Engl J Med 1999;341:410-8.
21
(22.Perski A, Olsson G, Landou C, de Faire U, Theorell T, Hamsten A. Minimum heart rate and coronary atherosclerosis: independent relationsto global severity and rate of progression of angiographic lesions in men with myocardial infarction at a young age. Am Heart J 1992;123:609-16.
22
ORIGINAL_ARTICLE
Ischemic Heart Disease in Patients with Diabetes Mellitus
https://smj.journals.ekb.eg/article_41796_4eab2a2fedfff612ec9a39a381d12370.pdf
2018-01-01
281
290
10.21608/smj.2018.41796
Alaa
Ghaleb
alaa_ahmed@med.sohag.edu.eg
1
Department of Internal Medicine, Faculty of Medicine, Sohag University.
AUTHOR
Elham
Hamed
elhamomar@med.sohag.edu.eg
2
Department of Clinical andChemical pathology, Sohag Faculty of Medicine, Sohag University.
AUTHOR
Ahmed
Boghdady
ahmed_boghdady@med.sohag.edu.eg
3
Department of Internal Medicine, Faculty of Medicine, Sohag University.
AUTHOR
Hassan
Hassanin
hassan_hassanain@med.sohag.edu.eg
4
Department of Internal Medicine, Faculty of Medicine, Sohag University.
AUTHOR
World Health Organization. World Health Statistics. Department of Measurement & Health Information Systems of the Information, Evidence and Research Cluster. Geneva: WHO Press; 2008. p. 29-31.
1
Adler AI, Stratton IM, Neil HA, Yudkin JS, Matthews DR, Cull CA, et al. Association of systolic blood pressure with macrovascular and microvascular complications of type 2 diabetes (UKPDS 36): prospective observational study. BMJ 2000; 321 : 412-9.
2
American Diabetes A. Standards of Medical Care in Diabetes--2008. Diabetes Care 2008; 31 (Suppl 1): S12-54.
3
American Diabetic Association: Standards of medical care in diabetes- 2009. Diabetes Care 2009;32(suppl 1):S13-S61.
4
Antithrombotic Trialists Collaboration. Collaborative meta-analysis of randomised trials of antiplatelet therapy for prevention of death, myocardial infarction, and stroke in high risk patients. BMJ 2002; 324 : 71-86.
5
Baigent C, Blackwell L, Collins R, Emberson J, Godwin J, Peto R, et al. Aspirin in the primary and secondary prevention of vascular disease: collaborative meta-analysis of individual participant data from randomised trials. Lancet 2009; 373 : 1849-60.
6
Baigent C, Keech A, Kearney PM, Blackwell L, Buck G, Pollicino C, et al. Efficacy and safety of cholesterol-lowering treatment: prospective meta-analysis of data from 90,056 participants in 14 randomised trials of statins. Lancet 2005; 366 : 1267-78.
7
Bhatt DL, Marso SP, Hirsch AT, Ringleb PA, Hacke W, Topol EJ. Amplified benefit of clopidogrel versus aspirin in patients with diabetes mellitus. Am J Cardio 2002; 90 : 625-8.
8
Buse JB, Rosenstock J. Prevention of cardiovascular outcomes in type 2 diabetes mellitus: trials on the horizon. Endocrinol Metab Clin North Am 2005; 34 : 221-35.
9
Chalmers J, Joshi R, Patel A. Advances in reducing the burden of vascular disease in type 2 diabetes. Clin Exp Pharmacol Physiol 2008; 35 : 434-7.
10
Chambers JC, Elliott P, Zabaneh D, Zhang W, Li Y, Froguel P, et al. Common genetic variation near MC4R is associated with waist circumference and insulin resistance. Nat Genet 2008; 40 : 716-8.
11
Colhoun HM, Betteridge DJ, Durrington PN, Hitman GA, Neil HA, Livingstone SJ, et al. Primary prevention of cardiovascular disease with atorvastatin in type 2 diabetes in the Collaborative Atorvastatin Diabetes Study (CARDS): multicentre randomised placebo-controlled trial. Lancet 2004; 364 : 685-96.
12
Collins R, Armitage J, Parish S, Sleigh P, Peto R; MRC/BHF Heart Protection Study of cholesterol-lowering with simvastatin in 5963 people with diabetes: a randomised placebo-controlled trial. Lancet 2003; 361 : 2005-16.
13
Collins R, Peto R, MacMahon S, Hebert P, Fiebach NH, Eberlein KA, et al. Blood pressure, stroke, and coronary heart disease. Part 2, Short-term reductions in blood pressure: overview of randomised drug trials in their epidemiological context. Lancet 1990; 335 : 827-38.
14
Deedwania PC, Fonseca VA. Diabetes, prediabetes, and cardiovascular risk: shifting the paradigm. Am J Med 2005; 118 : 939-47.
15
Diaz VA, Mainous AG, 3rd, Baker R, Carnemolla M, Majeed A. How does ethnicity affect the association between obesity and diabetes? Diabet Med 2007; 24 : 1199-204.
16
Duckworth W, Abraira C, Moritz T, Reda D, Emanuele N, Reaven PD, et al. Glucose control and vascular complications in veterans with type 2 diabetes. N Engl J Med 2009; 360 : 129-39.
17
Enas EA, Mehta J. Malignant coronary artery disease in young Asian Indians: thoughts on pathogenesis, prevention, and therapy. Coronary Artery Disease in Asian Indians (CADI) Study. Clin Cardiol 1993; 18 : 131-5.
18
Estacio RO, Coll JR, Tran ZV, Schrier RW. Effect of intensive blood pressure control with valsartan on urinary albumin excretion in normotensive patients with type 2 diabetes. Am J Hypertens 2006; 19 : 1241-8.
19
Gaede P, Vedel P, Larsen N, Jensen GV, Parving HH, Pedersen O: Multifactorial intervention and cardiovascular disease in patients with type 2 diabetes. N Engl J Med 348: 383–393, 2003.
20
Gaziano TA, Reddy KS, Paccaud F, Horton S, Chaturvedi V. Cardiovascular Disease. In: Jamison DT, Breman JG, Measham AR, Alleyne G, Claeson M, Evans DB, et al, editors. Disease control priorities in developing countries, 2nd ed. New York: Oxford University Press; 2006. p. 645-62.
21
Gerstein HC, Miller ME, Byington RP, Goff DC Jr, Bigger JT, Buse JB, et al. Effects of intensive glucose lowering in type 2 diabetes. N Engl J Med 2008; 358 : 2545-59.
22
Ghaffar A, Reddy KS, Singhi M. Burden of non-communicable diseases in South Asia. BMJ 2004; 328 : 807-10.
23
Ginsberg HN, Bonds DE, Lovato LC, Crouse JR, Elam MB, Linz PE, et al. Evolution of the Lipid Trial Protocol of the Action to Control Cardiovascular Risk in Diabetes (ACCORD) Trial. Am J Cardiol 2007; 99 (Suppl 1): S56-S67.
24
Gupta M, Brister S. Is South Asian ethnicity an independent cardiovascular risk factor? Can J Cardiol 2006; 22 : 193-7.
25
Gupta R, Gupta VP, Sarna M, Prakash H, Rastogi S, Gupta KD. Serial epidemiological surveys in an urban Indian population demonstrate increasing coronary risk factors among the lower socioeconomic strata. J Assoc Physicians India 2003; 51 : 470-7
26
Gupta R, Joshi P, Mohan V, Reddy KS, Yusuf S. Epidemiology and causation of coronary heart disease and stroke in India. Heart 2008; 94 : 16-26.
27
Gupta R, Kumar P. Global diabetes landscape - Type 2 diabetes mellitus in south Asia: Epidemiology, risk factors, and control. Insulin 2008; 3 : 78-94.
28
Haffner SJ, Cassells H. Hyperglycemia as a cardiovascular risk factor. Am J Med 2003; 115 (Suppl 8A): 6S-11S.
29
Hansson L, Zanchetti A, Carruthers SG, Dahlof B, Elmfeldt D, Julius S, et al. Effects of intensive blood-pressure lowering and low-dose aspirin in patients with hypertension: principal results of the Hypertension Optimal Treatment (HOT) randomised trial. HOT Study Group. Lancet 1998; 351 : 1755-62.
30
Holman RR, Paul SK, Bethel MA, Matthews DR, Neil HA. 10-year follow-up of intensive glucose control in type 2 diabetes. N Engl J Med 2008; 359 : 1577-89.
31
Iestra JA, Kromhout D, van der Schouw YT, Grobbee DE, Boshuizen HC, van Staveren WA. Effect size estimates of lifestyle and dietary changes on all-cause mortality in coronary artery disease patients: a systematic review. Circulation 2005; 112 : 924-34.
32
International Diabetes Federation (IDF). Diabetes atlas 4th ed. 2009. Available at: www.diabetesatlas.org. Joshi P, Islam S, Pais P, Reddy S, Dorairaj P, Kazmi K, et al. Risk factors
33
ORIGINAL_ARTICLE
Comparative study between posterior and modified posterior approaches of humeral diaphyseal fractures in adults
Introduction The optimal treatment of humeral shaft fractures continues to be debated. In the current investigation, we sought to determine the clinical and radiographic outcomes following the plate fixation of humeral shaft fractures utilizing the modified posterior approach. Materials and methods A retrospective review identified a consecutive series of 30 humeral shaft fractures (OTA20-A, 10-B, or 0-C) treated with plate fixation via a posterior (14 patients), ormodified posterior approach (16 patients) between 2016 and 2017 by a single surgeon. Demographics, operative reports, clinical follow-up, and preoperative radiographs were reviewed. Postoperative radiographs were assessed for angular deformity and time to union. Range of motion and strength testing were also reviewed. Results A total of 30 humeral shaft fractures were reviewed with a mean clinical follow-up of 4 months. The mean time to union was13.1 weeks and there3 patients developed radial nerve palsies in posterior approach group and one case in modified posterior approach postoperatively. Conclusionboth approaches could be used in the management of humeral diaphyseal middle or distal third fractures, And the modified posterior approach confirmed by our results minimizes the complication rate, allow early return of full range of elbow motion and full triceps muscle power and facilitates early return to normal activities of the patient with excellent functional out comes .
https://smj.journals.ekb.eg/article_41805_36ccfc72ec24c1f47cf92151f8aec739.pdf
2018-01-01
291
295
10.21608/smj.2018.41805
Emad
Nagib
1
Department of Orthopaedic and Traumatology , Faculty of Medicine , Sohag Univeristy.
AUTHOR
Ahmed
Shaker
ahmed_saleem@med.sohag.edu.eg
2
Department of Orthpaedic and Traumatology , Faculty of Medicine, Sohag University.
AUTHOR
Wael
salama
waeladel@med.sohag.edu.eg
3
Department of Orthopedics and Traumatology, Faculty of medicine, Sohag university, Egypt.
AUTHOR
Ahmed
Eldosoky
ahmed_eldesouky@med.sohag.edu.eg
4
Department of Orthpaedic and Traumatology , Faculty of Medicine, Sohag University.
AUTHOR
Shazly
Musa
shazli_mousa@med.sohag.edu.eg
5
Department of Orthopaedic and Traumatology , Faculty of Medicine , Sohag Univeristy.
AUTHOR
1 - Handbook of fractures, Kennethv A.Egol, Kenneth J. Koval and Joseph D.Zuckerman, fractures of the shaft of the humerus fourth edition Page 203:213, 1996
1
2 - Caldwell: The treatment of humeral fractures with Hanging cast Orthop. Trauma,10:16-13,1940.
2
3 - Epps Ch. Jr., Grant RE: Fractures of the shaft of the humerus .Chapter11 in fractures in adults, 3rd edition. Editors: Rockwood CA., Green DP, and Bucholz RW.
3
4 - Elizabeth B. Gausden, Alexander B.Christ ,Stephen J. Warner, et al The triceps-sparing posterior approach to plating humeral shaft fractures results in a high rate of union and low incidence of complications., Arc Orthop Trauma Surg 136:1683–1689 (2016
4
5- Muller ME,Allgower A, Scneider R,Willnegger H: Manual of internal fixation: techniques recommended by the AO-ASIF group.3rd edition.Berlin,Springer-Verlag,1991
5
6- MICHELLE GERWIN, ROBERT N. HOTCHKISS and ANDREW J. WEILAND.: Alternative Operative Exposures of the Posterior Aspect of the Humeral Diaphysis. With Reference to the Radial Nerve, J Bone Joint Surg Am78:1690-5,
6
7- Stanley Hoppenfeld, Piet deBoer et al, Surgical exposures in orthopedics, Fourth edition P 98 – 105
7
8- Yi JW, Oh JK, Han SB, Shin SJ, Oh CW, Yoon YC (2013) Healing process after rigid plate fixation of humeral shaft fractures revisited. Arch Orthop Trauma Surg 133:811–817
8
9-Wang X, Zhang P, Zhou Y, Zhu C (2014) Secondary radial nervepalsy after internal fixation of humeral shaft fractures. Eur JOrthop Surg Traumatol 24:331–333.
9
10-Yin P, Zhang L, Mao Z, Zhao Y, Zhang Q, Tao S, Liang X, Zhang H, Lv H, Li T, Tang P (2014) Comparison of lateral and posterior surgical approach in management of extra-articular distal humeral shaft fractures. Injury 45:1121–1125.
10
11-Singh AK, Narsaria N, Seth RR, Garg S (2014) Plate osteosynthesis of fractures of the shaft of the humerus: comparison of limited contact dynamic compression plates and locking compression plates. J Orthop Traumatol 15:117–122.
11
12-Wang C, Li J, Li Y, Dai G, Wang M (2015) Is minimally invasive plating osteosynthesis for humeral shaft fracture advantageous compared with the conventional open technique? J Shoulder Elb Surg 24:1741–1748.
12
ORIGINAL_ARTICLE
A Study of Prevalence of Obesity among Female Students in Sohag University
Introduction: Obesity is a medical case in which extra body fat has stored to the extent that it may have a harmful effect on health. People are generally measured obese when their body mass index (BMI), ameasurement obtained by dividing aperson's weight by the square of the person's height, is over 30 kg/m2, with the range 25–30 kg/m2 defined as overweight. Some East Asian countries use lower values. Aim of the work: Find out the prevalence of overweight and obesity among female students in Sohag University, and identify important risk factors. Patients and Methods: Cross sectional study, included a sample of female students aged 17-25 in the selected faculties in Sohag University, the study was carried out in Faculty of Medicine, Faculty of Nursery and Faculty of Education in Sohag University, the questionnaire was divided into five parts, the demography, dietary habits, physical activity, perceptions of body weight and beliefs of obesity and the record of self-reported and actual anthropometric body measurements. Results: Overweight and obesity were prevalent among the our study subjects as the prevelance was 38.5%, lack of physical activity, soft drink consumpton and marital status were significantly associated with obesity, our students preferred dairy products and fatty foods over vegetables and fruits. In addition, their “lack of time” was the most frequently mentioned barrier to eating a healthy diet and engaging in regular exercise. Life style modification is important to improve healthy habits earlier in life. Conclusion: Overweight and obesity were prevalent among the our study subjects as the prevelance was 38.5%.
https://smj.journals.ekb.eg/article_41810_716cc8e1f291fee826818527c6594db3.pdf
2018-01-01
297
311
10.21608/smj.2018.41810
Obesity
Female
Sohag university
Farida
Abdou
1
Department of Family Medicine, Faculty of Medicine, Sohag University.
AUTHOR
ahmed
elnahhas
ahmed_hamed@med.sohag.edu.eg
2
public health and community medicine department, faculty of medicine, Sohag University, sohag, egypt.
AUTHOR
Eman
Mohammed
eman_mahmoud@med.sohag.edu.eg
3
Department of Family Medicine, Faculty of Medicine, Sohag University.
AUTHOR
Nesreen
Mohammed
nesreen_mohamed@med.sohag.edu.eg
4
department, of Public Health and Community Medicine-Sohag University.
AUTHOR
1 .Kanazawa M, Yoshiike N, Osaka T, Numba Y, Zimmet P, Inoue S. Criteria and classification of obesity in Japan and Asia-Oceania. World review of nutrition and dietetics. 2005;94:1-12.
1
2 . Haslam DW, James WP. Obesity. Lancet. 2005;366(9492):1197-209.
2
3 .Musaiger AO, Hassan AS, Obeid O. The paradox of nutrition-related diseases in the Arab countries: the need for action. International journal of environmental research and public health. 2011;8(9):3637-71.
3
4. Sengupta A, Angeli F, Syamala TS, Dagnelie PC, van Schayck CP. Overweight and obesity prevalence among Indian women by place of residence and socio-economic status: Contrasting patterns from 'underweight states' and 'overweight states' of India. Social science & medicine. 2015;138:161-9.
4
5 .Tjepkema M. Adult obesity. Health reports. 2006;17(3):9-25. 6Berghofer A, Pischon T, Reinhold T, Apovian CM, Sharma AM, Willich SN. Obesity prevalence from aEuropean perspective: a systematic review. BMC public health. 2008;8:200.
5
7.Adesina AF, Peterside O, Anochie I, Akani NA. Weight status of adolescents in secondary schools in port Harcourt using Body Mass Index (BMI). Italian journal of pediatrics. 2012;38:31.
6
8 .Yahia N, Achkar A, Abdallah A, Rizk S. Eating habits and obesity among Lebanese university students. Nutrition journal. 2008;7:32.
