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ORIGINAL ARTICLE
Year : 2014  |  Volume : 34  |  Issue : 1  |  Page : 36-40

Tumor necrosis factor α promoter −308G/A polymorphism in patients with patchy alopecia areata


1 Department of Dermatology and Venereology, Faculty of Medicine, Ain Shams University, Cairo, Egypt
2 Department of Microbiology and Immunology, Faculty of Medicine, Ain Shams University, Cairo, Egypt

Correspondence Address:
Al-Hasan M El-Hefnawy
MD, Departments of Dermatology and Venereology, Faculty of Medicine, Ain Shams University, Cairo 12311
Egypt
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/1110-6530.137295

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Background Alopecia areata (AA) is a common recurrent inflammatory nonscarring hair loss disease with a worldwide prevalence ranging from 1 to 2%. Although the exact etiology of AA is unknown, there is evidence for both genetic and autoimmune components. Recently, tumor necrosis factor a (TNF-a) promoter −308 polymorphism was suggested to contribute to the pathogenesis of a wide range of autoimmune and infectious diseases. There is a plausible association between TNF-α polymorphism and AA. Objective The aim of the study was to determine TNF-α 308 gene polymorphism in patients with patchy AA. Patients and methods The present case-control study included 20 patients with patchy AA and 20 age-matched and sex-matched apparently healthy controls. TNF-α 308 gene polymorphism was detected by restricted fragment length polymorphism PCR in all of them. Results The mutant TNF-α 308 gene was found in 28.6% of patients with patchy AA and in 4.8% of controls, with statistically nonsignificant difference (P = 0.093). No statistically significant differences were found between patients with normal genotype and those with mutant genotype with respect to age, sex, disease duration, medical associations, family history of autoimmune diseases, or history of previous attacks. Statistically significant difference was found with respect to family history of AA and number of lesions. Conclusion TNF-α 308 gene polymorphism was present in small percentage of patients with patchy AA, with statistically nonsignificant difference from controls.


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