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Disease Markers
Volume 34 (2013), Issue 1, Pages 23-32
http://dx.doi.org/10.3233/DMA-2012-120946

Association between RAS Gene Polymorphisms (ACE I/D, AGT M235T) and Henoch-Schönlein Purpura in a Turkish Population

Sinem Nalbantoglu,1 Yılmaz Tabel,2 Sevgi Mir,3 Erkin Serdaroğlu,4 and Afig Berdeli1

1Molecular Medicine Laboratory, Children’s Hospital, Faculty of Medicine, Ege University, Bornova, Izmir, Turkey
2Department of Pediatrics, Faculty of Medicine, Inonu University, Malatya, Turkey
3Division of Pediatric Nephrology, Department of Pediatrics, Faculty of Medicine, Ege University, Bornova, Izmir, Turkey
4Izmir Dr. Behcet Uz Children's Hospital, Izmir, Turkey

Received 12 November 2012; Accepted 12 November 2012

Copyright © 2013 Hindawi Publishing Corporation. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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 and ACE I/D and AGT M235T polymorphisms. 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) of ACE I/D polymorphism between patients and controls, while no significant association was detected in genotype distribution (p > 0.05) and allele frequencies (p > 0.05) of the AGT M235T polymorphism. 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 with ACE I/D, and AGT M235T polymorphisms. Our findings suggest that ACE I/D polymorphism is significantly associated with HSP susceptibility.