7
9 .Horikawa C, Kodama S, Yachi Y, Heianza Y, Hirasawa R, Ibe Y, et al. Skipping breakfast and prevalence of overweight and obesity in Asian and Pacific regions: a meta-analysis. Preventive medicine. 2011;53(4-5):260-7.
8
10.Ganasegeran K, Al-Dubai SA, Qureshi AM, Al-abed AA, Am R, Aljunid SM. Social and psychological factors affecting eating habits among university students in a Malaysian medical school: a cross-sectional study. Nutrition journal. 2012;11:48.
9
11.Moy FM, Johari S, Ismail Y, Mahad R, Tie FH, Wan Ismail WA. Breakfast Skipping and Its Associated Factors among Undergraduates in a Public University in Kuala Lumpur. Malaysian journal of nutrition. 2009;15(2):165-74.
10
12.Malik VS, Schulze MB, Hu FB. Intake of sugar-sweetened beverages and weight gain: a systematic review. The American journal of clinical nutrition. 2006;84(2):274-88.
11
13.Pinto BM, Cherico NP, Szymanski L, Marcus BH. Longitudinal changes in college students' exercise participation. Journal of American college health : J of ACH. 1998;47(1):23-7.
12
14.ruz SY, Fabian C, Pagan I, Rios JL, Gonzalez AM, Betancourt J, et al. Physical activity and its associations with sociodemographic characteristics, dietary patterns, and perceived academic stress in students attending college in Puerto Rico. Puerto Rico health sciences journal. 2013;32(1):44-50.
13
15.Davy SR, Benes BA, Driskell JA. Sex differences in dieting trends, eating habits, and nutrition beliefs of a group of midwestern college students. Journal of the American Dietetic Association. 2006;106(10):1673-7.
14
16.Neutzling MB, Hallal PR, Araujo CL, Horta BL, Vieira Mde F, Menezes AM, et al. Infant feeding and obesity at 11 years: prospective birth cohort study. International journal of pediatric obesity : IJPO : an official journal of the International Association for the Study of Obesity. 2009;4(3):143-9.
15
17.Garaulet M, Martinez A, Victoria F, Perez-Llamas F, Ortega RM, Zamora S. Difference in dietary intake and activity level between normal-weight and overweight or obese adolescents. Journal of pediatric gastroenterology and nutrition. 2000;30(3):253-8.
16
18.Monteiro P, Victora C, Barros F.[Social, familial, and behavioral risk factors for obesity in adolescents]. Revista panamericana de salud publica = Pan American journal of public health. 2004;16(4):250-8.
17
19.Neutzling MB, Taddei JA, Gigante DP. Risk factors of obesity among Brazilian adolescents: a case-control study. Public health nutrition. 2003;6(8):743-9.
18
20.Silveira D, Taddei JA, Escrivao MA, Oliveira FL, Ancona-Lopez F. Risk factors for overweight among Brazilian adolescents of low-income families: a case-control study. Public health nutrition. 2006;9(4):421-8.
19
21.Chen G, Liu C, Yao J, Jiang Q, Chen N, Huang H, et al. Overweight, obesity, and their associations with insulin resistance and beta-cell function among Chinese: a cross-sectional study in China. Metabolism: clinical and experimental. 2010;59(12):1823-32.
20
22.Al-Rethaiaa AS, Fahmy AE, Al-Shwaiyat NM. Obesity and eating habits among college students in Saudi Arabia: a cross sectional study. Nutrition journal. 2010;9:39.
21
23.Siddiqi Z, Tiro JA, Shuval K. Understanding impediments and enablers to physical activity among African American adults: a systematic review of qualitative studies. Health education research. 2011;26(6):1010-24.
22
24.Janssen I, Katzmarzyk PT, Boyce WF, King MA, Pickett W. Overweight and obesity in Canadian adolescents and their associations with dietary habits and physical activity patterns. The Journal of adolescent health : official publication of the Society for Adolescent Medicine. 2004;35(5):360-7.
23
25.Neumark-Sztainer D, Story M, Resnick MD, Blum RW. Correlates of inadequate fruit and vegetable consumption among adolescents. Preventive medicine. 1996;25(5):497-505.
24
26. Arroyo Izaga M, Rocandio Pablo AM, Ansotegui Alday L, Pascual Apalauza E, Salces Beti I, Rebato Ochoa E. [Diet quality, overweight and obesity in university students]. Nutricion hospitalaria. 2006;21(6):673-9.
25
ORIGINAL_ARTICLE
Study of Ankle-Brachial Index Compared to Carotid Intima-Media Thickness as a Non-Invasive Technique to Predict the Severity of Coronary Atherosclerosis
https://smj.journals.ekb.eg/article_41816_ffa444fcdef546504eec74f2e2723bdf.pdf
2018-01-01
313
319
10.21608/smj.2018.41816
Mohamed
Elsayed
mohamed_elsayed@med.sohag.edu.eg
1
Department of Internal Medicine. faculty of medicine.sohag University.
AUTHOR
Roig CS, de Winther MP, Weber C, et al. Atherosclerotic plaque destabilization mechanism, models, and therapeutic strategies. Circ Res. 2014; 114: 214-26.
1
Norgren L, Hiatt WR, Dormandy JA, et al. Trans Atlantic Inter-society Consensus for the management of peripheral arterial disease (TASC II). J Vasc Surg. 2007; 45 (Suppl S): S5-67.
2
Heald CL, Fowkes FG, Murray GD, et al. Risk of mortality and cardiovascular disease associated with the ankle brachial index: Systematic review. Atherosclerosis. 2006; 189: 61-9.
3
Hirsch AT, Criqui MH, Treat-Jacobson D, et al. Peripheral arterial disease detection, awareness, and treatment in primary care. JAMA. 2001; 286: 1317-24.
4
Lamina C, Meisinger C, Heid IM, et al. Association of ankle brachial index and plaques in the carotid and femoral arteries with cardiovascular events and total mortality in a population-based study with 13 years of follow up. Eur Heart J. 2006; 27: 2580-7.
5
Ueki Y, Miura T, Miyashita Y, et al. Predictive value of combining the ankle brachial index and SYNTAX score for the prediction of outcome after percutaneous coronary intervention (from the SHINANO Registry). Am J Cardiol. 2016; 117: 179-85.
6
Chang ST, Chu CM, Hsu JT, et al. Role of ankle-brachial pressure index as a predictor of coronary artery disease severity in patients with diabetes mellitus. Canadian Journal of Cardiology, 2009; 25(9): S301-
7
AK Agarwal, Manjeet Singh, Vivek Arya, et al. Prevalence of peripheral Arterial Disease and its correlation with coronary artery disease. JAPI, 2010; 60: 45-50.
8
Lee AJ, Price JF, Russell MJ, et al. Improved prediction of fatal myocardial infarction using the ankle brachial index in addition to conventional risk factors: the Edinburgh Artery Study. Circulation. 2004; 110 (19): 3075 - 3080.
9
Leng GC, Fowkes FG, Lee AJ, et al. Use of ankle brachial pressure index to predict cardiovascular events and death: a cohort study. BMJ. 1996; 313:1440 -1444.
10
Papamichael CM, Lekakis JP, Stamatelopoulos KS, et al. Ankle-brachial index as a predictor of the extent of coronary atherosclerosis and cardiovascular events in patients with coronary artery disease. Am J Cardiol . 2000; 8 6(6):615 - 618.
11
Criqui MH, McClelland RL, McDermott MM, et al. The ankle-brachial index and incident cardiovascular events in the MESA (Multi-Ethnic Study of Atherosclerosis). J Am CollCardiol. 2010; 56 (18):1506 - 1512.
12
Kasliwal RR, Bansal M, Gupta H, et al. Association of carotid intima- media thickness with left main coronary artery disease. Indian Heart J. 2007; 59 (1):50 - 55.
13
Wang D, Yang H, Quinones MJ, et al. A genome-wide scan for carotid artery intima-media thickness: the Mexican - American Coronary Artery Disease Family Study. Stroke. 2005;36 (3): 540 - 545.
14
Liviakis L, Pogue B, Paramsothy P, et al. Carotid intima-media thickness for the practicing lipidologist. J ClinLipidol. 2010; 4 (1): 24 - 35.
15
Kablak-Ziembicka A, Tracz W, Przewlocki T, et al. Association of increased carotid intima- media thickness with the extent of coronary artery disease.Heart. 2004; 90(11):1286 – 1290
16
Heuten H, Goovaerts I, Ennekens G, et al. Carotid artery intima- media thickness is associated with coronary artery disease. ActaCardiol. 2008;63( 3):309 – 313.
17
Hayashi C, Ogawa O, Kubo S, et al. Ankle brachial pressure index and carotid intima- media thickness as atherosclerosis markers in Japanese diabetics. Diabetes Res ClinPract. 2004; 66 (3): 269-275.
18
Pignoli P, Tremoli E, Poli A, et al. Intimal plus media l thickness of the arterial wall: a direct measurement with ultrasound imag ing. Circulation. 1986;74:1399 – 1406
19
Greenland P, Alpert JS, Beller GA, et al; American College of Cardiology Foundation; American Heart Association. 2010 ACCF/AHA guideline for assessment of cardiovascular risk in asymptomatic adults: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardio l. 2010; 56:e50 – e103.
20
Stein JH, Korcarz CE, Hurst RT, et al. Use of carotid ultrasound to identify subclinical vascular dis-ease and evaluate cardiovascular disease risk: A consensus statement from the American Society of Echocardiography Carotid Intima-Media Thickness Task Force: Endorsed by the Society for Vascular Medicine. J Am Soc Echocardiogr 2008; 21: 93 – 111; quiz 189 – 190.
21
Weintraub W.S., Karlsberg R.P., Tcheng J.E., et al. ACCF/AHA 2011 key data elements and definitions of a base cardiovascular vocabulary for electronic health records: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Clinical Data Standards. J. Am. Coll. Cardiol. 2011; 58(2):202–222.
22
Criqui MH, Denenberg JO, Langer RD, et al. The epidemiology of peripheral arterial disease: Importance of identifying the population at risk. Vasc Med 1997; 2: 221 – 226.
23
McKenna M, Wolfson S, Kuller L. The ratio of ankle and arm arterial pressure as an independent predictor of mortality. Atherosclerosis 1991; 87: 119 – 128.
24
Criqui MH, Langer RD, Fronek A, et al. Mortality over a period of 10 years in patients with peripheral arterial disease. N Engl J Med 1992; 326: 381 – 386.
25
Ikeda N, Kogame N, Iijima R, et al. Carotid artery intima-media thickness and plaque score can predict the SYNTAX score. Eur Heart J 2012; 33: 113 – 119.
26
Howard G, Burke GL, Evans GW, et al. Relations of intimal-medial thickness among sites within the carotid artery as evaluated by B-mode ultrasound: ARIC Investigators: Atherosclerosis Risk in Communities. Stroke 1994; 25: 1581 – 1587.
27
Cacoub PP, Abola MT, Baumgartner I, et al. Cardiovascular risk factor control and outcomes in peripheral artery disease patients in the Reduction of Atherothrombosis for Continued Health (REACH) Registry. Atherosclerosis 2009; 204: e86 – e92.
28
Singh M, Lennon RJ, Darbar D, et al. Effect of peripheral arterial disease in patients undergoing percutaneous coronary intervention with intracoronary stents. Mayo Clin Proc 2004; 79: 1113 – 1118.
29
Morice MC, Serruys PW, Kappetein AP, et al. Outcomes in patients with de novo left main disease treated with either percutaneous coronary intervention using paclitaxel-eluting stents or coronary artery bypass graft treatment in the Synergy Between Percutaneous Coronary Intervention with TAXUS and Cardiac Surgery (SYNTAX) trial. Circulation 2010; 121: 2645 – 2653.
30
Valgimigli M, Serruys PW, Tsuchida K, et al. Cyphering the complexity of coronary artery disease using the syntax score to predict clinical outcome in patients with three-vessel lumen obstruction undergoing percutaneous coronary intervention. Am J Cardiol 2007; 99: 1072 – 1081.
31
ORIGINAL_ARTICLE
Molecular characterization of mutation in the parC and gyrB genes that confer fluoroquinolone resistance in Streptococcus pneumonia isolates
Resistance of Streptococcus pneumoniae to multiple antibacterial agents, including β-lactams, macrolides, tetracyclines, and co-trimoxazole, has emerged worldwide in the 1980s and 1990s and has emphasized the need for new therapeutic alternatives, such as newer fluoroquinolones. Older fluoroquinolones, such as ciprofloxacin and ofloxacin, have been widely used in the last 2 decades, but their activity against gram-positive pathogens is limited. Newer fluoroquinolones, such as levofloxacin, gatifloxacin, moxifloxacin, and gemifloxacin, have enhanced activity against most respiratory pathogens, and some are being more widely used to treat respiratory tract infections. Therefore, the emergence of fluoroquinolone-resistant S. pneumoniae strains, although worldwide prevalence is low, is a concern to clinicians who manage respiratory tract infections. Aim of the work: The aim of this study was to determine the prevalence of fluoroquinolone resistance Streptococcus pneumoniae (FQRSP) and to examine the genetic relatedness of pneumococcal isolates with parC and gyrB genes mutations in different specimens. Patients and Methods: In this study, Biometra Thermal Cyclar-T Gradient Software PCR system version 4 together with DNASIS 2.6 Sequence Analysis Programs were used to investigate the presence of mutations at quinolone resistance-determining regions of topoisomerase IV and DNA gyrase on 78 S. pneumoniae strains, Among 78 isolates 37 (47.4%) of S. pneumonia isolates were Fluroquinolones susceptible, 12 (15.4%) were with variable susceptibility and 29 (37.2%) were Fluroquinolones resistant. Results: Our study illustrate the role of mutation in the parC & gyrB genes and the effect of mutations in the both genes in fluoroquinolone resistance among S. pneumoniae isolates. Conclusion: Results indicated that there is a significant correlation between quinolone resistance development and mutations in the parC gene and in less significance in the gyrB genes .
https://smj.journals.ekb.eg/article_41821_3a91a239a906032e4e7baefa9b4dcb62.pdf
2018-01-01
321
334
10.21608/smj.2018.41821
GyrB
ParC
Streptococcus pneumonia
Fluoroquinolones
Laila
Yousef
lailamohamed@med.sohag.edu.eg
1
Department of Clinical and Chemical pathology, Faculty of Medicine, Sohag University.
AUTHOR
Ghada
Ismael
2
Department of Clinical Pathology, Faculty of Medicine, Ain Shams University.
AUTHOR
Ashraf
Mohammed
ashraf_abdallah@med.sohag.edu.eg
3
Department of Clinical Pathology, Faculty of Medicine, Sohag University.
AUTHOR
Mohammed
Mahmoud
mohamedhamdy@med.sohag.edu.eg
4
Department of Clinical Pathology, Faculty of Medicine, Sohag University.
AUTHOR
1. Mandell LA, Wunderink RG, Anzueto A, Bartlett JG, Campbell GD, Dean NC, et al. Infectious Diseases Society of America/American Thoracic Society consensus guidelines on the management of community-acquired pneumonia in adults. Clinical infectious diseases : an official publication of the Infectious Diseases Society of America. 2007;44 Suppl 2:S27-72.
1
2. Patel SN, McGeer A, Melano R, Tyrrell GJ, Green K, Pillai DR, et al. Susceptibility of Streptococcus pneumoniae to fluoroquinolones in Canada. Antimicrobial agents and chemotherapy. 2011;55(8):3703-8.
2
3. Morrissey I, Farrell DJ, Bakker S, Buckridge S, Felmingham D. Molecular characterization and antimicrobial susceptibility of fluoroquinolone-resistant or -susceptible Streptococcus pneumoniae from Hong Kong. Antimicrobial agents and chemotherapy. 2003;47(4):1433-5.
3
4. de la Campa AG, Balsalobre L, Ardanuy C, Fenoll A, Perez-Trallero E, Linares J, et al. Fluoroquinolone resistance in penicillin-resistant Streptococcus pneumoniae clones, Spain. Emerging infectious diseases. 2004;10(10):1751-9.
4
5. Fisher LM, Gould KA, Pan XS, Patel S, Heaton VJ. Analysis of dual active fluoroquinolones in Streptococcus pneumoniae. The Journal of antimicrobial chemotherapy. 2003;52(2):312-3; author reply 3-4.
5
6. Andersson MI, MacGowan AP. Development of the quinolones. The Journal of antimicrobial chemotherapy. 2003;51 Suppl 1:1-11.
6
7. Collins MD, Hutson RA, Hoyles L, Falsen E, Nikolaitchouk N, Foster G. Streptococcus ovis sp. nov., isolated from sheep. International journal of systematic and evolutionary microbiology. 2001;51(Pt 3):1147-50.
7
8. Zhanel GG, Palatnick L, Nichol KA, Bellyou T, Low DE, Hoban DJ. Antimicrobial resistance in respiratory tract Streptococcus pneumoniae isolates: results of the Canadian Respiratory Organism Susceptibility Study, 1997 to 2002. Antimicrobial agents and chemotherapy. 2003;47(6):1867-74.
8
9. Tettelin H, Nelson KE, Paulsen IT, Eisen JA, Read TD, Peterson S, et al. Complete genome sequence of a virulent isolate of Streptococcus pneumoniae. Science. 2001;293(5529):498-506.
9
10. Hoskins J, Alborn WE, Jr., Arnold J, Blaszczak LC, Burgett S, DeHoff BS, et al. Genome of the bacterium Streptococcus pneumoniae strain R6. Journal of bacteriology. 2001;183(19):5709-17.
