Analysis of the Tumor Necrosis Factor-alpha Promoter Polymorphismin Children with Henoch-Schonlein Purpura.
- Author:
Hye Ran YANG
1
;
Jae Sung KO
;
Jeong Kee SEO
Author Information
1. Department of Pediatrics, Seoul National University College of Medicine, Seoul, Korea. jkseo@snu.ac.kr
- Publication Type:Original Article
- Keywords:
Henoch-Schonlein purpura;
Tumor necrosis factor-alpha;
Polymorphism;
Children
- MeSH:
Child*;
Enzyme-Linked Immunosorbent Assay;
Gastrointestinal Tract;
Genetic Predisposition to Disease;
Humans;
Joints;
Kidney;
Purpura, Schoenlein-Henoch*;
Skin;
Systemic Vasculitis;
Tumor Necrosis Factor-alpha*
- From:Korean Journal of Pediatric Gastroenterology and Nutrition
2007;10(1):11-19
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
PURPOSE: 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-alpha) is regarded as an important cytokine contributing to the disease. The goal of this study was to determine the role of TNF-alpha in the pathogenesis of HSP, and to evaluate the TNF-alpha polymorphism for genetic susceptibility to HSP. METHODS: From March 2004 to November 2005, 40 children with HSP and 32 healthy controls were included. Serum TNF-alpha levels were measured using the ELISA method during the acute and convalescent phase of HSP. The genotypic and allelic frequencies of the TNF-alpha gene polymorphisms at positions -308 and -238 were evaluated in patients and controls. RESULTS: Serum TNF-alpha 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-alpha levels and the clinical scores of HSP (r=0.310, p=0.070). The genotypic frequency of the TNF-alpha - 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-alpha -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). CONCLUSION: TNF-alpha is assumed to be the main cytokine associated with the pathogenesis of HSP during the acute phase. However, the presence of TNF-alpha gene polymorphisms at positions -308 and -238 did not distinguish children with HSP from normal controls.
