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  • Title: Tumor necrosis factor alpha promoter-308G/A polymorphism in Mexican patients with patchy alopecia areata.
    Author: Cristina CS, Mauricio SS, Armando LR, Celia SD, Clara RI, Rocío OL, Oliverio W, Jorge OC.
    Journal: Int J Dermatol; 2012 May; 51(5):571-5. PubMed ID: 22515582.
    Abstract:
    BACKGROUND: Alopecia areata (AA) is a chronic inflammatory condition characterized by hair loss, most frequently from the scalp. Its etiopathogenesis is currently unknown, but inflammatory traits and associations with autoimmune diseases suggest that AA shares a similar origin. The tumor necrosis factor alpha (TNFα) gene, located on chromosome 6 within the major histocompatibility complex class III gene, may carry previously described polymorphisms--particularly in the promoter region, such as TNFα-308G/A--known to be risk factors in a wide variety of inflammatory pathologies. In Mexican populations, this polymorphism has been associated with augmented TNFα production and, thus, renders carriers more susceptible to developing autoimmune diseases; however, as yet it has not been associated with AA. OBJECTIVES: To assess a possible association between the presence of TNFα-308G/A and patchy AA. MATERIALS AND METHODS: Blood samples were taken from 59 patients affected by patchy AA and 103 control subjects without AA, all from the northeastern Mexican population. Genomic DNA was isolated using the phenol-chloroform method and samples subjected to polymerase chain reaction-restriction fragment length polymorphism in order to detect the TNFα-308G/A polymorphism. RESULTS: TNFα-308G/A (TNF2) allele [odds ratio (OR) = 3.22, P = 0.026, 95% confidence interval (CI) = 0.99-11.61], when segregated in the heterozygous (TNF1/TNF2) genotype (OR = 3.53, P = 0.023, 95% CI = 1.01-12.89) confers a significant risk for developing AA, compared with the genotype TNF1/TNF1 observed in controls (OR = 0.28, P = 0.023, 95% CI = 0.08-0.99). CONCLUSIONS: Our data suggest that there is a plausible association between the presence of the TNFα-308G/A polymorphism and a higher susceptibility for developing patchy AA. This risk might be due to overproduction of TNFα, which would facilitate an autoimmune response against the hair follicle.
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