Angiotensin converting enzyme insertion/deletion polymorphism in preterm labor

Preterm labour is labour resulting birth before 37 completed weeks of gestational age. Preterm birth is the single largest cause of perinatal mortality and morbidity in non-anamalous infants in developed nations. It is likely the result of interactions between specific genes and the maternal and fetal factors. Angiotensin converting enzyme (ACE) is a zinc metallopeptidase widely distributed on the surface of various cells. It plays an essential role in production of angiotensin II. The wide distribution and multifunctional properties of this peptide suggest that ACE would be involved in various pathophysiological conditions. The discovery that ACE levels are under genetic control ushered in a new era of investigation; most studies focused on an insertion/deletion (/D) polymorphism in intron 16 of the ACE gene as a marker for a functional polymorphism. ACE has been found in many tissues including human placenta and uterus. Plasma ACE activity has been observed to increase in pregnancy. Myometrium from labouring women has been observed to be more sensitive to the contractile effects of A-II than myometrium from non laboring women. Here we speculated that changes in ACE activity due to /D polymorphism might be a factor related to preterm uterine contractions in preterm labor patients. We examined the role of ACE /D polymorphism in preterm labor in a group of Turkish subjects. Seventy four patients with preterm labor and 86 control subjects were analysed by polymerase chain reaction (PCR). A significant association was not found between ACE /D polymorphism and preterm labor. Thus, the /D polymorphism of the ACE gene may not have a role in molecular pathogenesis of preterm labor patients.