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

Nalbantoglu S., TABEL Y. , Mir S., BERDELİ A.

CYTOKINE, cilt.62, ss.160-164, 2013 (SCI İndekslerine Giren Dergi) identifier identifier identifier

  • Cilt numarası: 62 Konu: 1
  • Basım Tarihi: 2013
  • Doi Numarası: 10.1016/j.cyto.2013.02.024
  • Dergi Adı: CYTOKINE
  • Sayfa Sayıları: ss.160-164


Henoch-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.