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

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... ere 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.