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Effect of paraoxonase 1 gene polymorphisms on clinical course of Henoch-Schonlein purpura.

Authors: Yilmaz, A  Emre, S  Agachan, B  Bilge, I  Yilmaz, H  Ergen, A  Isbir, T  Sirin, A 
Citation: Yilmaz A, etal., J Nephrol. 2009 Nov-Dec;22(6):726-32.
Pubmed: (View Article at PubMed) PMID:19967651

BACKGROUND: Henoch-Schonlein purpura (HSP) is a systemic vasculitis; its pathogenesis is still unknown. Oxidative stress may play a role in the pathogenesis of HSP. Paraoxonase1 (PON1) is an antioxidant enzyme. Two polymorphisms have been defined in the coding region of the PON1 gene, Q/R192 and L/M55. In the present study, we aimed to investigate the effect of PON1 gene polymorphisms on the course and renal involvement of HSP in Turkish children. METHOD: Forty-six patients with HSP were compared with 34 healthy children regarding the distribution of PON1 polymorphisms. RESULTS: PON1 Q/R192 genotype distribution was 58.6% QQ, 32.6% QR and 8.8% RR in the HSP group and 14.3% QQ, 50% QR and 35.7% RR in the control group. The frequency of QQ genotype was higher in the HSP group, and the presence of QQ genotype increased the risk by 3.42-fold for developing HSP (p=0.000, Fisher exact test; odds ratio [OR] = 2.048; 95% confidence interval [95% CI], 1.396-3.00). PON1 L/M55 genotype distribution was 50% LL, 43.5% LM and 6.5% MM in the HSP group and 48% LL, 26% LM and 26% MM in the control group. The frequency of MM genotype was lower in the HSP group, and the presence of MM genotype decreased the risk by 7.38-fold for developing HSP (p=0.009, Fisher exact test; OR=7.380, 95% CI, 1.474-36.953). CONCLUSION: PON1 polymorphisms may contribute to the pathogenesis and course of HSP, but we suggest that further investigations with larger patient groups are required to confirm our results.


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CRRD Object Information
CRRD ID: 11552576
Created: 2016-10-11
Species: All species
Last Modified: 2016-10-11
Status: ACTIVE


RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.