Abstract
Henoch-Schönlein purpura (HSP) is a small-vessel vasculitis of autoimmune hypersensitivity, and renin-angiotensin system (RAS) regulates vascular homeostasis and inflammation with activation of cytokine release. Thus, we aimed to investigate the association between HSP andACE I/DandAGT M235Tpolymorphisms. Genotyping was determined by allele specific PCR and PCR-RFLP. We obtained a significant difference in genotype distribution (p= 0.003) and allele frequencies (p< 0.001) ofACE I/Dpolymorphism between patients and controls, while no significant association was detected in genotype distribution (p> 0.05) and allele frequencies (p> 0.05) of theAGT M235Tpolymorphism. Risk assessment showed significant risk for HSP in the subjects both with the ID + DD genotype (p= 0.019, OR: 2.288, 95% CI: 1.136–4.609) and D allele (OR: D vs. I: 2.0528, 95% CI: 1.3632–3.0912,p= 0.001) while no significant risk was obtained for HSP in the subjects both with the MT + TT genotype (p= 0.312, OR: 1.3905, 95% CI: 0.7326–2.6391) and T allele (OR: T vs. M: 1.065, 95% CI: 0.729–1.557,p= 0.743). Furthermore, when patients were stratified by the presence of certain systemic complications of HSP, no significant association was detected withACE I/D, andAGT M235Tpolymorphisms. Our findings suggest thatACE I/Dpolymorphism is significantly associated with HSP susceptibility.
Highlights
Henoch-Schonlein purpura (HSP) is a rare, nonthrombocytopenic, leukocytoclastic, lgA mediated small-vessel vasculitis of autoimmune hypersensitivity [1]
HSP patients who were homozygous for the deletion allele (DD) presented a significantly higher prevalence of HSP compared to patients homozygous for the insertion allele (II) or heterozygous (ID)
The association between DD genotype/D allele and HSP was consistent as shown by a high odds ratio, but the genotype-phenotype correlation analysis showed no significant association between ACE I/D, AGT M235T, and main clinical manifestations of HSP
Summary
Henoch-Schonlein purpura (HSP) is a rare, nonthrombocytopenic, leukocytoclastic, lgA mediated small-vessel vasculitis of autoimmune hypersensitivity [1]. HSP typically involves small vessels, and main-. Ly affects skin, joints, gastrointestinal (GI) tract, and kidneys some of which progress to renal insufficiency especially in the adulthood. Rare complications of HSP include central and peripheral nervous system and pulmonary complications [2,3,4]. Immune and inflammatory response activation is a common feature of systemic vasculitis, and HSP is the result of a complex series of inflammatory and immunologic processes. Important roles of pro-inflammatory cytokines and the renin-angiotensin system (RAS) components were shown on HSP pathogenesis [5,6].
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