10
11. Kargar M, Moein Jahromi F, Doosti A, Handali S. Molecular Investigation of Quinolone Resistance of Quinolone Resistance-Determining Region in Streptococcus pneumoniae Strains Isolated from Iran Using Polymerase Chain Reaction-Restriction Fragment Length Polymorphism Method. Osong public health and research perspectives. 2014;5(5):245-50.
11
12. Bast DJ, Low DE, Duncan CL, Kilburn L, Mandell LA, Davidson RJ, et al. Fluoroquinolone resistance in clinical isolates of Streptococcus pneumoniae: contributions of type II topoisomerase mutations and efflux to levels of resistance. Antimicrobial agents and chemotherapy. 2000;44(11):3049-54.
12
13. Broskey J, Coleman K, Gwynn MN, McCloskey L, Traini C, Voelker L, et al. Efflux and target mutations as quinolone resistance mechanisms in clinical isolates of Streptococcus pneumoniae. The Journal of antimicrobial chemotherapy. 2000;45 Suppl 1:95-9.
13
14. Brueggemann AB, Coffman SL, Rhomberg P, Huynh H, Almer L, Nilius A, et al. Fluoroquinolone resistance in Streptococcus pneumoniae in United States since 1994-1995. Antimicrobial agents and chemotherapy. 2002;46(3):680-8.
14
15. Beekmann SE, Heilmann KP, Richter SS, Garcia-de-Lomas J, Doern GV, Group GS. Antimicrobial resistance in Streptococcus pneumoniae, Haemophilus influenzae, Moraxella catarrhalis and group A beta-haemolytic streptococci in 2002-2003. Results of the multinational GRASP Surveillance Program. International journal of antimicrobial agents. 2005;25(2):148-56.
15
16. Jones ME, Sahm DF, Martin N, Scheuring S, Heisig P, Thornsberry C, et al. Prevalence of gyrA, gyrB, parC, and parE mutations in clinical isolates of Streptococcus pneumoniae with decreased susceptibilities to different fluoroquinolones and originating from Worldwide Surveillance Studies during the 1997-1998 respiratory season. Antimicrobial agents and chemotherapy. 2000;44(2):462-6.
16
17. Korzheva N, Davies TA, Goldschmidt R. Novel Ser79Leu and Ser81Ile substitutions in the quinolone resistance-determining regions of ParC topoisomerase IV and GyrA DNA gyrase subunits from recent fluoroquinolone-resistant Streptococcus pneumoniae clinical isolates. Antimicrobial agents and chemotherapy. 2005;49(6):2479-86.
17
18. Davies TA, Evangelista A, Pfleger S, Bush K, Sahm DF, Goldschmidt R. Prevalence of single mutations in topoisomerase type II genes among levofloxacin-susceptible clinical strains of Streptococcus pneumoniae isolated in the United States in 1992 to 1996 and 1999 to 2000. Antimicrobial agents and chemotherapy. 2002;46(1):119-24.
18
19. Lim S, Bast D, McGeer A, de Azavedo J, Low DE. Antimicrobial susceptibility breakpoints and first-step parC mutations in Streptococcus pneumoniae: redefining fluoroquinolone resistance. Emerging infectious diseases. 2003;9(7):833-7.
19
20. Doern GV, Richter SS, Miller A, Miller N, Rice C, Heilmann K, et al. Antimicrobial resistance among Streptococcus pneumoniae in the United States: have we begun to turn the corner on resistance to certain antimicrobial classes? Clinical infectious diseases : an official publication of the Infectious Diseases Society of America. 2005;41(2):139-48.
20
21. De Vecchi E, Nicola L, Ossola F, Drago L. In vitro selection of resistance in Streptococcus pneumoniae at in vivo fluoroquinolone concentrations. The Journal of antimicrobial chemotherapy. 2009;63(4):721-7.
21
22. Sierra JM, Cabeza JG, Ruiz Chaler M, Montero T, Hernandez J, Mensa J, et al. The selection of resistance to and the mutagenicity of different fluoroquinolones in Staphylococcus aureus and Streptococcus pneumoniae. Clinical microbiology and infection : the official publication of the European Society of Clinical Microbiology and Infectious Diseases. 2005;11(9):750-8.
22
23. Brino L, Urzhumtsev A, Mousli M, Bronner C, Mitschler A, Oudet P, et al. Dimerization of Escherichia coli DNA-gyrase B provides a structural mechanism for activating the ATPase catalytic center. The Journal of biological chemistry. 2000;275(13):9468-75.
23
24. Fass D, Bogden CE, Berger JM. Quaternary changes in topoisomerase II may direct orthogonal movement of two DNA strands. Nature structural biology. 1999;6(4):322-6.
24
25. Hosaka M, Kinoshita S, Toyama A, Otsuki M, Nishino T. Antibacterial properties of AM-1155, a new 8-methoxy quinolone. The Journal of antimicrobial chemotherapy. 1995;36(2):293-301.
25
26. Stass H, Dalhoff A, Kubitza D, Schuhly U. Pharmacokinetics, safety, and tolerability of ascending single doses of moxifloxacin, a new 8-methoxy quinolone, administered to healthy subjects. Antimicrobial agents and chemotherapy. 1998;42(8):2060-5.
26
27. Yoshida H, Bogaki M, Nakamura M, Nakamura S. Quinolone resistance-determining region in the DNA gyrase gyrA gene of Escherichia coli. Antimicrobial agents and chemotherapy. 1990;34(6):1271-2.
27
28. Fukushima KY, Hirakata Y, Sugahara K, Yanagihara K, Kondo A, Kohno S, et al. Rapid screening of topoisomerase gene mutations by a novel melting curve analysis method for early warning of fluoroquinolone-resistant Streptococcus pneumoniae emergence. Journal of clinical microbiology. 2006;44(12):4553-8.
28
ORIGINAL_ARTICLE
MANAGEMENT OF SUPRACONDYLAR FRACTURE HUMERUS WITH Pink Pulseless Hand in Children.
The management of children with a pink pulseless hand in severely displaced supracondylar humeral fractures remains controversial regarding immediate exploration of the brachial artery and revascularization during fracture fixation or just closed reduction of the fracture and percutaneous pinning and follow up of limb perfusion.Between 2012 and 2016 we followed 52 children with displaced supracondylar fracture humerus. All patients had absent radial pulse with an otherwise well perfused hand. The radial pulse was returned in all patients, without surgical exploration after closed reduction of the fracture and percutaneous pinning .It takes variable periods from 1week to 2 months . Radial pulse recovery may be due to recanalization of brachial artery or by collaterals. So closed reduction of the fracture, percutaneous pinning and observation is a good option of treatment pediatric supracondylar humeral fractures with a pink pulseless hand without need to do early revascularization procedures.
https://smj.journals.ekb.eg/article_41979_176a8d574753a55a5aeb9423e5124def.pdf
2018-01-01
337
341
10.21608/smj.2018.41979
Mohamed
Atea
1
Department of Orthopedics, Sohag University ,Sohag , Egypt.
AUTHOR
Ashraf
Ahmed
ashraf_marzouk@med.sohag.edu.eg
2
Department of Orthopedics, Sohag University ,Sohag , Egypt.
AUTHOR
Ahmed
Eldosoky
ahmed_eldesouky@med.sohag.edu.eg
3
Department of Orthpaedic and Traumatology , Faculty of Medicine, Sohag University.
AUTHOR
Mohamed
Abdel-Wanis
mohamed_abdelwanees@med.sohag.edu.eg
4
Department of Orthpaedic and Traumatology , Faculty of Medicine, Sohag University.
AUTHOR
1. Noaman HH, . Microsurgical reconstruction of brachial artery injuries in displaced supracondylar fracture humerus in children. J Microsurgery 2006 .26:498-505
1
2. 2.Lee YH, Lee SK, Kim BS, Chun MS, Baek GH, Gong HS. Three lateral divergent or parallel pin fixations for the treatment of displaced supracondylar humerus fractures in children. J Pediatr Orthop 2008;28:417-422.
2
3. Schoenecker PL, Delgado E, Rotman M, Sicard GA, Capelli AM(1996) Pulseless arm in association with totally displaced supracondylar fracture. J Orthop Trauma 10:410–415
3
4. Campbell CC, Waters PM, Emans JB, Kasser JR, Millis MB (1995) Neurovascular injury and displacement in type III supracondylar humerus fractures. J Pediatr Orthop 15:47–52 toward a goal of prevention. J Pediatr Orthop 16:99–103
4
5. Culp RW, Osterman AL, Davidson RS, Skirven T, Bora FW Jr(1990) Neural injuries associated with supracondylar fractures of the humerus in children. J Bone Joint Surg Am 72:1211–1215
5
6. Brown IC, Zinar DM (1995) Traumatic and iatrogenic neurological complications after supracondylar humerus fractures in children. J Pediatr Orthop 15:440–443
6
7. Ristic S, Strauch RJ, Rosenwasser MP (2000) The assessment and treatment of nerve dysfunction after trauma around the elbow. Clin Orthop Relat Res 370:138–153
7
8. Wilkins (1996) Fractures and dislocations of the elbow region. In: Rockwood CA,Wilkins KE, King RE (eds) Fractures in children, vol 3, 4th edn. Lippincott-Raven, Philadelphia, pp 363–575
8
9. Felsenreich F (1931) Kindlichesuprakondylarefrakturen und posttraumatische deformitäten des ellebo engelenk.
9
10. Gartland JJ (1959) Management of supracondylar fractures of the humerus in children. Surg Gynecol Obstet 109:145–154
10
11. Garbuz DS, Leitch K, Wright LG (1996) The treatment of supracondylar fractures in children with an absent radial pulse. J Pediatr Orthop 16:594–596
11
12. Gosens T, Bongers KJ (2003) Neurovascular complications and functional outcome in displaced supracondylar fractures of the humerus in children. Injury 34:267–273
12
13. Malviya A, Simmons D, Vallamshetla R, Bache CE (2006) Pink pulseless hand following supracondylar fractures: an audit of British practice. J Pediatr Orthop B 15:62–64
13
14. Sabharwal S, Tredwell SJ, Beauchamp RD, Mackenzie WG, Jakubec DM, Cairns R, LeBlanc JG (1997) Management of pulseless pink hand in pediatric supracondylar fractures of humerus. J Pediatr Orthop 17:303–310
14
15. Shaw BA, Kasser JR, Emans JB, Rand FF (1990) Management of vascular injuries in displaced supracondylar humerus fractures without arteriography. J Orthop Trauma 4:25–29
15
16. Pirone AM, Graham HK, Krajbich JI (1988) Management of displaced extension-type supracondylar fractures of the humerus in children. J Bone Joint Surg Am 70:641–650
16
17. Marck KW, Kooijman AM, Binnendijk B (1986) Brachial artery rupture following supracondylar fracture of the humerus. Neth J Surg 38:81–84
17
18. Broudy S, Jupiter J, May JW Jr (1979) Management of supracondylar fracture with brachial artery thrombosis in a child: case report and literature review. J Orthop Trauma 19:540–554
18
19. Ramachandran M, Birch R, Eastwood DM (2006) Clinical outcome of nerve of injuries associated with supracondylar fractures the humerus in children: the experience of a specialist referral centre. J Bone Joint Surg Br 88:90–94
19
20. Garbuz DS, Leitch K, Wright LG. The treatment of supracondylar fractures in children with an absent radial pulse. J Pediatr Orthop. 1996;16:594–596.
20
21. Malviya A, Simmons D, Vallamshetla R, Bache CE. Pink pulseless hand following supracondylar fractures: an audit of British practice. J Pediatr Orthop B. 2006;15:62–64.
21
22. Sabharwal S, Tredwell SJ, Beauchamp RD, Mackenzie WG, Jakubec DM, Cairns R, LeBlanc JG. Management of pulseless pink hand in pediatric supracondylar fractures of humerus. J Pediatr Orthop. 1997;17:303–310. doi: 10.1097/00004694-199705000-00007.
22
ORIGINAL_ARTICLE
The use of modified humeral intramedullary interlocking nail in adolescent and elder children femoral shaft fracture
https://smj.journals.ekb.eg/article_41980_d3e27a641c539e2fd327047415474f33.pdf
2018-01-01
343
347
10.21608/smj.2018.41980
Mohamed
Derar
1
Department of Orthopedic surgery, Faculty of Medicine, Sohag university.
AUTHOR
Mohamed
Kenway
mohamed_ahmed8@med.sohag.edu.eg
2
Department of Orthopedic surgery, Faculty of Medicine, Sohag university.
AUTHOR
Yasser
EL Sagher
3
Department of Orthopedic surgery, Faculty of Medicine, Sohag university.
AUTHOR
Shazly
Musa
shazli_mousa@med.sohag.edu.eg
4
Department of Orthopedic surgery, Faculty of Medicine, Sohag university.
AUTHOR
Flynn JM, Skaggs DL. Femoral shaft fractures. In: Flynn JM, Skaggs DL, Waters PM, eds. Rockwood and Wilkins' Fractures in Children. Philadelphia: Lippincott Williams and Wilkins; 2015:987-1023.
1
Kocher MS, Sink EL, Blasier RD, et al. Treatment of pediatric diaphyseal femur fractures. The Journal of the American Academy of Orthopaedic Surgeons. Nov 2009;17(11):718-725.
2
Wright JG. The treatment of femoral shaft fractures in children: a systematic overview and critical appraisal of the literature. Canadian journal of surgery. Journal canadien de chirurgie. Jun 2000;43(3):180-189.
3
Flynn JM, Skaggs DL. Femoral shaft fractures. In: Flynn JM, Skaggs DL, Waters PM, eds. Rockwood and Wilkins' Fractures in Children. Philadelphia: Lippincott Williams and Wilkins; 2015:987-1023.
4
Kocher MS, Sink EL, Blasier RD, et al. Treatment of pediatric diaphyseal femur fractures. The Journal of the American Academy of Orthopaedic Surgeons. Nov 2009;17(11):718-725.
5
Wright JG. The treatment of femoral shaft fractures in children: a systematic overview and critical appraisal of the literature. Canadian journal of surgery. Journal canadien de chirurgie. Jun 2000;43(3):180-189.
6
Sahlin Y (1990) Occurrence of fractures in a defined population: a 1-year study. Injury 21(3):158–160.
7
McCartney D, Hinton A, Heinrich SD (1994) Operative stabilization of pediatric femur fractures. OrthopClin North Am 25(4):635–650
8
Flynn JM, Hresko T, Reynolds RA, Blasier RD, Davidson R, Kasser J (2001) Titanium elastic nails for pediatric femur fractures: a multicenter study of early results with analysis of complications. J PediatrOrthop 21(1):4–8
9
Kanlic E, Cruz M (2007) Current concepts in pediatric femur fracture treatment. Orthopedics 30(12):1015–1019
10
Rasool MN, Govender S, Naidoo KS (1989) Treatment of femoral shaft fractures in children by early spica casting. S Afr Med J 76(3):96–99
11
Wright JG, Wang EE, Owen JL, Stephens D, Graham HK, Hanlon M, Nattrass GR, Reynolds RA, Coyte P (2005) Treatments for paediatric femoral fractures: a randomised trial. Lancet 365(9465):1153–1158. doi:10.1016/S0140-6736(05)71878-X
12
Podeszwa DA, Mooney JF 3rd, Cramer KE, Mendelow MJ (2004) Comparison of Pavlik harness application and immediate spica casting for femur fractures in infants. J PediatrOrthop 24(5):460–462
13
Burton VW, Fordyce AJ (1972) Immobilization of femoral shaft fractures in children aged 2–10 years. Injury 4(1):47–53
14
Stannard JP, Christensen KP, Wilkins KE (1995) Femur fractures in infants: a new therapeutic approach. J PediatrOrthop 15(4): 461–466.
15
Ramseier LE et al (2007) Treatment of open femur fractures in children: comparison between external fixator and intramedullary nailing. J PediatrOrthop 27(7):748–750
16
ORIGINAL_ARTICLE
Factors Affecting the Outcome in the Management of Cervicofacial Infection
Introduction Facial cellulitis and abscesses are common in public health problems and early recognition and management is critical, as they are becoming more severe with a noticeable increase in hospitalization. Aim of work detection of factor affecting outcome in the management of cervicofacial infections and complication to reduce associated mortality and morbidity. Patient and method This study was a prospective study which was conducted at Sohag University Hospital, General Surgery Department. It included patients with cervicofacial infection of odontogenic or non-odontogenic origin either localized or diffuse infection attended to at the Oral and Maxillofacial Surgery Clinic or the Accident and Emergency Unit from October 2016 to October 2017. Results This study included 35 cases, the submandibular space was the most common single site affected (11-34.29%), followed by bilateral or multi- space involvement presented (13-37.14%) of study patients, Diabetes mellitus was the most common associated co- morbidity among study population (12-34.29%), and other systemic diseases (6-17.14%). Conclusion Diabetes, bad general condition, impaired laboratory parameters including an elevated blood sugar level and metabolic acidosis at time of admission were found to be significant risk factors for development of post intervention complications and/ or delayed recovery.
https://smj.journals.ekb.eg/article_42001_f2e8de17883f0ec8b38a03b1d57eab47.pdf
2018-01-01
349
355
10.21608/smj.2018.42001
cervicofacial infection
deep neck space infection
DM
odontogenic infection
Trismus
Mohammed
Abbas
1
Department of surgery, Faculty of medicine, Sohag university.
