Lack of association between macrophage migration inhibitory factor gene promoter (-173 G/C) polymorphism and childhood Henoch-Schonlein purpura in Turkish patients

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dc.authorwosidTabel, Yilmaz/AAF-9801-2020
dc.contributor.authorNalbantoglu, Sinem
dc.contributor.authorTabel, Yilmaz
dc.contributor.authorMir, Sevgi
dc.contributor.authorBerdeli, Afig
dc.date.accessioned2024-08-04T20:37:32Z
dc.date.available2024-08-04T20:37:32Z
dc.date.issued2013
dc.departmentİnönü Üniversitesien_US
dc.description.abstractHenoch-Schonlein purpura (HSP) is a small-vessel vasculitis of autoimmune hypersensitivity with rash, arthritis, abdominal pain and renal involvements. Macrophage migration inhibitory factor (MIF) is a immunoregulatory proinflammatory cytokine, and a major mediator at the inflammatory sites. The pathogenesis of HSP has not been fully elucidated. Here we aimed to assess the influence of macrophage migration inhibitory factor gene (-173 G/C). polymorphism in the susceptibility and clinical expression of patients with Henoch-Schonlein purpura (HSP). HSP patients (n:139) and ethnically matched healthy controls (n:100) were genotyped by PCR-RFLP. Genotype analysis of both polymorphisms did not reveal a significant deviation from Hardy-Weinberg equilibrium in any group (p > 0.05). No significant difference was obtained in genotype distribution (p > 0.05) and allele frequencies (p > 0.05) between patients and controls. A statistically significant genotype-phenotype correlation was not obtained when HSP patients were stratified by the presence of certain systemic complications and the macrophage migration inhibitory factor gene (-173 G/C) polymorphism (p > 0.05). A significant risk was not observed in the subjects both with the GC + CC genotype (p = 0.06, OR: 0.5538, 95% CI: 0.2985-1.0274) and C allele (odds ratio: C vs. G: 1.799, 95% CI: 1.002-3.23, p = 0.05). Our findings suggest that MIF gene -173 G/C polymorphism is not associated with HSP in the present Turkish population. (C) 2013 Elsevier Ltd. All rights reserved.en_US
dc.identifier.doi10.1016/j.cyto.2013.02.024
dc.identifier.endpage164en_US
dc.identifier.issn1043-4666
dc.identifier.issn1096-0023
dc.identifier.issue1en_US
dc.identifier.pmid23523092en_US
dc.identifier.scopus2-s2.0-84875804718en_US
dc.identifier.scopusqualityQ2en_US
dc.identifier.startpage160en_US
dc.identifier.urihttps://doi.org/10.1016/j.cyto.2013.02.024
dc.identifier.urihttps://hdl.handle.net/11616/96004
dc.identifier.volume62en_US
dc.identifier.wosWOS:000317795000025en_US
dc.identifier.wosqualityQ2en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherAcademic Press Ltd- Elsevier Science Ltden_US
dc.relation.ispartofCytokineen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectHenoch-Schonlein purpura (HSP)en_US
dc.subjectMacrophage migration inhibitory factor (MIF)en_US
dc.subjectSingle nucleotide polymorphism (SNP)en_US
dc.subjectOrgan involvementsen_US
dc.subjectGenotype-phenotype correlationen_US
dc.titleLack of association between macrophage migration inhibitory factor gene promoter (-173 G/C) polymorphism and childhood Henoch-Schonlein purpura in Turkish patientsen_US
dc.typeArticleen_US

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