Background. Imbalanced pro- and anti-inflammatory systems can unfavourably condition carrying of pregnancy and provoke gestation complications, such as premature rupture of membranes.Objectives. Assessing the contribution of SNP variants -137G>C (rs187238), -607G>T (rs1946518) and -656A>C (rs5744228) of the IL-18 gene promoter to the incidence of extremely preterm premature rupture of membranes.Methods. A case-control study enrolled 120 pregnant women managed at the Perinatal Centre. The women were divided in two cohorts. The study cohort comprised 80 women with premature rupture of membranes at 22–27 weeks 6 days’ gestation hospitalised in a high-risk pregnancy unit, a control cohort consisted of 40 women with physiological pregnancy at 22–27 weeks 6 days’ gestation following outpatient counselling. The cohorts had comparable obstetric and gynaecological histories. The study exclusion criteria were: multiple gestation, foetal chromosomal anomalies, congenital foetal malformations, pregnancy due to assisted reproduction. Genotyping was performed at positions -137G>C, -607G>T and -656A>C of the IL-18 gene promoter with determining a peripheral blood IL-18 level in cohorts.Results. The premature rupture of membranes cohort had a statistically higher serum interleukin-18 concentration compared to control (p = 0.001). Genotyping of the IL-18 gene promoter revealed a statistically higher rate of homozygous -137G>C mutation (CC genotype) in the premature rupture of membranes cohort at 22–27 weeks 6 days’ term (p <0.001), 67 vs. 27% in control.Conclusion. A homozygous IL-18 -137G>C polymorphic variant associated with elevated blood IL-18 levels is statistically more common in pregnant women having premature rupture of membranes at 22–27 weeks 6 days’ gestation.
Correction to: Risk factors of premature rupture of membranes in public hospitals at Mekele city, Tigray, a case control study
