Tumor necrosis factor alpha promoter-308G/A polymorphism in Mexican patients with patchy alopecia areata

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.

To assess a possible association between the presence of TNFα-308G/A and patchy AA.

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.

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).

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.