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

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★ Association between −173 G/C SNP of MIF gene and HSP risk is suggested. ★ PCR-RFLP method and sytatistical risk assessment are used. ★ No association is obtained between GC+CC genotype/C allele and HSP development. ★ Genetic association between the MIF gene and HSP pathogenesis is not detected. ★ Search for possible candidate genes in HSP in various ethnicities is required.

Henoch–Schönlein 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–Schönlein 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.

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