Association between RAS gene polymorphisms (ACE I/D, AGT M235T) and Henoch-Schonlein purpura in a Turkish population

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dc.authoridSerdaroglu, Erkin/0000-0002-6863-8866
dc.authoridSerdaroglu, Erkin/0000-0002-6863-8866
dc.authorwosidTabel, Yilmaz/AAF-9801-2020
dc.authorwosidSerdaroglu, Erkin/N-3838-2019
dc.authorwosidSerdaroglu, Erkin/E-9547-2016
dc.contributor.authorNalbantoglu, Sinem
dc.contributor.authorTabel, Yilmaz
dc.contributor.authorMir, Sevgi
dc.contributor.authorSerdaroglu, Erkin
dc.contributor.authorBerdeli, Afig
dc.date.accessioned2024-08-04T20:37:23Z
dc.date.available2024-08-04T20:37:23Z
dc.date.issued2013
dc.departmentİnönü Üniversitesien_US
dc.description.abstractHenoch-Schonlein 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.en_US
dc.identifier.doi10.1155/2013/624757
dc.identifier.endpage32en_US
dc.identifier.issn0278-0240
dc.identifier.issn1875-8630
dc.identifier.issue1en_US
dc.identifier.pmid23151617en_US
dc.identifier.scopus2-s2.0-84872288348en_US
dc.identifier.scopusqualityQ2en_US
dc.identifier.startpage23en_US
dc.identifier.urihttps://doi.org/10.1155/2013/624757
dc.identifier.urihttps://hdl.handle.net/11616/95921
dc.identifier.volume34en_US
dc.identifier.wosWOS:000312597200004en_US
dc.identifier.wosqualityQ2en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherHindawi Ltden_US
dc.relation.ispartofDisease Markersen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/openAccessen_US
dc.subjectHenoch-Schonlein purpura (HSP)en_US
dc.subjectACE I/Den_US
dc.subjectAGT M235Ten_US
dc.subjectSingle Nucleotide Polymorphism (SNP)en_US
dc.subjectorgan involvementsen_US
dc.subjectGenotype-phenotype correlationen_US
dc.titleAssociation between RAS gene polymorphisms (ACE I/D, AGT M235T) and Henoch-Schonlein purpura in a Turkish populationen_US
dc.typeArticleen_US

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