AUTHOR
Tarek
Ftohy
tarek_elsayed@med.sohag.edu.eg
2
General Surgery Faculty of Medicine , Sohag university.
AUTHOR
Ahmed
Ahmed
ahmed_ahmed2@med.sohag.edu.eg
3
Department, of General Surgery , Faculty of Medicine, Sohag University
AUTHOR
Kamal
El-Sharkawy
kamal_mohamed@med.sohag.edu.eg
4
Department of General Surgery, Faculty of Medicine, Sohag University.
AUTHOR
1.Adekeye EO and Adekeye JO. The pathogenesis and microbiology of idiopathic cervicofacial abscesses. J Oral Maxillofac Surg. 1982; 40:100-6}}
1
2.Al-Malik M and Al-Sarheed M. Pattern of management of oro-facial infection in children: A retrospective. Saudi Journal of Biological Sciences. 2017; 24:1375-9
2
3.Aloosi S, Abdullah H and Yaqub F . Factors influencingManagement Outcome of Hospital-ised Patients with Odontogenic Infection.2017; vol 4
3
4.Bakathir A A, Moos K F, Ayoub A F . et al. Factors Contributing to the Spread of Odontogenic Infections: A prospective pilot study. Sultan Qaboos University medical journal. 2009; 9 296-304
4
5.Bakir S, Tanriverdi M H, Gun R. et al. Deep neck space infections: a retrospective review of 173 cases. American journal of otolaryngology. 2012; 33 56-63
5
6.Fomete B, Agbara R, Osunde D O. et al. Cervicofacial infection in a Nigerian tertiary health institution: a retrospective analysis of 77 cases. Journal of the Korean Association of Oral and Maxillofacial Surgeons. 2015; 41 293-8
6
7.Herr RD, Serious Soft Tissue Infections of the Head and Neck, American Family Physician, September 1991;60:830-34
7
8.Juncar M, Popa A R, Baciut M F. et al. Evolution assessment of head and neck infections in diabetic patients--a case control study. Journal of cranio-maxillo-facial surgery : official publication of the European Association for Cranio-Maxillo-Facial Surgery. 2014; 42 498-502
8
9.Kamat R D, Dhupar V, Akkara F.et al. A comparative analysis of odontogenic maxillofacial infections in diabetic and nondiabetic patients: an institutional study. J Korean Assoc Oral Maxillofac Surg. 2015; 41 176-80
9
10.Karkos PD, Leong SC, Beer H, et al. Challenging airways in deep neck space infections. Am J Otolaryngol 2007; 28:415e8.
10
11.McDonald C, Hennedige A, Henry A.et al. Management of cervicofacial infections: a survey of current practice in maxillofacial units in the UK. British Journal of Oral and Maxillofacial Surgery. 2017; 55 940-5
11
12.Peters E S, Fong B, Wormuth D W . et al. Risk factors affecting hospital length of stay in patients with odontogenic maxillofacial infections. Journal of oral and maxillofacial surgery : official journal of the American Association of Oral and Maxillofacial Surgeons. 1996; 54 1386-91; discussion 91-2.
12
13.Bakathir AA, Moos KF, Ayoub AF, et al . Factors Contributing to the Spread of Odontogenic Infections: A prospective pilot study. Sultan Qaboos Univ Med J 2009;9(3):296-304.
13
14.Cachovan G, Nergiz I, Thuss U. et al. Penetration of moxifloxacin into rat mandibular bone and soft tissue. Acta Odontol Scand (2009); 67(3):182-6.
14
15.Paster BJ, Falkler JW Jr, Enwonwu CO, et al. Prevalent bacterial species and novel phylotypes in advanced noma lesions. J Clin Microbiol. 2002; 40:2187-2191.
15
16.Sette-Dias AC, Maldonado AJT, Aguiar EGd. et al. Profile of patients hospitalized with odontogenic infections in a public hospital in Belo Horizonte, Brazil. J Clin Exp Dent.2012; 4(5):271-4.
16
17.Wang J, Ahani A and Pogrel MA. A five-year retrospective study of odontogenic maxillofacial infections in a large urban public hospital. Int J Oral Maxillofacial Surg. 2005; 34:646-9
17
18.Zamiri B, Bron. HS, Hill. HS. et al. Prevalence of Odontogenic Deep Head and Neck Spaces Infection and its Correlation with Length of Hospital Stay. Shiraz Univ Dent J 2012; 13(1):29-35.
18
ORIGINAL_ARTICLE
Oncoplastic breast surgery:current strategies and outcome
Oncoplastic surgery has emerged as a new approach to allow wide excision for breast conserving surgery without compromising the natural shape of the breast. It is based on integration of plastic surgery techniques for immediate breast reshaping after wide excision for breast cancer. Objective:To study the different methods of oncoplastic surgery for breast reconstruction to achieve better aesthetic outcome and improve quality of life. Patients and Methods: Thirty patients with breast cancer, treated at Sohag University Hospital between July 2016 to May 2017 were included in this study. The oncoplastic techniques performed were Local glandular tissue displacement in (60%), latissimus dorsi flap (LD) in (16.6%), superior pedicle flap in(10%), implant insertion in (6.6%) and Transverse rectus abdominus myocutanous flap (TRAM) in (6.6%). The choice of the oncoplastic techniques depends on the achievement of free safety margins, the breast volume, and its ptotic degree. Results: The number of patients included in the study were thirty. The median age was 43 years (range; 20–60 ys). There were three major complications that require repeating the oncoplastic techniques. Recorded complications included wound infection (5/30, 16.6 %) donor site seroma (10/30, 33.3 %), postoperative haematoma (1/30, 3.3%), flap ischemia and necrosis (1/30, 3.3%). The 12-months subjective patient satisfaction was excellent in 27 (90%) patients, and bad in 3 (10 %) patients. There were two local recurrence, no systemic metastasis after an average follow-up duration of 12 months. Conclusion:Restoring the defect after resection of the breast cancer can be safely achieved using oncoplastic procedures including the previous techniques with immediate breast reconstruction. In our patients, these procedures yield a satisfactory aesthetic outcome with lower morbidity.
https://smj.journals.ekb.eg/article_42037_3492f2c01c5f4ce3e422143fe3a3eee4.pdf
2018-01-01
357
365
10.21608/smj.2018.42037
Oncoplastic breast surgery
Breast conservative surgery
LD flap
TRAM flap
Mahmoud
Abd El Baky
1
Department of surgery, Faculty of medicine, Sohag university.
AUTHOR
Ahmed
Aldardeer
ahmed_eldardeer@med.sohag.edu.eg
2
Department, of Surgery Faculty of, Medicine University of, Sohag.
AUTHOR
Ayman
Ali
ayman_ali@med.sohag.edu.eg
3
Department of surgery, Faculty of medicine, Sohag university.
AUTHOR
Alaa
Redwan
profalaaredwan@yahoo.com
4
Department, Faculty, of Medicine General Surgery, Sohag University.
AUTHOR
1-Fisher B, Jeong JH, Anderson S, et al., (2002). Twenty-five year follow-up of a randomized trial comparing radical mastectomy, total mastectomy, and total mastectomy followed by irradiation. N Engl J Med; 347:567-75.
1
2-Clough KB, Ihrai T, Oden S, et al., (2012). Oncoplastic surgery for breast cancer based on tumour location and a quadrant per- quadrant atlas. Br J Surg; 99:1389-95.
2
3- Losken A, Pinell-White X, Hart AM, et al., (2014). The oncoplastic reduction approach to breast conservation therapy: benefits for margin control. Aesthet Surg J;34:1185-91.
3
4- Barnea Y, Inbal A, Barsuk D, et al., (2014). Oncoplastic reduction using the vertical scar superior-medial pedicle pattern technique for immediate partial breast reconstruction. Can J Surg 2014; 57:E134-40.
4
5- Chan SW, Cheung PS, Lam SH, (2010). Cosmetic outcome and percentage of breast volume excision in oncoplastic breast conserving surgery. World J Surg; 34:1447-52.
5
6- Clough KB, Lewis JS, Couturaud B, et al., (2003). Oncoplastic techniques allow extensive resection for breast-conserving therapy of breast carcinomas. Ann Surg; 237:26–34.
6
7- Jamal K. Almasad, and Bareqa Salah, (2008). Breast Reconstruction by Local flaps after Conserving Surgery for Breast Cancer: An Added Asset to Oncoplastic Techniques, The Breast Journal, Volume 14 Number 4, 340–344.
7
8- Omar Farouk, Essam Attia1, Sameh Roshdy1, et al., (2015). The outcome of oncoplastic techniques in defect reconstruction after resection of central breast tumors, World Journal of Surgical Oncology P: 13–285.
8
9- Pezzi CM, Kukora JS, Audet IM, et al, (2004). Breast conservation surgery using nipple-areolar resection for central breast cancers. Arch Surg; 139:32-7.
9
10- Stavrou D, Weissman O, Polyniki A, (2009). Quality of life after breast cancer surgery with or without reconstruction. Eplasty; 9:e18.
10
11- Saira Khawaja, Abrar Saiyed, Darmiga Thayabaran et al, (2015). A Comparison Between Oncoplastic Breast Conserving Surgery and Standard Wide Local Excision: A UK Experience. Breast Can Curr Res 1:1.
11
12- Lee AH, (2005). Why is carcinoma of the breast more frequent in the upper outer quadrant? A case series based on needle core biopsy diagnoses. Breast. Apr; 14(2):151-2.
12
13- Rainsbury R. M, (2007). “Surgery Insight: oncoplastic breast conserving reconstruction—indications, benefits, choices and outcomes” Nature Clinical Practice Oncology, vol. 4, no. 11, pp. 657–664.
13
14- Tuomo, Masetti R, and Silverstein M. J. (2009). “Oncoplastic approaches to partial mastectomy: an overview of volume displacement techniques,” The Lancet Oncology, vol. 6, no. 3, pp. 145–157.
14
15- Clough KB, Ihrai T, Oden S, et al, (2012). Oncoplastic surgery for breast cancer based on tumour location and a quadrant per- quadrant atlas. Br J Surg;99:1389-95.
15
16- MG Berry, AD Fitoussi, A Curnier, et al, (2010). J Plast Reconstr Aesthet Surg 2010; 63:1233–1243.
16
17- Clough KB, Kroll SS, Audretsch W, (1999). An approach to the repair of partial mastectomy defects.Plast Reconstr Surg;104:409-20.
17
18- Anderson BO, Masetti R, Silverstein MJ, (2005). Oncoplastic approaches to partial mastectomy: an overview of volume displacement techniques. Lancet Oncol;6:145-57.
18
19- McCulley SJ, Macmillan RD, (2005). Planning and use of therapeutic mammoplasty Nottingham approach. Br J Plast Surg;58:889-901.
19
ORIGINAL_ARTICLE
Microneedling as a monotherapy in treatment of male androgenetic alopecia
https://smj.journals.ekb.eg/article_42045_1077226ee9d5f75e30faa2fa0374d1dd.pdf
2018-01-01
367
373
10.21608/smj.2018.42045
ESSAMELDIN
NADA
essameldin_nada@med.sohag.edu.eg
1
DERMATOLOGY, Venereology and Andrology, Faculty of Medicine , sohag university.
AUTHOR
Reham
El Sharkawy
reham_elsharkawy@med.sohag.edu.eg
2
Departments of Dermatology, Venereology and Andrology, Faculty of Medicine, Sohag University.
AUTHOR
Wafaa
Abd El- Maged
wafaa_mohamed@med.sohag.edu.eg
3
Department of Dermatology, Venereology and Andrology, Faculty of Medicine, Sohag University.
AUTHOR
Ashraf
Abd El-Latif
ashraf_abdelwahab@med.sohag.edu.eg
4
Department of Dermatology, Venereology and Andrology- Faculty of Medicine- Sohag University.
AUTHOR
Marwa
Abo Elmagd
marwaaly@med.sohag.edu.eg
5
Department of Dermatology, Venereology and Andrology, Faculty of Medicine, Sohag University.
AUTHOR
1. Hunt N and Mchale S: The psychological impact of alopecia.BMJ. 2005; 331(7522): 951-3.
1
2. Gubelin Harcha W, Barboza Martinez J, Tsai TF, Katsuoka K, Kawashima M: A randomized, active- and placebo-controlled study of the efficacy and safety of different doses of dutasteride versus placebo and finasteride in the treatment of male subjects with androgenetic alopecia.J Am Acad Dermatol. 2014; 70(3): 489-98.e3.
2
3. Kim MW, Shin IS, Yoon HS, Cho S and Park HS: Lipid profile in patients with androgenetic alopecia: a meta-analysis.J Eur Acad Dermatol Venereol. 2017; 31(6): 942-51.
3
4. Gkini MA, Kouskoukis AE, Tripsianis G, Rigopoulos D and Kouskoukis K: Study of platelet-rich plasma injections in the treatment of androgenetic alopecia through an one-year period.J Cutan Aesthet Surg. 2014; 7(4): 213-9.
4
5. Leiros GJ, Attorresi AI and Balana ME: Hair follicle stem cell differentiation is inhibited through cross-talk between Wnt/beta-catenin and androgen signalling in dermal papilla cells from patients with androgenetic alopecia.Br J Dermatol. 2012; 166(5): 1035-42.
5
6. Dhurat R, Sukesh M, Avhad G, Dandale A, Pal A: A randomized evaluator blinded study of effect of microneedling in androgenetic alopecia: a pilot study.Int J Trichology. 2013; 5(1): 6-11.
6
7. Fertig RM and Gamret AC: Microneedling for the treatment of hair loss? 2017.
7
8. Ayatollahi A, Hosseini H, Shahdi M, Ahmadnasrollahi S, Nassirikashani M: Platelet-rich Plasma by Single Spin Process in Male Pattern Androgenetic Alopecia: Is it an Effective Treatment? Indian Dermatol Online J. 2017; 8(6): 460-464.
8
9. Costa IM and Costa MC: Microneedling for varicella scars in a dark-skinned teenager.Dermatol Surg. 2014; 40(3): 333-4.
9
10. Budamakuntla L, Loganathan E, Suresh DH, Shanmugam S, Suryanarayan S: A Randomised, Open-label, Comparative Study of Tranexamic Acid Microinjections and Tranexamic Acid with Microneedling in Patients with Melasma.J Cutan Aesthet Surg. 2013; 6(3): 139-43.
10
11. Iriarte C, Awosika O, Rengifo-Pardo M and Ehrlich A: Review of applications of microneedling in dermatology.Clin Cosmet Investig Dermatol. 2017; 10: 289-98.
11
12. Motofei IG, Rowland DL, Baconi DL, Tampa M, Sarbu MI: Androgenetic alopecia; drug safety and therapeutic strategies.Expert Opin Drug Saf. 2018.
12
13. Escobar-Chavez JJ, Bonilla-Martinez D, Villegas-Gonzalez MA, Molina-Trinidad E, Casas-Alancaster N: Microneedles: a valuable physical enhancer to increase transdermal drug delivery.J Clin Pharmacol. 2011; 51(7): 964-77.
13
14. Matarasso A, Pfeifer TM and Plastic Surgery Educational Foundation DC: Mesotherapy for body contouring.Plast Reconstr Surg. 2005; 115(5): 1420-4.
14
15. Dhurat R and Mathapati S: Response to Microneedling Treatment in Men with Androgenetic Alopecia Who Failed to Respond to Conventional Therapy.Indian J Dermatol. 2015; 60(3): 260-3.
15
16. Shapiro J, Wiseman M and Lui H: Practical management of hair loss.Can Fam Physician. 2000; 46: 1469-77.
16
17. Sehgal VN, Kak R, Aggarwal A, Srivastava G and Rajput P: Male pattern androgenetic alopecia in an Indian context: a perspective study.J Eur Acad Dermatol Venereol. 2007; 21(4): 473-9.
17
18. Hillmann K and Blume-Peytavi U: Diagnosis of hair disorders.Semin Cutan Med Surg. 2009; 28(1): 33-8.
18
19. Barber B, Kaufman K, Kozloff R, Girman C and Guess H: A hair growth questionnaire for use in the evaluation of therapeutic effects in men.J Dermatol Treat. 1998; 9(3): 181-186.
19
20. Lucky AW, Piacquadio DJ, Ditre CM, Dunlap F, Kantor I: A randomized, placebo-controlled trial of 5% and 2% topical minoxidil solutions in the treatment of female pattern hair loss.J Am Acad Dermatol. 2004; 50(4): 541-53.
20
21. Sobhy N, Aly H, El Shafee A and El Deeb M: Evaluation of the effect of injection of dutasteride as mesotherapeutic tool in treatment of androgenetic alopecia in males.Our Dermatol Online. 2013; 4(1): 40-5.1. Muller DC, Giles GG, Sinclair R, Hopper JL, English DR: Age-dependent associations between androgenetic alopecia and prostate cancer risk.Cancer Epidemiol Biomarkers Prev. 2013; 22(2): 209-15.
21
22. Hunt N and Mchale S: The psychological impact of alopecia.BMJ. 2005; 331(7522): 951-3.
22
23. Gubelin Harcha W, Barboza Martinez J, Tsai TF, Katsuoka K, Kawashima M: A randomized, active- and placebo-controlled study of the efficacy and safety of different doses of dutasteride versus placebo and finasteride in the treatment of male subjects with androgenetic alopecia.J Am Acad Dermatol. 2014; 70(3): 489-498.e3.
