title: Effect of paraoxonase 1 gene polymorphisms on clinical course of Henoch-Schönlein purpura.
abstract: BACKGROUND
  Henoch-Schönlein 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.
  
  
  METHODS
  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).
  
  
  CONCLUSIONS
  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.
authors.affiliation: Pediatric Nephrology Department, Bakirkoy Maternity and Children Hospital, Istanbul, Turkey. alevyy@yahoo.com
authors.forename: Alev
authors.initials: A
authors.lastname: Yilmaz
authors.forename: Sevinc
authors.initials: S
authors.lastname: Emre
authors.forename: Bedia
authors.initials: B
authors.lastname: Agachan
authors.forename: Ilmay
authors.initials: I
authors.lastname: Bilge
authors.forename: Hulya
authors.initials: H
authors.lastname: Yilmaz
authors.forename: Arzu
authors.initials: A
authors.lastname: Ergen
authors.forename: Turgay
authors.initials: T
authors.lastname: Isbir
authors.forename: Aydan
authors.initials: A
authors.lastname: Sirin
mesh_terms: D000293:Adolescent; D043303:Aryldialkylphosphatase / Q000235:genetics* / Q000378:metabolism; D016022:Case-Control Studies; D002648:Child; D002675:Child, Preschool; D018450:Disease Progression; D005260:Female; D005787:Gene Frequency; D005820:Genetic Testing; D006579:Heterozygote; D006720:Homozygote; D006801:Humans; D011695:IgA Vasculitis / Q000150:complications / Q000201:enzymology / Q000235:genetics* / Q000473:pathology; D008297:Male; D009393:Nephritis / Q000201:enzymology / Q000235:genetics* / Q000473:pathology; D016017:Odds Ratio; D016366:Open Reading Frames; D010641:Phenotype; D011110:Polymorphism, Genetic; D011507:Proteinuria / Q000201:enzymology / Q000235:genetics; D018570:Risk Assessment; D012307:Risk Factors; D014421:Turkey
chemical_list: D043303:Aryldialkylphosphatase; C468406:PON1 protein, human