OBJECTIVE: To assess the influence of endothelial nitric oxide synthase (eNOS) polymorphisms in the susceptibility and clinical expression of patients with cutaneous vasculitis fulfilling classification criteria for Henoch-Schönlein purpura (HSP). METHODS: Fifty patients from Northwest Spain with primary cutaneous vasculitis classified as HSP were studied. Patients and ethnically matched controls (n = 117) were genotyped by polymerase chain reaction techniques for a variable-number tandem-repeat polymorphism in intron 4, a T/C polymorphism at position -786 in the promoter region, and a polymorphism in exon 7 (298Glu/Asp or 5557G/T) of the eNOS gene. RESULTS: No differences in allele or genotype frequencies for any of the individual eNOS polymorphisms were observed between patients fulfilling HSP classification criteria and controls, or when patients were stratified for the presence of nephritis or joint or gastrointestinal manifestations. In the HSP group no linkage disequilibrium between these polymorphisms was found. No significant difference in haplotype frequencies was observed between patients and controls. CONCLUSION: Our results do not support a role for these polymorphisms in the susceptibility to HSP.
OBJECTIVE: To assess the influence of endothelial nitric oxide synthase (eNOS) polymorphisms in the susceptibility and clinical expression of patients with cutaneous vasculitis fulfilling classification criteria for Henoch-Schönlein purpura (HSP). METHODS: Fifty patients from Northwest Spain with primary cutaneous vasculitis classified as HSP were studied. Patients and ethnically matched controls (n = 117) were genotyped by polymerase chain reaction techniques for a variable-number tandem-repeat polymorphism in intron 4, a T/C polymorphism at position -786 in the promoter region, and a polymorphism in exon 7 (298Glu/Asp or 5557G/T) of the eNOS gene. RESULTS: No differences in allele or genotype frequencies for any of the individual eNOS polymorphisms were observed between patients fulfilling HSP classification criteria and controls, or when patients were stratified for the presence of nephritis or joint or gastrointestinal manifestations. In the HSP group no linkage disequilibrium between these polymorphisms was found. No significant difference in haplotype frequencies was observed between patients and controls. CONCLUSION: Our results do not support a role for these polymorphisms in the susceptibility to HSP.