23
24. Kim MW, Shin IS, Yoon HS, Cho S and Park HS: Lipid profile in patients with androgenetic alopecia: a meta-analysis.J Eur Acad Dermatol Venereol. 2017; 31(6): 942-951.
24
25. Gkini MA, Kouskoukis AE, Tripsianis G, Rigopoulos D and Kouskoukis K: Study of platelet-rich plasma injections in the treatment of androgenetic alopecia through an one-year period.J Cutan Aesthet Surg. 2014; 7(4): 213-9.
25
26. Dhurat R, Sukesh M, Avhad G, Dandale A, Pal A: A randomized evaluator blinded study of effect of microneedling in androgenetic alopecia: a pilot study.Int J Trichology. 2013; 5(1): 6-11.
26
27. Arif T, Dorjay K, Adil M and Sami M: Dutasteride in Androgenetic Alopecia: An Update.Curr Clin Pharmacol. 2017; 12(1): 31-35.
27
28. Abdallah M, El-Zawahry K and Besar H: Mesotherapy using dutasteride-containing solution in male pattern hair loss: A controlled pilot study.J Pan Arab Leag Dermatol. 2009; 20: 137-45.
28
29. Sobhy N, Aly H, El Shafee A and El Deeb M: Evaluation of the effect of injection of dutasteride as mesotherapeutic tool in treatment of androgenetic alopecia in males.Our Dermatol Online. 2013; 4(1): 40-5.
29
30. Saceda-Corralo D, Rodrigues-Barata AR, Vano-Galvan S and Jaen-Olasolo P: Mesotherapy with Dutasteride in the Treatment of Androgenetic Alopecia.Int J Trichology. 2017; 9(3): 143-145.
30
31. Fertig RM and Gamret AC: Microneedling for the treatment of hair loss? 2017.
31
32. Dhurat R and Mathapati S: Response to Microneedling Treatment in Men with Androgenetic Alopecia Who Failed to Respond to Conventional Therapy.Indian J Dermatol. 2015; 60(3): 260-3.
32
33. Shapiro J, Wiseman M and Lui H: Practical management of hair loss.Can Fam Physician. 2000; 46: 1469-77.
33
34. Sehgal VN, Kak R, Aggarwal A, Srivastava G and Rajput P: Male pattern androgenetic alopecia in an Indian context: a perspective study.J Eur Acad Dermatol Venereol. 2007; 21(4): 473-9.
34
35. Barber B, Kaufman K, Kozloff R, Girman C and Guess H: A hair growth questionnaire for use in the evaluation of therapeutic effects in men.J Dermatol Treat. 1998; 9(3): 181-186.
35
36. Lucky AW, Piacquadio DJ, Ditre CM, Dunlap F, Kantor I: A randomized, placebo-controlled trial of 5% and 2% topical minoxidil solutions in the treatment of female pattern hair loss.J Am Acad Dermatol. 2004; 50(4): 541-53.
36
37. Mounsey AL and Reed SW: Diagnosing and treating hair loss.Am Fam Physician. 2009; 80(4): 356-62.
37
38. Andriole GL and Kirby R: Safety and tolerability of the dual 5alpha-reductase inhibitor dutasteride in the treatment of benign prostatic hyperplasia.Eur Urol. 2003; 44(1): 82-8.
38
39. Eun HC, Kwon OS, Yeon JH, Shin HS, Kim BY: Efficacy, safety, and tolerability of dutasteride 0.5 mg once daily in male patients with male pattern hair loss: a randomized, double-blind, placebo-controlled, phase III study.J Am Acad Dermatol. 2010; 63(2): 252-8.
39
40. Amory JK, Wang C, Swerdloff RS, Anawalt BD, Matsumoto AM: The effect of 5alpha-reductase inhibition with dutasteride and finasteride on semen parameters and serum hormones in healthy men.J Clin Endocrinol Metab. 2007; 92(5): 1659-65.
40
41.Olsen EA: Female pattern hair loss.J Am AcadDermatol. 2001; 45(3 Suppl):s70-80
41
ORIGINAL_ARTICLE
Association of osteopontin promoter polymorphism and aggresivness in breast cancer
Osteopontin (OPN) is an extracellularmatrix protein that is overexpressed in various cancers and promotes oncogenic features including cell proliferation, survival, migration, and angiogenesis, among others. OPN can participate in the regulation of the tumor microenvironment, affecting both cancer and neighboring cells. Here, we review The role of single-nucleotide polymorphism (SNP)-443 of the OPN gene in cancer aggressiveness.
https://smj.journals.ekb.eg/article_42049_6179996784565298af078fddbde59104.pdf
2018-01-01
375
379
10.21608/smj.2018.42049
Madeha
Zakhary
1
Department, of Medical Biochemistry, Faculty of Medicine, Assuit university.
AUTHOR
Aida
Mahmoud
aida_mahmoud@med.sohag.edu.eg
2
Department, of Medical Biochemistry, Faculty of Medicine, Sohag university.
AUTHOR
Wael
Ahmed
3
Department of General Surgery, Faculty of Medicine, Sohag university.
AUTHOR
Marwa
Hashim
marwa_hashem@med.sohag.edu.eg
4
Department of Biochemistry and microbiology, Facaulty of Medicine, Sohag University.
AUTHOR
1. Wood L.D., Parsons D.W., Jones S. et al.(2007)"The genomic landscapes of human breast and colorectal cancers". Science 318:1108–1113.
1
2. Sottoriva A., Kang H., Ma Z., et al. (2015)"A Big Bang model of human colorectal tumor growth". Nat. Genet. 47 :209–216.
2
3. Gimba E.R. and Tilli T.M.(2013)" Human osteopontin splicing isoforms: known roles, potential clinical applications and activated signaling pathways". Cancer Lett. 331:11–17.
3
4. Sodek J. , Ganss B. and McKee M.D.(2000) Osteopontin, Crit. Rev. Oral Biol. Med. 11:279–303.
4
5. Bandopadhyay M. , Bulbule A. , Butti R. , et al.(2014)" Osteopontin as a therapeutic target for cancer, Expert Opin. Ther. Targets 18: 883–895.
5
6. Weber G.F. , Lett G.S., Haubein N.C. (2010)."Osteopontin is amarker for cancer aggressiveness and patient survival". Br. J. Cancer 103:861–869.
6
7. Cao DX, Li ZJ, Jiang XO, et al.(2012)." Osteopontin as potential biomarker and therapeutic target in gastric and liver cancers". World J Gastroenterol;18(30):3923-3930 Carcinoma". Cancer;83:2521.
7
8. Kiefer MC, Bauer DM and Barr PJ (1989). "The cDNA and derived amino acid sequence for human osteopontin.". Nucleic Acids Res. 17 (1): 3306 . doi:10.1093 /nar/17.8.3306 .
8
9. Crosby AH, Edwards SJ, Murray JC and Dixon MJ (1995). "Genomic organization of the human osteopontin gene : exclusion of the locus from a causative role in the pathogenesis of dentinogenesis imperfect typeII". Genomics. 27 (1):155160 .
9
10. Merry K, Dodds R, Littlewood A and Gowen M (1993). "Expression of Osteopontin mRNA by osteoclasts and osteoblasts in modelling adult human bone". J Cell Sci. 104 (4): 1013–1020.
10
11. Nakashima K, Zhou X, Kunkel G et al.(2002). "The novel zinc finger-containing transcription factor osterix is required for osteoblast differentiation and bone formation" . Cell. 108 (1):1729.
11
12. Ducy P, Zhang R, Geoffroy V, Ridall AL and Karsenty G (1997). "Osf2/Cbfa1:a transcriptional activator of osteoblast differentiation" . Cell. 89 (1): 747–754.
12
13. Yucha C and Guthrie D (2003). "Renal homeostasis of calcium" . Nephrol Nurs J. 30 (1): 755–764.
13
14. Chang P.L. and Prince C.W. (1991) "1α,25-Dihydroxyvitamin D3 Stimulates Synthesis and Secretion of Nonphosphorylated Osteopontin (Secreted Phosphoprotein 1) in Mouse JB6 Epidermal Cells" Cancer Research 51.NO.8.PP: 2144-2150.
14
15. Fatherazi S, Matsa-Dunn D, Foster BL et al. (2009). "Phosphate regulates osteopontin gene transcription" . JDentRes. 88 (1):39-44.
15
16. Guo H, Cai CQ, Schroeder RA and Kuo PC (2001). "Osteopontin is a negative feedback regulator of nitric oxide synthesis in murine macrophages" . JImmunol . 166 (1):1079-1086.
16
17. Ricardo SD, Franzoni DF, Roesener CD, Crisman JM and Diamond JR (2000). "Angiotensinogen and AT(1) antisense inhibition of osteopontin translation in rat proximal tubular cells" . Am J Physiol Renal Physiol. 278 (1): 708–716.
17
18. Sodhi CP, Phadke SA, Batlle D and Sahai A (2001). "Hypoxia and high glucose cause exaggerated mesangial cell growth and collagen synthesis: role of osteopontin". Am J Physiol Renal Physiol . 280 (1):667674.
18
19. Briones-Orta M.A. , Avendaño-Vázquez S. , Aparicio-Bautista D.I. et al.(2017) "Osteopontin splice variants and polymorphisms in cancer progression and prognosis." Biochimica et Biophysica Acta (BBA) - Reviews on Cancer 1868(1): 93-108.A.
19
20. Ramchandani D and Weber GF. (2013)" An osteopontin promoter polymorphism is associated with aggressiveness in breast cancer". Oncol Rep.;30(4):1860-8. doi: 10.3892/or.2013.2632. Epub 2013 Jul 23.
20
21. He, L., and Wang, Y. (2016). "Association of OPN rs11730582 polymorphism with cancer risk: a meta-analysis". OncoTargets and Therapy, 9, 1275–1280.
21
22. Sherry S.T., Ward M.H., Kholodov M., et al.(2001) "dbSNP: theNCBI database of genetic variation, Nucleic Acids Res. 29:308–311.
22
23. Schultz J., Lorenz P., Ibrahim S.M., et al. (2009)." The functional−443T/C osteopontin promoter polymorphism influences osteopontin gene expression in melanoma cells via binding of c-Myb transcription factor". Mol.Carcinog. 48 :14–23.
23
24. Liu Y., Lei H. , Zhang J., Wang J., Li K. and Dong W. (2015)"Associations between the genetic polymorphisms of osteopontin promoter and susceptibility to cancer in Chinese population: a meta-analysis". PLoS One 10 , e0135318.
24
25. Yang G. , Peng X. , Guo P. and Yang G.(2015) "Association of osteopontin polymorphism with cancer risk: a meta-analysis". Int. J. Clin. Exp. Med. 8 :20911–20917.
25
ORIGINAL_ARTICLE
Evaluation of some biomarkers in breast cancer patients
Background. Osteopontin (OPN) is an extracellularmatrix protein that is overexpressed in various cancers and promotes onco-genic features including cell proliferation, survival, migration, and angiogenesis. Here, we analyzed the correlation between the expression pattern of (osteopontin and CA15.3) and clinic-pathological status of breast cancer and other standard prognostic factors. Patients and methods. A case control study with 60 female breast cancer patients and 20 controls. All patients were subjected to complete medical history uptake , clinical examination and laboratory investigations include histopathological type of cancer, hormone receptor status ,CA 15-3 serum concentratios and osteopontin plasma level by ELISA. Results. Our study showed that osteopontin plasma level was significantly different among breast cancers and controls (p<0.0001) but no association between osteopontin plasma level and histological type , stage or grade. Also we found significant association between CA 15-3 and cancer stage (p<0.000). Interestingly CA15.3 serum concentrations increased in hormone receptor positive cancer. Conclusion. OPN and CA15.3 are overexpressed in breast cancer. OPN overexpression is associated with poor prognosis. Moreover CA15.3 has minimal prognostic value in non metastatic breast cancer.
https://smj.journals.ekb.eg/article_42078_a27a9b54f154efc5297ab95b75239b5b.pdf
2018-01-01
381
386
10.21608/smj.2018.42078
Madeha
Zakhary
1
Department OF Medical Biochemistry Faculty of Medicine. Assuit university.
AUTHOR
Aida
Mahmoud
aida_mahmoud@med.sohag.edu.eg
2
Department, of Medical Biochemistry, Faculty of Medicine, Sohag university.
AUTHOR
Wael
Ahmed
3
Department, OF General Surgery, Faculty of Medicine, Sohag university.
AUTHOR
Marwa
Hashim
marwa_hashem@med.sohag.edu.eg
4
Department of Biochemistry and microbiology, Facaulty of Medicine, Sohag University.
AUTHOR
1- Wang, C.-H., Li, J.-Z., & Zhang, W. (2014). "Breast cancer molecular subtypes of Uygur and Han in Xinjiang of China". International Journal of Clinical and Experimental Medicine, 7(4), 1116–1121.
1
2- Marques, R. C. B.; Costa-Rama, E. ;Viswanathan S. et al. (2018). "Voltammetric immunosensor for the simultaneous analysis of the breast cancer biomarkers CA 15-3 and HER2-ECD" J. Sensors and Actuators B: Chemical. Vol.255 no. 918-925.
2
3- Ahmed M and Kundu GC (2010). "osteopontin selectively regulates p70S6K/mTORphosphorylation leading to NF-κB dependentAP-1-mediated ICAM-1 expression in breast cancer cells " Molecular Cancer, 9:101.
3
4- Xu Y.Y., Zhang Y.Y., Lu W.F., Mi Y.J. and Chen Y.Q.. (2015)" Prognostic value of osteopontin expression in breast cancer: A meta-analysis" .Molecular and Clinical Oncology 3: 357-362.
4
5- Miller, E., Lee, H. J., Lulla, A., Hernandez, L., Gokare, P., & Lim, B. (2014). Current treatment of early breast cancer: adjuvant and neoadjuvant therapy. F1000Research, 3, 198. http://doi.org/10.12688/f1000research.4340.1
5
6- Pacheco , J.G.; Silva, M.S.V.; Freitas, M. et al. (2018)." Molecularly imprinted electrochemical sensor for the point-of-care detection of a breast cancer biomarker (CA 15-3)"J. Sensors and Actuators B: Chemical. Vol. 256 no. 905-912.
6
7- THORAT, D., SAHU, A., BEHERA, R., et al. (2013). Association of osteopontin and cyclooxygenase-2 expression with breast cancer subtypes and their use as potential biomarkers. Oncology Letters, 6(6), 1559–1564.
7
8- GENG, B., LIANG, M.-M., YE, X.-B., & ZHAO, W.-Y. (2015). Association of CA 15-3 and CEA with clinicopathological parameters in patients with metastatic breast cancer. Molecular and Clinical Oncology, 3(1), 232–236.
8
9- Liu Y. , Lei H. , Zhang J. et al. (2015)" Associations between the Genetic Polymorphisms of Osteopontin Promoter and Susceptibility to Cancer in Chinese Population: A Meta-Analysis". PLoS ONE 10(8). : e0135318. doi:10.1371/journal.pone.0135318.
9
10- Bramwell V.H., Tuck A.B., Chapman J.-A.W. et al. (2014)"Assessment of osteopontin in early breast cancer:correlative study in a randomised clinical trial" . Breast Cancer Research , 16:R8
10
11- Brouckaert, O., Laenen, A., Wildiers, H. et al. (2013) "The prognostic role of preoperative and (early) postoperatively change in CA15.3 serum levels in a single hospital cohort of primary operable breast cancers" J. The Breast vol.22(3):254-262.
11
12- Li , H. , Chen k. ,Su F.et al. (2014). "Preoperative CA 15-3 levels predict the prognosis of nonmetastatic luminal A breast cancer." Journal of Surgical Research 189(1): 48-56.
12
ORIGINAL_ARTICLE
Topical dutasteride with microneedling in treatment of male androgenetic alopecia
https://smj.journals.ekb.eg/article_42083_24b61cbba4be9982db23c318414034c0.pdf
2018-01-01
387
400
10.21608/smj.2018.42083
ESSAMELDIN
NADA
essameldin_nada@med.sohag.edu.eg
1
Department, OF DERMATOLOGY, Venereology and Andrology, Faculty of Medicine , sohag university.
AUTHOR
Reham
El Sharkawy
reham_elsharkawy@med.sohag.edu.eg
2
Departments of Dermatology, Venereology and Andrology, Faculty of Medicine, Sohag University.
AUTHOR
Wafaa
Abd El- Maged
wafaa_mohamed@med.sohag.edu.eg
3
Department of Dermatology, Venereology and Andrology, Faculty of Medicine, Sohag University.
AUTHOR
Marwa
Abo Elmagd
marwaaly@med.sohag.edu.eg
4
Department of Dermatology, Venereology and Andrology, Faculty of Medicine, Sohag University.
AUTHOR
1. Muller DC, Giles GG, Sinclair R, Hopper JL, English DR: Age-dependent associations between androgenetic alopecia and prostate cancer risk. Cancer Epidemiol Biomarkers Prev. 2013; 22(2): 209-15.
1
2. Hunt N and Mchale S: The psychological impact of alopecia. BMJ. 2005; 331(7522): 951-3.
2
3. Gubelin Harcha W, Barboza Martinez J, Tsai TF, Katsuoka K, Kawashima M: A randomized, active- and placebo-controlled study of the efficacy and safety of different doses of dutasteride versus placebo and finasteride in the treatment of male subjects with androgenetic alopecia. J Am Acad Dermatol. 2014; 70(3): 489-498.e3.
