title: Association between RAS gene polymorphisms (ACE I/D, AGT M235T) and Henoch-Schönlein purpura in a Turkish population.
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% T vs. M: 1.065, 95% CI: 0.7326-2.6391) and T allele (OR: 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.
authors.affiliation: Molecular Medicine Laboratory, Children's Hospital, Faculty of Medicine, Ege University, Bornova, Izmir, Turkey. nalbantoglusinem@gmail.com
authors.forename: Sinem
authors.initials: S
authors.lastname: Nalbantoglu
authors.forename: Yılmaz
authors.initials: Y
authors.lastname: Tabel
authors.forename: Sevgi
authors.initials: S
authors.lastname: Mir
authors.forename: Erkin
authors.initials: E
authors.lastname: Serdaroğlu
authors.forename: Afig
authors.initials: A
authors.lastname: Berdeli
mesh_terms: D000293:Adolescent; D000328:Adult; D019943:Amino Acid Substitution; D000808:Angiotensinogen / Q000235:genetics*; D016022:Case-Control Studies; D002648:Child; D002675:Child, Preschool; D004252:DNA Mutational Analysis; D005260:Female; D005787:Gene Frequency; D056726:Genetic Association Studies; D020022:Genetic Predisposition to Disease; D006801:Humans; D054643:INDEL Mutation; D011695:IgA Vasculitis / Q000201:enzymology / Q000235:genetics*; D008297:Male; D008875:Middle Aged; D007703:Peptidyl-Dipeptidase A / Q000235:genetics*; D020641:Polymorphism, Single Nucleotide; D012084:Renin-Angiotensin System / Q000235:genetics*; D012307:Risk Factors; D014421:Turkey; D055815:Young Adult
chemical_list: C534931:AGT protein, human; D000808:Angiotensinogen; C488034:ACE protein, human; D007703:Peptidyl-Dipeptidase A