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Int J Dermatol ; 49(10): 1133-40, 2010 Oct.
Article in English | MEDLINE | ID: mdl-20931685

ABSTRACT

BACKGROUND: The strongest genetic marker for psoriasis is Cw*06. Polymorphisms in the tumor necrosis factor (TNF)-alpha promoter region, especially replacement of guanine with adenine in positions -238 and -308 are related to higher TNF-alpha production and higher risk for psoriasis in Caucasoid populations, not found in Asians. We performed a case-control study of 69 patients with psoriasis type I and 70 controls, characterized clinical progression along 10-years of follow-up in mild or severe disease and determined HLA class I, II, and TNF single nucleotide polymorphisms (SNPs) -238 and -308 polymorphisms to demonstrate whether these polymorphisms may be genetic risk for susceptibility to psoriasis or severity of the disease in Brazilians. METHODS: Polymorphisms were identified using PCR/SSP. Alleles, genotypes, and haplotypes frequencies were compared using Fisher's test. RESULTS: More severe disease was found in male patients. It may be suggested that alleles B*37, Cw*06, Cw*12, and DRB1*07 were associated with severe disease course, while B*57 with mild disease. No statistical difference was found between the patients and controls regarding polymorphisms frequencies in TNF SNPs. This study pointed to a higher TNF-238 G/G genotype frequency (OR: 3.21; CI: 1.06­9.71; P = 0.04) in the group with severe disease. CONCLUSIONS: Polymorphisms in the TNF-alpha SNPs do not seem to be a more important genetic risk factor for psoriasis than the already known Cw*06 in Brazilian patients, but these markers may be related to clinical manifestations.


Subject(s)
Genetic Predisposition to Disease , HLA Antigens/genetics , Polymorphism, Single Nucleotide , Psoriasis/genetics , Severity of Illness Index , Tumor Necrosis Factor-alpha/genetics , Adolescent , Adult , Brazil , Case-Control Studies , Female , Follow-Up Studies , Gene Frequency , Genetic Markers , Genotype , Haplotypes , Humans , Male , Middle Aged , Polymerase Chain Reaction , Promoter Regions, Genetic , Young Adult
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