3
4. Kim MW, Shin IS, Yoon HS, Cho S and Park HS: Lipid profile in patients with androgenetic alopecia: a meta-analysis. J Eur Acad Dermatol Venereol. 2017; 31(6): 942-951.
4
5. Gkini MA, Kouskoukis AE, Tripsianis G, Rigopoulos D and Kouskoukis K: Study of platelet-rich plasma injections in the treatment of androgenetic alopecia through an one-year period. J Cutan Aesthet Surg. 2014; 7(4): 213-9.
5
6. Dhurat R, Sukesh M, Avhad G, Dandale A, Pal A: A randomized evaluator blinded study of effect of microneedling in androgenetic alopecia: a pilot study. Int J Trichology. 2013; 5(1): 6-11.
6
7. Arif T, Dorjay K, Adil M and Sami M: Dutasteride in Androgenetic Alopecia: An Update. Curr Clin Pharmacol. 2017; 12(1): 31-35.
7
8. Abdallah M, El-Zawahry K and Besar H: Mesotherapy using dutasteride-containing solution in male pattern hair loss: A controlled pilot study. J Pan Arab Leag Dermatol. 2009; 20: 137-45.
8
9. Sobhy N, Aly H, El Shafee A and El Deeb M: Evaluation of the effect of injection of dutasteride as mesotherapeutic tool in treatment of androgenetic alopecia in males. Our Dermatol Online. 2013; 4(1): 40-5.
9
10. Saceda-Corralo D, Rodrigues-Barata AR, Vano-Galvan S and Jaen-Olasolo P: Mesotherapy with Dutasteride in the Treatment of Androgenetic Alopecia. Int J Trichology. 2017; 9(3): 143-145.
10
11. Fertig RM and Gamret AC: Microneedling for the treatment of hair loss? 2017.
11
12. Dhurat R and Mathapati S: Response to Microneedling Treatment in Men with Androgenetic Alopecia Who Failed to Respond to Conventional Therapy. Indian J Dermatol. 2015; 60(3): 260-3.
12
13. Shapiro J, Wiseman M and Lui H: Practical management of hair loss. Can Fam Physician. 2000; 46: 1469-77.
13
14. Sehgal VN, Kak R, Aggarwal A, Srivastava G and Rajput P: Male pattern androgenetic alopecia in an Indian context: a perspective study. J Eur Acad Dermatol Venereol. 2007; 21(4): 473-9.
14
15. Barber B, Kaufman K, Kozloff R, Girman C and Guess H: A hair growth questionnaire for use in the evaluation of therapeutic effects in men. J Dermatol Treat. 1998; 9(3): 181-186.
15
16. Lucky AW, Piacquadio DJ, Ditre CM, Dunlap F, Kantor I: A randomized, placebo-controlled trial of 5% and 2% topical minoxidil solutions in the treatment of female pattern hair loss. J Am Acad Dermatol. 2004; 50(4): 541-53.
16
17. Mounsey AL and Reed SW: Diagnosing and treating hair loss. Am Fam Physician. 2009; 80(4): 356-62.
17
18. Andriole GL and Kirby R: Safety and tolerability of the dual 5alpha-reductase inhibitor dutasteride in the treatment of benign prostatic hyperplasia. Eur Urol. 2003; 44(1): 82
18
19. Eun HC, Kwon OS, Yeon JH, Shin HS, Kim BY: Efficacy, safety, and tolerability of dutasteride 0.5 mg once daily in male patients with male pattern hair loss: a randomized, double-blind, placebo-controlled, phase III study. J Am Acad Dermatol. 2010; 63(2): 252-8.
19
20. Amory JK, Wang C, Swerdloff RS, Anawalt BD, Matsumoto AM: The effect of 5alpha-reductase inhibition with dutasteride and finasteride on semen parameters and serum hormones in healthy men. J Clin Endocrinol Metab. 2007; 92(5): 1659-65.
20
21. Olsen EA: Female pattern hair loss. J Am Acad Dermatol. 2001; 45(3 Suppl): S70-80.
21
ORIGINAL_ARTICLE
Nerve growth factor (NGF) expression in correlation with severity of pruritus in cirrhotic patients
Background:Hepatic pruritus is a very common symptom among different chronic liver diseases, particularly in those related to cholestasis. Its prevalence is variable among liver diseases, ranging from 5% in chronic hepatitis C virus infection to 70% in primary biliary cirrhosis. Its etiopathogenesis remains poorly understood.Nerve growth factor (NGF) is a member of neurotrophins. many studies clearly demonstrate their role in pruritus. Nerve growth factor (NGF) is overexpressed in prurigonodularis and its therapeutic administration is pruritogenic. In atopic dermatitis, NGF is released by keratinocytes, mast cells and fibroblasts and plasma levels of NGF are also elevated and correlate with disease activity.This study examines the hypothesis that expression of NGF protein is altered in cirrhotic patients with pruritus. Patients and Methods: To test our hypothesis, we examined the expression patterns of NGF protein in cirrhotic patients with pruritus, cirrhotic patients without pruritus and corresponding healthy (control). skin biopsies (20 specimens each) were evaluated using immunoperoxidase staining techniques. Results: We found variations between the skins of cirrhotic patients with and without pruritus and healthy skin. In healthy skin, the expression of NGF protein was strong (basal cell keratinocytes), moderate (spinouslayer), and weak or abscent (granular cell layer). In contrast, marked expression of NGF protein was observed in all layers of skin (total NGF epidermis and dermis) incirrhotic patients with pruritus in comparison with cirrhotic patients without pruritus and healthy control and this was statistically significant. NGF protein expression was strong (basal cell keratinocytes), moderate (spinous layer), and weak or abscent (granular cell layer). The expression of NGF protein was strong in the adnexal structures. Conclusions: We report, for the first time, increased expression of NGF protein in the epidermal keratinocytes of cirrhotic patients with pruritus skin. Our findings suggest possible roles for this protienin pathophysiology of hepatic pruritus. The clinical ramifications of these observations mandate further investigations.
https://smj.journals.ekb.eg/article_42251_fe116eb3b70a0cd3c5fe26915e705197.pdf
2018-01-01
403
410
10.21608/smj.2018.42251
ESSAMELDIN
NADA
essameldin_nada@med.sohag.edu.eg
1
DERMATOLOGY, Venereology and Andrology, Faculty of Medicine , sohag university.
AUTHOR
Hanan
Assaf
hanan_asaf@med.sohag.edu.eg
2
Department of Dermatology, Venereology and Andrology, Sohag Faculty of Medicine, Sohag University.
AUTHOR
Reham
El Sharkawy
reham_elsharkawy@med.sohag.edu.eg
3
Departments of Dermatology, Venereology and Andrology, Faculty of Medicine, Sohag University.
AUTHOR
Amr
Zaghloul
amr_hashem@med.sohag.edu.eg
4
Department of Tropical Medicine and Gastroenterology, Faculty of Medicine, Sohag University.
AUTHOR
Marwa
Abd El Meged
5
Department of Dermatology, Venereology and Andrology, Sohag Faculty of Medicine, Sohag University.
AUTHOR
Mahmoud
Abd El Wahed
6
Department of pathology, Assuit Faculty of Medicine, Assuit University.
AUTHOR
Asmaa
Ahmed
7
Department of pathology, Assuit Faculty of Medicine, Assuit University.
AUTHOR
1- Lindor KD, Gershwin ME, Poupon R, Kaplan M, Bergasa NV, Heathcote EJ(2009): American Association for Study of Liver Diseases. Primary biliary cirrhosis. Hepatology.;50(1):291-308 .
1
2- ones D(2012): Pathogenesis of cholestatic itch: old questions, new
2
answers, and future opportunities. Hepatology.;56(4):1194-6 .
3
3- Kremer AE, Feramisco J, Reeh PW, Beuers U, Oude Elferink RP(2014): Receptors, cells and circuits involved in pruritus of systemic
4
disorders. BiochimBiophysActa.; 1842(7):869-92.
5
4- Oude Elferink RP, Bolier R, Beuers UH(2015):Lysophosphatidic acid and signaling in sensory neurons. BiochimBiophysActa.; 1851(1):61-5.
6
5- Azevedo R, Takamatsu F, Kondo M, Ferraz M, Mattar R, Cestari S, SalzedasNetto A, Souza P, Pinto W, RezendeFilho F, Oliveira A (2017): Pruritus in cholestasis. Rev Soc Bras Clin Med.;15(1):61-7.
7
6- Raap U and Kapp A (2010): Neuroimmunological findings in allergic skin diseases. CurrOpin Allergy ClinImmunol 5:419–24
8
7- Pincelli C, Yaar M (1997): Nerve growth factor: its significance in cutaneous biology.JInvestigDermatolSympProc 2:61–8.
9
8- Teng K and Hempstead B (2004): Neurotrophins and their receptors: signaling trios in complex biological systems. Cell Mol Life Sci.;61:35-48.
10
9- Zegarska B, Lelińska A, Tyrakowski T (2006). Clinical and experimental aspects of cutaneous neurogenic inflammation. Pharmacol Rep.;58:13-21.
11
10- Nockher W and Renz H (2003):Neurotrophins in inflammatory lung diseases: modulators of cell differentiation and neuroimmune interactions. Cytokine Growth Factor Rev; 14: 559-78.
12
11-Suarez A, Feramisco J, Koo J, Steinhoff M (2012)Psychoneuroimmunology of Psychological Stress and Atopic Dermatitis: Pathophysiologic and Therapeutic Updates. Acta dermato- venereologica.;92(1):7-15
13
12- Adly M, Assaf H, Nada E, Soliman M, Hussein M (2006): Expression of nerve growth factor and its high-affinity receptor, tyrosine kinase Aproteins, in the human scalp skin. J CutanPathol; 33: 559–568 .
14
13- Dou Y, Hagstromer L, Emtestam L. Increased nerve growth factor and its receptors in atopic dermatitis: an immunohistochemical study. Arch Dermatol Res 2006; 298: 31-7.
15
14-Hodeib A, El-Samad Z, Hanafy H, El-Latief A, El-bendary A, Abu-Raya A: Nerve growth factor, neuropeptides and cutaneous nerves in atopic dermatitis. Indian J Dermatol 2010;55:135-9.
16
15- Toyoda M, Nakamura M, Makino T, Hino T, Kagoura M, Morohashi M (2002): Nerve growth factor and substance P are useful plasma markers of disease activity in atopic dermatitis. Br J Dermatol.; 147:71-9.
17
16- Schulte-Herbrüggen O, Floster-Holst R, von Elstermann M, Augustin M, Hellweg R: Clinical relevance of nerve growth factor serum levels in patients with atopic dermatitis and psoriasis. IntArch Allergy Immunol. 2007; 144 (3):211–216.
18
17- Levi-Montalcini R, Dal Toso R, Della Valle F, Skaper SD, Alberta L. Update of the NGF saga. J Neurol Sci. 1995; 130 (2):119–127.
19
18- Joachim R, Kuhlmei A, Dinh Q, Handjiski B, Fischer T, Peters E: Neuronal plasticity of the brain–skin connection stress-triggered upregulation of neuropeptides in dorsal root ganglia and skin via nerve growth factor-dependent pathways. J Mol Med. 2007; 85 (12):1369–1378.
20
ORIGINAL_ARTICLE
Gut microbiome in chronic kidney disease
https://smj.journals.ekb.eg/article_42518_b99dc76e0f8a486f978232d8936a6abe.pdf
2018-01-01
415
420
10.21608/smj.2018.42518
Noher
Abass
nahirmohamed@med.sohag.edu.eg
1
Department of Internal Medicine, Sohag Faculty of Medicine, Sohag University.
AUTHOR
Bäckhed F, Ley RE, Sonnenburg JL,Peterson DA, Gordon JI: Host-bacterial utualism in the human intestine. Science 2005; 307: 1915–1920.
1
Ley RE, Turnbaugh PJ, Klein S, Gordon JI: Microbial ecology: Human gut microbes associated with obesity. Nature 2006; 444: 1022–1023.
2
Qin J, Li Y, Cai Z, Li S, Zhu J, Zhang F, Liang S, ZhangW, Guan Y: Ametagenome-wide association study of gut microbiota in type 2 diabetes. Nature 2012; 490: 55–60.
3
Frank DN, St Amand AL, Feldman RA, Boedeker EC, Harpaz N, Pace NR: Molecular-phylogenetic characterization of microbial community imbalances in human inflammatory bowel diseases. Proc Natl Acad Sci US A 2007; 104: 13780–13785.
4
Wang Z, Klipfell E, Bennett BJ, Koeth R, Levison BS, Dugar B, Feldstein AE, Britt EB, Fu X, Chung YM,WuY, Schauer P, Smith JD, Allayee H, TangWH, Di Donato JA, Lusis AJ, Hazen SL: Gut flora metabolism of phosphatidylcholine promotes cardiovascular disease. Nature 2011; 472: 57–63
5
Vaziri ND,Wong J, Pahl M, Piceno YM, Yuan J, De Santis TZ, Ni Z, Nguyen TH, Andersen GL: Chronic kidney disease alters intestinal microbial flora. Kidney Int 2013; 83: 308–315.
6
De Felippo C, Cavalieri D, Di Paola M, Ramazzotti M, Poullet JB, Massart S, Collini S, Pieraccini G & Lionetti P : Impact of diet in shaping gut microbiota revealed by a comparative study in children from Europe and rural Africa. Proc Natl Acad Sci USA 2010; 107, 14691–14696.
7
Dethlefsen L & Relman DA : Incomplete recovery and individualized responses of the human distal gut microbiota to repeated antibiotic perturbation. Proc Natl Acad Sci USA 2011; 108 Suppl 1 , 4554–4561.
8
Goodrich JK,Waters JL, Poole AC, Sutter JL, Koren O, Blekhman R, Beaumont M, Van Treuren W, Knight R, Bell JT, Spector TD, Clark AG & Ley RE : Human genetics shape the gut microbiome. Cell 2014; 159, 789–799.
9
Amar J, Lange C, Payros G, Garret C, Chabo C, Lantieri O, Courtney M, Marre M, harles MA, Balkau B & Burcelin R : Blood microbiota dysbiosis is associated with the onset of cardiovascular events in a large general population: the D.E.S.I.R. study. PLoS One 2013; 8: e54461.
10
De Angelis M, Montemurno E, Piccolo M, Vannini L, Lauriero G, Maranzano V, Gozzi G, Serrazanetti D, Dalfino G, Gobbetti M & Gesualdo L :Microbiota and metabolome associated with immunoglobulin A nephropathy (IgAN). PLoS One 2014;9: e99006.
11
Zheng X, Zhao A, Xie G, Chi Y, Zhao L, Li H,Wang C, Bao Y, JiaW, Luther M, Su , Nicholson JK & JiaW: Melamine-induced renal toxicity is mediated by the gut microbiota. Sci Transl Med 2013;5: 172- 22.
12
Andrade-Oliveira V, Amano MT, Correa-Costa M, Castoldi A, Felizardo RJ, de Almeida DC, Bassi EJ, Moraes-Vieira PM, Hiyane MI, Rodas AC, Peron JP, Aguiar CF, Reis MA, Ribeiro WR, Valduga CJ, Curi R, Vinolo MA, Ferreira CM& Cˆamara NO : Gut bacteria products prevent AKI induced by ischemia–reperfusion. J Am Soc Nephrol 2015;26: 1877–1888.
13
Vaziri ND,Wong J, Pahl M, Piceno YM, Yuan J, Desantis TZ: Chronic kidney disease alters intestinal microbial flora. Kidney Int.2013; 83(2):308–15.
14
Hida M, Aiba Y, Sawamura S, Suzuki N, Satoh T: Inhibition of the accumulation of uremic toxins in the blood and their precursors in the feces after oral administration of Lebenin, a lactic acid bacteria preparation, to uremic patients undergoing hemodialysis. Nephron. 1996;74(2):349–55.
15
Schepers E, Glorieux G, Vanholder R: The gut: the forgotten organ in uremia? Blood Purif. 2010;29(2):130–6.
16
Ramezani A & Raj DS : The gut microbiome, kidney disease, and targeted interventions. J Am Soc Nephrol 2014; 25: 657–670.
17
Wu MJ, Chang CS, Cheng CH, Chen CH, LeeWC, Hsu YH, Shu KH & Tang MJ : Colonic transit time in long-term dialysis patients. Am J Kidney Dis 2004; 44: 322–327.
18
Alderman MH, Cohen H, Madhavan S & Kivlighn S : Serum uric acid and cardiovascular events in successfullytreated hypertensive patients. Hypertension 1999; 34:144–150.
19
Wong J, Piceno YM, DeSantis TZ, Pahl M, Andersen GL & Vaziri ND : Expansion of urease- and uricase-containing, indole- and p-cresol-forming and contraction of short-chain fatty acid-producing intestinal microbiota in ESRD. Am J Nephrol 2014;39: 230–237.
20
Ramezani A,Massy ZA, Meijers B, Evenepoel P, Vanholder R, Raj DS: Role of the gut microbiome in uremia: a potential therapeutic target. Am J Kidney Dis. 2016; 67(3):483–98.
21
Carrero JJ, Stenvinkel P: Inflammation in end-stage renal disease- what have we learned in 10 years? Semin Dial. 2010; 23(5):498–509.
