title: Tumor necrosis factor alpha promoter-308G/A polymorphism in Mexican patients with patchy alopecia areata.
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.
  
  
  OBJECTIVE
  To assess a possible association between the presence of TNFα-308G/A and patchy AA.
  
  
  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.
authors.affiliation: Departamento de Dermatología, Hospital Universitario Dr José Eleuterio González, Monterrey, NL, México.
authors.forename: Cantú-Salinas
authors.initials: CS
authors.lastname: Cristina
authors.forename: Salinas-Santander
authors.initials: SS
authors.lastname: Mauricio
authors.forename: Lagos-Rodríguez
authors.initials: LR
authors.lastname: Armando
authors.forename: Sánchez-Domínguez
authors.initials: SD
authors.lastname: Celia
authors.forename: Rios-Ibarra
authors.initials: RI
authors.lastname: Clara
authors.forename: Ortiz-López
authors.initials: OL
authors.lastname: Rocío
authors.forename: Welsh
authors.initials: W
authors.lastname: Oliverio
authors.forename: Ocampo-Candiani
authors.initials: OC
authors.lastname: Jorge
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D000483:Alleles; D000506:Alopecia Areata / Q000235:genetics*; D002648:Child; D002675:Child, Preschool; D016001:Confidence Intervals; D005260:Female; D005838:Genotype; D006801:Humans; D008297:Male; D008800:Mexico; D008875:Middle Aged; D016017:Odds Ratio; D020641:Polymorphism, Single Nucleotide; D011401:Promoter Regions, Genetic / Q000235:genetics*; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics*; D055815:Young Adult
chemical_list: D014409:Tumor Necrosis Factor-alpha