Henoch-Schonlein purpura (HSP) is a systemic vasculitis involving the skin, joints, gastrointestinal tract, and kidney. Although the pathogenesis of HSP is still unclear, tumor necrosis factor (TNF-α) is regarded as an important cytokine contributing to the disease. The goal of this study was to determine the role of TNF-α in the pathogenesis of HSP, and to evaluate the TNF-α polymorphism for genetic susceptibility to HSP.

From March 2004 to November 2005, 40 children with HSP and 32 healthy controls were included. Serum TNF-α levels were measured using the ELISA method during the acute and convalescent phase of HSP. The genotypic and allelic frequencies of the TNF-α gene polymorphisms at positions −308 and −238 were evaluated in patients and controls.

Serum TNF-α levels were 23.17±11.31 pg/mL in the acute phase of children with HSP and 10.56±5.59 pg/mL in the convalescent phase (p=0.000). There was no significant correlation between the serum TNF-α levels and the clinical scores of HSP (r=0.310, p=0.070). The genotypic frequency of the TNF-α −308 polymorphism in children with HSP was not significantly different compared to healthy controls (GG 80%, GA 20% vs. GG 93.8%, GA 6.2%; p=0.094). The genotypic frequency of the TNF-α −238 polymorphism in children with HSP was not significantly different (GG 97.5%, GA 2.5% vs. GG 93.8%, GA 6.3%; p=0.429).

TNF-α is assumed to be the main cytokine associated with the pathogenesis of HSP during the acute phase. However, the presence of TNF-α gene polymorphisms at positions −308 and −238 did not distinguish children with HSP from normal controls.