22
Koren O, Spor A, Felin J, Fak F, Stombaugh J, Tremaroli V:Human oral, gut, and plaque microbiota in patients with atherosclerosis. Proc Natl Acad Sci U S A. 2011;108(Suppl 1):4592–8.
23
Wiedermann CJ, Kiechl S, Dunzendorfer S, Schratzberger P, EggerG, Oberhollenzer F: Association of endotoxemia with carotid atherosclerosis and cardiovascular disease: prospective results from the Bruneck Study. J Am Coll Cardiol. 1999; 34(7):1975–81.
24
Poesen Rl, Ramezani A, Claes K, Augustijns P, Kuypers D, Barrows : Associations of soluble CD14 and endotoxin with mortality, cardiovascular disease, and progression of kidney disease among patients with chronic kidney disease. CJASN. 2015; In Press.
25
Lin CJ,Wu V,Wu PC,Wu CJ : Meta-analysis of the associations of p-cresyl sulfate (PCS) and indoxyl sulfate (IS) with cardiovascular events and all-cause mortality in patients with chronic renal failure . PLoS One. 2015;10(7):e0132589.
26
Velasquez MT, Ramezani A, Manal A, Raj DS:Trimethylamine NOxide:The Good, the Bad and the Unknown. Toxins (Basel). 2016; 8(11).
27
Tang WH, Wang Z, Kennedy DJ, Wu Y, Buffa JA, Agatisa-Boyle B: Gut microbiota-dependent trimethylamine N-oxide (TMAO) pathway contributes to both development of renal insufficiency and mortality risk in chronic kidney disease. Circ Res. 2015;116(3):448–55.
28
Tang WH, Wang Z, Fan Y, Levison B, Hazen JE, Donahue LM: Prognostic value of elevated levels of intestinal microbegenerated metabolite trimethylamine-N-oxide in patients with heart failure: refining the gut hypothesis. J Am Coll Cardiol. 2014; 64(18):1908–14.
29
Yang T, Santisteban MM, Rodriguez V, Li E, Ahmari N, Carvajal JM: Gut dysbiosis is linked to hypertension. Hypertension. 2015; 65(6):1331–40.
30
Macfarlane S, Macfarlane GT: Regulation of short-chain fatty acid production. Proc Nutr Soc. 2003; 62(1):67–72.
31
Le PE, Loison C, Struyf S, Springael JY, annoy V, DecobecqME: Functional characterization of human receptors for short chain fatty acids and their role in polymorphonuclear cell activation. J Biol Chem. 2003; 278(28):25481–9.
32
Round JL, Mazmanian SK:The gut microbiota shapes intestinal immune responses during health and disease. Nat Rev Immunol. 2009; 9(5):313–23.
33
Mortensen FV, Nielsen H,MulvanyMJ, Hessov I: Short chain fatty acids dilate isolated human colonic resistance arteries. Gut. 1990; 31(12):1391–4.
34
Pluznick JL, Zou DJ, Zhang X, Yan Q, Rodriguez-Gil DJ, Eisner C et al: Functional expression of the olfactory signaling system in the kidney. Proc Natl Acad Sci U S A 2009; 106(6):2059–2064.
35
Gibson GR, Probert HM, Loo JV, Rastall RA, Roberfroid MB: Dietary modulation of the human colonic microbiota: Updating the concept of prebiotics. Nutr Res Rev 2004; 17: 259–275.
36
Silk DB, Davis A, Vulevic J, Tzortzis G, Gibson GR: Clinical trial: the effects of a trans-galactooligosaccharide prebiotic on faecal microbiota and symptoms in irritabl bowel syndrome. Aliment Pharmacol Ther 2009; 29: 508–518.
37
Cani PD, Neyrinck AM, Fava F, Knauf C, Burcelin RG, Tuohy KM,GibsonGR, elzenne NM: Selective increases of bifidobacteria in gut microflora improve high-fat-diet-induced diabetes in mice through a mechanism associated with endotoxaemia. Diabetologia 2007; 50: 2374–2383.
38
Krishnamurthy VM, WeiG, Baird BC,Murtaugh M, Chonchol MB, Raphael KL, Greene T, Beddhu S: High dietary fiber intake is associated with decreased inflammation and all cause mortality in patients with chronic kidney disease. Kidney Int 2012; 81: 300–306.
39
Food and Agriculture Organization of the United Nations (FAO). Health and nutritional properties of probiotics in food including powder milk with live lactic acid bacteria. Available at: Accessed October 30, 2013.
40
van Baarlen P, Troost FJ, van Hemert S, vander Meer C, de Vos WM, de Groot PJ, Hooiveld GJ, Brummer RJ, Kleerebezem M; van BP: Differential NF-kappaB pathways induction by Lactobacillus plantarum in the duodenum of healthy humans correlating with immune tolerance. Proc Natl Acad Sci U S A 2009; 106: 2371–2376.
41
Evenepoel P, Bammens B, Verbeke K,Vanrenterghem Y: Acarbose treatmentlowers generation and serum concentrations of the protein-bound solute p-cresol: a pilot study. Kidney Int 2006; 70: 192–198.
42
Persky SE, Brandt LJ: Treatment of recurrent Clostridium difficile-associated diarrhea by administration of donated stool directly through a colonoscope. Am J Gastroenterol 2000; 95: 3283–3285.
43
ORIGINAL_ARTICLE
Study of Pulmonary Hypertension in Hemodialysis patients in Sohag University Hospital
https://smj.journals.ekb.eg/article_42519_88372dc5ac53e1833f2b20041083daac.pdf
2018-01-01
423
429
10.21608/smj.2018.42519
Lotfy
Abo Dahab
loutfy_abodahab@med.sohag.edu.eg
1
Department of Internal Medicine, Faculty of Medicine, Sohag University.
AUTHOR
Ahmed
Boghdady
ahmed_boghdady@med.sohag.edu.eg
2
Department of Internal Medicine, Faculty of Medicine, Sohag University.
AUTHOR
Nayel
Zaki
nail_elsaghier@med.sohag.edu.eg
3
Department of Internal Medicine, Faculty of Medicine, Sohag University.
AUTHOR
Noher
Abass
nahirmohamed@med.sohag.edu.eg
4
Department of Internal Medicine, Sohag Faculty of Medicine, Sohag University.
AUTHOR
Hill N.R, Fatoba S.T, Oke J.L, Hirst J.A, O’Callaghan C.A, Lasserson D.S: Global Prevalence of Chronic Kidney Disease, Systematic Review and Meta Analysis. PLoS ONE 2016; 11(7).
1
Navaneethan S.D, Roy J, Tao K, Brecklin C.S, Chen J, Deo R, Flack J.M, Ojo A.O, Plappert T.J, Raj D.S, Saydain G, Sondheimer J.H, Sood R, Steigerwalt S.P, Townsend R.R, Dweik R.A, Rahman M: Chronic Renal Insufficiency Cohort Investigators: Prevalence, predictors, and outcomes of pulmonary hypertension in CKD. J Am Soc Nephrol 2016; 27: 877- 886
2
Selvaraj S, Shah S.J, Ommerborn MJ: Pulmonary hypertension is associated with a higher risk of heart failure hospitalization and mortality in patients with chronic kidney disease: The Jackson Heart Study. Circ Heart Fail 2017; 6-10.
3
Stallworthy E.J, Pilmore H.L, Webster M.W: Do echocardiographic parameters predict mortality in patients with end-stage renal disease? Transplantation. 2013; 95 (10): 1225–1232.
4
Kawar B, Ellam T, Jackson C, Kiely D.G: Pulmonary hypertension in renal disease: Epidemiology, potential mechanisms and implications. Am J Nephrol 2013; 37: 281–290.
5
Humbert M, Gerry Coghlan J, Khanna D: Early detection and management of pulmonary arterial hypertension. Eur Respir Rev 2012; 21: 306–312.
6
Lawrence G, Rudski, Wyman W.L, Jonathan Afilalo, Lanqi Hua, Mark D. Handschumacher, Krishnaswamy Chandrasekaran, Scott D, Solomon, Eric K. Louie, and Nelson B. Schiller: Guidelines for the Echocardiographic Assessment of the right heart in adults American Society of EchocardiographyEndorsed by the European Association of Echocardiography. J Am Soc Echocardiogr 2010; 23:685-713.
7
Yigla M, Nakhoul F, Sabag A, Tov N, Gorevich B, Abassi Z, Reisner S.A: Pulmonary hypertension in patients with end-stage renal disease, Chest 2003; 123 (5): 1577–1582.
8
Mahdavi-Mazdeh.M, Alijavad-Mousavi.S, Yahyazadeh.H, Azadi.M, Yoosef nejad.H, Ataiipoor.Y: Pulmonary hypertension in hemodialysis patients. Saudi J. Kidney Dis. Transpl 2008;19: 189–193.
9
Abdelwhab S, Elshinnawy S: Pulmonary hypertension in chronic renal failure patients. Am. J. Nephrol 2008;28: 990–997.
10
Sise M.E, Courtwright A.M, Channick R.N: Pulmonary hypertension in patients with chronic and end-stage kidney disease. Kidney Int 2013; 84: 682–692.
11
Stauffer M.E, Fan T: Prevalence of anemia in chronic kidney disease in the United States. PLoS One.2014; 9: e84943.
12
Tsai Y.C, Tsai J.C, Chen S.C, Chiu Y.W, Hwang S.J, Hung C.C, Chen T.H, Kuo M.C, Chen H.C: Association of fluid overload with kidney disease progression in advanced CKD: a prospective cohort study. Am J Kidney Dis 2014; 63: 68–75.
13
Magdy M.Emara, Mohamad A. Habeb, Alsayed Ahmed Alnahal, Tarek A. Elshazly, Faisal O. Alatawi, Amer S. Masoud: Prevalence of pulmonary hypertension in patients with chronic kidney disease on and without dialysis. Egyptian Journal of Chest Diseases and Tuberculosis 2013; 62: 761–768
14
Tarrass F, Benjelloun M, Medkouri G, Hachim K, Benghanem M.G: Doppler echocardiograph evaluation of pulmonary hypertension in patients undergoing hemodialysis. Hemodial Int2006; 10: 356-359.
15
Kumbar L, Fein P.A, Rafiq M.A, Borawski C, Chattopadhyay J: Pulmonary hypertension in peritoneal dialysis patients. Adv Perit Dial 2007:23: 127-131.
16
Jawad Kadhem Manuti: Pulmonary Hypertension in Patients with Chronic Renal Failure. IRAQI J MED SCI 7(2009): 104-108.
17
Abdallah E.A, Waked E, Metwaly A, Khalek A.A: Role of arterio-venous shunt in the pathogenesis of pulmonary hypertension in patients with end stage renal disease. Kidney 2010; 19: 239.
18
min M, Fawzy A, Hamid M.A, Elhendy A: Pulmonary hypertension in patients with chronic renal failure, role of parathyroid hormone and pulmonary artery calcifications. Chest 2003; 124: 2093-2097.
19
Buemi M, Senatore M, Gallo G.C, Crasc E, Campo S, Sturiale A, Coppolino G, Bolignano D, Frisina N : Pulmonary hypertension and erythropoietin. Kidney Blood Press Res 2007; 30(4):248–252.
20
Mousavi S.S, Tamadon M.R, Nasri H, Ardalan M.R: Impact of parathyroid hormone on pulmonary artery pressure in hemodialysis patients. J Parathyr Dis. 2014; 2: 71-2.
21
Demir M, Uyan U, Keçeoçlu S, Demir C: The relationship between vitamin D deficiency and pulmonary hypertension. Prague Med Rep 2013; 114:154-61.
22
Park M, Hsu C.Y, Li Y, Mishra R.K, Keane M, Rosas S.E, Dries D, Xie D, Chen J, He J, Anderson A, Go A.S, Shlipak M.G: Associations between kidney function and sub-clinical cardiac abnormalities in CKD. J Am Soc Nephrol 2012; 23:1725–1734.
23
Paoletti E, Specchia C, Di Maio G, Bellino D, Damasio B, Cassottana P, Cannella G: The worsening of left ventricular hypertrophy is the strongest predictor of sudden cardiac death in haemodialysis patients: a 10 year survey. Nephrol Dial Transplant 2004; 19: 1829–1834.
24
ORIGINAL_ARTICLE
Review on Collection , Preservation and Fowarding of Biological Samples for Toxicological Analysis
Forensic Toxicology is the study and practice of the application of toxicology to the purposes of the law. The relevance of any finding is determined, in the first instance, by the nature and integrity of the specimen(s) submitted for analysis. This means that there are several specific challenges to select and collect specimens for ante-mortem
and post-mortem toxicology investigation. Post-mortem specimens may be numerous and can endow some special difficulties compared to clinical specimens, namely those resulting from autolytic and putrefactive changes. Storage stability is also an important issue to be considered during the pre-analytic phase, since its consideration should facilitate the assessment of sample quality and the analytical result obtained from that sample. The knowledge on degradation mechanisms and methods to increase storage stability may enable the forensic toxicologist to circumvent possible difficulties. Therefore, advantages and limitations of specimen preservation procedures are thoroughly discussed in this review. Presently, harmonized protocols for sampling in suspected intoxications would have obvious utility. In the present review an overview is given on sampling procedures for routinely collected specimens as well as on alternative specimens that may provide additional information on the route and timing of exposure to a specific xenobiotic. Last, but not least, how to forward a correct report and how to interpret a toxicological results is provided. This comprehensive review article is intented as a significant help for forensic toxicologists to accomplish their frequently overwhelming mission.
https://smj.journals.ekb.eg/article_42520_ad2abd4b3401991089c172c5604e19f1.pdf
2018-01-01
431
438
10.21608/smj.2018.42520
sampling
collection
Preservation
toxicological analysis
Maha
Hilal
maha_abdelaziz@med.sohag.edu.eg
1
Department of Forensic Medicine & Clinical Toxicology, Faculty of Medicine, Sohag, University.
AUTHOR
Essam
Abdullah
essam_abdallah@med.sohag.edu.eg
2
Lecturer of Forensic Medicine & Clinical Toxicoogy, Faculty of Medicine - Sohag University.
AUTHOR
Reda
El Sayed
reda_abdelrasowl@med.sohag.edu.eg
3
Department of, Forensic Medicine & Clinical Toxicology Faculty of Medicine, Sohag University, Egypt.
AUTHOR
Hend
Salman
hend-mohamed@med.sohag.edu.eg
4
Demonstrator in the Department of Forensic Medicine & Clinical Toxicoogy, Faculty of Medicine - Sohag University.
AUTHOR
A White Paper of the American Society of Addiction Medicine (ASAM) (2013): Drug testing in addiction treatment. Current Applications of Drug Testing and Promising New Opportunities. Vol.IV:46-55.
1
Baselt, R.C. (2008): Peripherally-acting drugs and common toxic chemicals. Disposition of Drugs and Toxic Chemicals in Man. 8th ed. Vol.2. Foster City, CA: Biomedical Publications: 560-1690.
2
Casavant, M.J.(2002): Urine drug screening in adolescents. Pediatr. Clin. North Am.,49: 317-327.
3
Coe, J.L. (1993): Postmortem chemistry update. Emphasis on forensic application. Am. J. Forensic Med. Pathol., 14:91–117.
4
Cooper, G.A.A.; Sue Paterson and Osselton, M.D.(2010): The United Kingdom and Ireland Association of Forensic Toxicologists . Forensic toxicology laboratory guidelines. Science and Justice. 50:166–176.
5
Daniel, C.R.; Piraccini, B.M. and Tosti, A. (2004): The nail and hair in forensic science. J. Am. Acad. Dermatol., 50:258–261.
6
Dinis-Oliveira, R.J.; Carvalho, F.; Duarte, J. A.; Remião, F., Marques, A.; Santos, A. and Magalhães, T. (2010): Collection of biological samples in forensic toxicology, Toxicology Mechanisms and Methods, 20 (7): 363-414.
7
Drummer, O.H. and Gerostamoulos, J. (2002): Postmortem drug analysis: analytical and toxicological aspects. Ther Drug Monit., 24:199–209.
8
Flanagan, R.J. and Connally G. (2005): Interpretation of analytical toxicology results in life and at postmortem. J. Toxicol Rev., 24(1):63-71.
9
Flanagan, R.J.; Taylor, A.; Watson, I.D. and Whelpton, R. (2007): Sample collection, transport and storage. Fundamentals of Analytical Toxicology.Ch.2, West Sussex: John Wiley & Sons Ltd: 21-47.
10
Gallardo, E. and Queiroz, J.A. (2008): The role of alternative specimens in toxicological analysis. Biomed. Chromatogr., 22:795–821.
11
Gourlay, D. L. and Heit, H. A. (2009): Commentary on unexpected urine drug testing results in a hospice patient on high dose morphine therapy. Clinical Chemistry, 55(10), 1767-1769.
12
Gronewold, A.; Dettling, A.; Haffner, H.T. and Skopp, G. (2009): Doxepin and nordoxepin concentrations in body fluids and tissues in doxepin associated deaths. Forensic Sci. Int., 190:74–79.
13
Health and Human Service /Medical Review Officer (HHS. MRO.), (2004): Urine drug testing. Medical Review Officer Manual for Federal Agency Workplace Drug Testing Programs. Ch.3. 6-19.
14
Helper, B.R. and Isenschmid, D.S. (2008): Specimen selection,collection,preservation and security. In: Karch, S.B. Editor. Postmortem Toxicology of Abused Drugs. 1st edition.Ch.2, Boca Raton, FL: CRC Press:13-31.
15
Henderson, GL. (1993): Mechanisms of drug incorporation into hair. Forensic Sci Int., 63:19–29.
16
Jickells, S. and Negrusz, A.; Moffat, A.C.; Osselton, M.D.; Widdop, B.; (2008): Introduction to forensic toxicology. In: Jickells, S. and Negrusz, A. (eds.). Clarke's Analytical Forensic Toxicology,3rd. edition. Ch.1. London:Pharmaceutical Press. Vol.1: 1-11.
17
Karinen, R.; Oiestad, EL.; Andresen, W.; Wethe, G.; Smith-Kielland, A. and Christophersen, A. (2010): Comparison of ethanol and other drugs of abuse concentrations in whole blood stored in Venoject glass and plastic and Venosafe plastic evacuated tubes. J. Anal. Toxicol., 34: 420–428.
18
Kellermann, A.L.; Fihn, S.D.; Logerfo,J.P. and Copass, M.K.(1988): Utilization and yield of drug screening in the emergency department. American Journal of Emergency Medicine. 6 (1): 14-20.
19
Kerrigan, S. (2008) : Sampling, storage and stability. In : Jickells, S. and Negrusz, A. (eds.). Clarke’s Analytical Forensic Toxicology, 1st edition. vol. 1. ch.13. London , Pharmaceutical Press: 335-356.
20
Leikin, JB. and Watson, WA. (2003): Post-mortem toxicology: what the dead can and cannot tell us. J. Toxicol. Clin. Toxicol., 41:47–56.
21
Levine, B. and Jufer, R. (2008): Drugs of abuse testing in vitreous humor. In: Jenkins, A.J. and Caplan, Y.H. (eds.). Drug Testing in Alternate Biological Specimens. ch.7.USA, Humana Press: 117-128.
22
Malamud, D. and Tabak, L. (1993): Saliva as a diagnostic fluid. Ann. NY. Acad. Sci., 694:11–12.
23
Moffat, A.C.; Osselton, M.D. and Widdop, B. (2013): Introduction to forensic toxicology. In: Negrusz, A. and Cooper, G. Clarke’s Analytical Forensic Toxicology. 2nd edition. vol.1. ch.1. London: Pharmaceutical Press:1-10.
24
Pesce, A.; West, C.; Egan, C.K. and Strickland, J.( 2012): Interpretation of urine drug testing in pain patients. Pain Med.,13:868-885.
25
Politi, L. ; Groppi, A.; Polettini, A. and Montagna M.(2004): A rapid screening procedure for drugs and poisons in gastric contents by direct injection-HPLC analysis. Forensic Science International, 141 : 115–120
26
Skopp, G.(2004): preanalytic aspect in postmortem toxicologicy Forensic Sci. Int.; 142:75-100.
27
Society of Forensic Toxicologists/American Academy of Forensic Sciences (SOFT/AAFS) (2006):Forensic Toxicology Laboratory Guidelines.1-24 . www.soft-tox.org.
28
Stimpfl, T.; Muller, K.; Gergov, M.; LeBeau, M.; Polettini, A.; Sporkert, F. and Weinmann W.(2007): Recommendations on Sample Preparation of Biological Specimens for Systematic Toxicological Analysis. TIAFT – The International Association of Forensic Toxicologists . TIAFT-Bulletin 41 (2): 1-11.
29
Swiss Committee for Drugs of Abuse Testing(SCDAT)(2012): Guidelines for Drugs of Abuse Testing., 1-62.
30
Tominaga, M.; Michiue, T.; Ishikawa, T.; Inamori-Kawamoto, O.; Oritani, Sh. and Maeda, H. (2015): Evaluation of postmortem drug concentrations in cerebrospinal fluid compared with blood and pericardial fluid. Forensic Science International, 254 : 118–125.
31
Triunfante, P.; Soares, M.E.; Santos, A.; Tavares, S.; Carmo, H. and Bastos Mde, L. (2009): Mercury fatal intoxication: two case reports. Forensic Sci. Int., 184:1-6.
32
University of California (UC) Davis analytical laboratory(2010): Introduction and over view. Quality Manual. Rev.0004.02: 3-18
33
World Health Organization (1995): International program in chemicalsafty,BasicAnalyticalToxicology,http://www.who.int/ipcs/publications/training_poisons/ _toxicology.
34
ORIGINAL_ARTICLE
Evaluation of cardiac function in patients with thalassemia intermedia: A prospective hospital based study
Background:B-Thalassemia is an inherited hemoglobin disorder caused by impaired synthesis of the b-globin chain and resulting in chronic hemolytic anemia.In the absence of regular treatment of thalassemia intermedia patients the diastolic performance of the left ventricle is maintained stable, while the pressure of pulmonary arteries continues to rise which is the main cause of death in these patients. 2D, M mode echocardiographyand tissueDopplerare method for evaluating the cardiac function in patients with thalassemia intermedia. Objective: Our main objective in this study is to evaluate the cardiac function in patients with thalassemia intermedia by 2D, M mode echocardiography and Doppler methods. Methods: This case-control study was conducted on 46 thalassemic patients (mean age: 9.7 ± 4.6years) and 46 healthy individuals (mean age: 10.3 ± 4.1 years) as a control group from October 2016 toSeptember 2017 in the Pediatric haematology Clinics and inpatients of Pediatric Department.There was no sign of cardiac involvement by physical examination, chest x-ray and ECG in patients. Echocardiographic parameters were measured in groups, and finally data was analyzed by SPSS software. Results:The mean of left ventricular myocardial performance index (LMPI) ((P- value<0.001) and left ventricular mass index (LVMI) ((P- value<0.001) have statistically significant differencebetween two groups. Mean of interventricular septal dimension in diastole (IVSD), left ventricular posterior wall thickness in diastole (LVPWD) and interventricular septal dimension in systole (IVSS) were also statistically significant with a P-value of, <0.001, 0.042, 0.05). Conclusion: the systolic and diastolic performance of thalassemia intermedia patients is affected earlier in comparison with control group in some parameters including LVMPI, EF, FS, IVSD, IVSS, LVPWDD and RVMPI. For more evaluation, more quantitative and comprehensive research suggested by evaluation of specific effective factors to psychosocial health of these patients. Study Limitation * Age group: we conduct only the pediatric age group thalassemia intermedia, and as we know the most of complication appear in older age * Number of patient: we conduct only46 patient in our study. *Lack of material potential: availability of other facilities like T* and MRI as echocardiography is not able to replace them even echocardiographic abnormalities are found.
https://smj.journals.ekb.eg/article_42525_5d882dc5bb636b5dceefbb41cf213bbc.pdf
2018-01-01
439
444
10.21608/smj.2018.42525
thalassemia intermedia in children
Complications of TI
cardiac function
echocardiography and Dopplerstudies
Alzahraa
Ahmed
elzahraa_sharaf@med.sohag.edu.eg
1
Department of Pediatric haematology Unit, Pediatric Department,Faculty of Medicine, Sohag University, Sohag, Egypt.
AUTHOR
Safaa
Ali
safaa_ahmed@med.sohag.edu.eg
2
Department of Pediatric , Faculty of Medicine,Sohag University, Sohag, Egypt.
AUTHOR
Walaa
Madkoor
3
Department of Pediatric ,Faculty of Medicine, Sohag University, Sohag Egypt.
AUTHOR
Aessopos A , Farmakis D, Deftereos S, Tsironi M, Tassiopoulos S, Moyssakis I, Karagiorga M. Thalassemia Heart Disease: A Comparative Evaluation of Thalassemia Major and Thalassemia Intermedia. Chest. 2005; 127(5):1523-1530.
1
Aessopos A, Berdoukas V. Cardiac function and iron chelation in thalassemia major and intermedia: a review of the underlying pathophysiology and approach to chelation management. Mediterranean Journal of Hematology and Infectious Diseases.2009; 49 (2):137-143.
2
Aessopos A, Tsironi M, Andreopoulos A, Farmakis D. Heart disease in thalassemia intermedia. Hemoglobin. 2009; 33(1):170-6.
3
Bosi G, Crepaz R, Gamberini MR, Fortini M, Scarcias, Bonsante E. Left Ventricular remodeling and Systolic and diastolic Function in young adult with beta thalassemia Major: A Doppler echocardiographic assessment and correlation with hematologic data. Heart. 2003; 89(7):262-6.
4
Challenor VF, Conway N, Monro JL. The surgical treatment of restrictive cardiomyopathy in pseudoxanthoma elasticum. Br Heart J. 2004; 59:266-269.
5
Ehlers KH, Levin AR, Markenson AL. Longitudinal study of cardiac function in thalassemia major. Ann N Y Acad Sci. 2006; 344:397-404.
6
Isner JM, Carter BL, Bankoff MS, Konstam MA, Salem DN. Computed tomography in the diagnosis of pericardial heart disease. Ann Intern Med.1982; 97:473-479
7
Kanavakis E, Traeger-Synodinos J, Tzetis M, Metaxotou-Mavromati A, Ladis V, Kattamis C.Molecular characterization of homozygous (high hba2) beta-thalassemia intermedia in Greece. Pediatric Hematol Onco. 2007;l:135-158.
8
Mahdi, Safa A, Laith S, Faraj, Hasanein H, Ghali. Significance of Red Blood Cell Indices in Beta-Thalassaemia Trait. Mustansiriya Medical Journal.215; 14:27-30.
9
Marshall A. Lichtman Ernest Beutler, Thomas J.Williams. Hematology. In: Kaushansky SK, Josef T.7th ed. 2006: 633-6.
10
Modell B, Berdoukas V. The Clinical Approach to Thalassemia. New York, NY: Grune & Stratton.1984.3:115-130.
11
Nouri NM, Naderi M, Emamdadi A, Fadaie M, Rajaie S. Comparison of Cardiac Function in Young Patients with Thalassemia Intermedia and Healthy Individuals Using Echocardiography Method. Iranian journal of blood and cancer. 2012; 4(4):157-161.
12
Nouri NM, Naderi M , Rajaie S, Dorgalaleh A , Tabibian Sh. Evaluation of Cardiac Function in Patients with Thalassemia Intermedia. Iranian Journal of Pediatric Hematology Oncology. 2013; l3 (1):193-199.
13
Ocal B, Oguz D, Karademir S, Birgen D, Yüksek N, Ertem U. Myocardial performance index combining systolic and diastolic myocardial performance in doxorubicin-treated patients and its correlation to conventional echo/Doppler indices. Pediatr Cardiol. 2002; 23(5):522-7.
14
Shawky RM, Kamal TM. Thalassemia intermedia: An overview. Egyptian Journal of Medical Human Genetics. 2012; 13: 245–255.
15
Vaccari M, Crepaz R, Fortini M, Gamberini MR, Scarcia S, Pitscheider W,. Left ventricular remodeling, systolic function and diastolic function in young adults with beta thalassemia intermedia: a Doppler echocardiography study. Chest 2002; 121(2): 506-12.
16
Zurlo MG, DE Stefano P, Borgna-Pignatti. Survival and causes of death in thalassemia major. Lancet. 1999; 2:27-30.
17
ORIGINAL_ARTICLE
Histopathological evaluation of skin in cirrhotic patients with pruritus
Background: Cirrhosis often is a silent disease Clinical symptoms at presentation may include jaundice of the eyes or skin, pruritus, gastrointestinal bleeding, coagulopathy, increasing abdominal girth, and mental status changes. Pruritus may be the presenting symptom, arising years before any other classic clinical and laboratory markers of hepatic dysfunction. This study examines the clinical, laboratory and histopathological changes in the skins of cirrhotic patients with pruritus in comparison with cirrhotic patients without pruritus and healthy control skins . Patients and Methods: To evaluate clinical, laboratory and histopathological changes in cirrhotic patients with pruritus, cirrhotic patients without pruritus and corresponding healthy (control). skin biopsies (20 specimens each) using hematoxylin and eosin stain and to study mast cell density using gimesa stain. Results: In the skin biopsy specimens of the cirrhotic patients with pruritus we found several histological changes including: epidermal hyperplasia (acanthosis) ,vascular ectasia(dilated dermal blood vessels), hypertrophied dermal nerve endings, mixed inflammatory cellular infilterate and lymphocytic vasculopathy (swelling of the endothelial cell lining of the blood vessels without fibrinoid necrosis, leucocytoclasia or extravasation of red blood cells). Evaluation of mast cell count in Gimesa stained skin sections revealed an increased numbers of these cells in the group of cirrhotic patients with pruritus ( N=5-10). The cells noted in perivascular, perineural and interstitial distribution (between collagen bundles). Conclusions: We report, for the first time, some histopathologial changes in the skins of cirrhotic patients with pruritus in comparison with cirrhotic patients without pruritus and healthy control skins .
https://smj.journals.ekb.eg/article_42529_fa33077822e6f05ca719099bdc318829.pdf
2018-01-01
447
452
10.21608/smj.2018.42529
ESSAMELDIN
NADA
essameldin_nada@med.sohag.edu.eg
1
DERMATOLOGY, Venereology and Andrology, Faculty of Medicine , sohag university.
AUTHOR
Hanan
Assaf
hanan_asaf@med.sohag.edu.eg
2
Department of Dermatology, Venereology and Andrology, Sohag Faculty of Medicine, Sohag University.
AUTHOR
Reham
El Sharkawy
reham_elsharkawy@med.sohag.edu.eg
3
Departments of Dermatology, Venereology and Andrology, Faculty of Medicine, Sohag University.
AUTHOR
Amr
Zaghloul
amr_hashem@med.sohag.edu.eg
4
Department of Tropical Medicine and Gastroenterology, Faculty of Medicine, Sohag University.
AUTHOR
Marwa
Abd El Meged
marwamohamed@med.sohag.edu.eg
5
Department of Dermatology, Venereology and Andrology, Sohag Faculty of Medicine, Sohag University.
AUTHOR
Mahmoud
Abd El Wahed
6
Department of pathology, Assuit Faculty of Medicine, Assuit University.
AUTHOR
Asmaa
Ahmed
7
Department of pathology, Assuit Faculty of Medicine, Assuit University.
AUTHOR
Malekzadeh R, Mohamadnejad M, Rakhshani N, Nasseri-Moghaddam S, Merat S, Tavangar SM, et al (2004): Reversibility of cirrhosis in chronic hepatitis B. Clin Gastroenterol Hepatol;2:344-7.
1
Heidelbaugh J and Sherbondy M (2006). Cirrhosis and chronic liver failure. Part II: Complications and treatment. Am Fam Physician;74:765-74,779.
2
Diehl A. Alcoholic and nonalcoholic steatohepatitis. Goldman L,Ausiello D (2004), eds. Cecil Textbook of Medicine. 22nd ed. Philadelphia, Pa.: Saunders,:935-6.
3
Amin M, Shahat M, El-Garem N, Soliman A, Obaia E (2017): Assessment of serum level cholinesterase as a biomarker of liver cirrhosis in Egyptian cirrhotic patients Gastroenterology Insights; volume 8:6914
4
Rosselli M and Zuckermann M (2011). Liver cirrhosis. Best Pract Res Clin Gastroenterol.;25:281–290.
5
Jones D (2012): Pathogenesis of cholestatic itch: old questions, new answers, and future opportunities. Hepatology.;56(4):1194-6.
6
Bergasa N (2005): The pruritus of cholestasis. J Hepatol.;43(6): 1078-88.
7
Bergasa N (2011): The itch of liver disease. Semin. Cutan. Med. Surg30: 93– 8
8
Mela A, Mancuso A, Burroughs AK (2003): Review article: pruritus in cholestasis and other liver diseases. Aliment Pharmacol Ther.;17(7):857-70.
9
Beuers U, Kremer AE, Bolier R, Elferink RP (2014):Pruritus in cholestasis: facts and fiction. Hepatology.;60(1):399-407.
10
Metz M and Ständer S (2010): Chronic pruritus – pathogenesis, clinical aspects and treatment. J Eur Acad Dermatol Venerol.;24(11):1249-60.
11
Paus R, Theoharides TC, Arck PC (2006):Neuroimmune endocrine circuitry of the ‘‘brain-skin connection’’.Trends Immunol 15:1–13
12
Kremer AE, Elferink RP, Beuers U (2011): Pathophysiology and current management of pruritud in liver disease. Clin Res Hepatol Gastroenterol.;35:89-97
13
European Association for the study of the liver (2009): EASL Clinical Practice guidelines: Management of liver diseases. J Hepatol.;51(2):237-40.
14
Dawson P and Karpen S (2014):Bile acids reach out to the spinal cord: new insights to the pathogenesis of itch and analgesia in cholestatic liver disease. Hepatology. ;59:1638–41.
15
Khalil S, Youssef M, Mekkawy M, Abdelmalek M (2015): Liver Cirrhosis: Impact Of Nutritional Regimen On Patients Outcome. IOSR Journal of Nursing and Health Science (IOSR-JNHS) e-ISSN: 2320–1959.p- ISSN: 2320–1940 Volume 4, Issue 2 Ver. III (Mar.-Apr. 2015), PP 22-35.
16
O’Keefee C, Baird AW, Nolan N, Mccomick PA (2004):Cholestatic pruritus: the role of cutaneous mast cells and nerves. Aliment Pharmacol Ther.;19(12):1293-300.
17
Lindor K, Gershwin M, Poupon R, Kaplan M, Bergasa N, Heathcote E (2009): American Association for Study of Liver Diseases. Primary biliary cirrhosis. Hepatology.;50(1):291-308.
18