Research of past decades has shown that pregnancy miscarriage (PM) and placental insufficiency (PI) underlie severe obstetric pathologies that result in complications of fetal development. The occurrence of PI developed during previous PMs varied from 47.6 to 77.3%. Pregnancy miscarriage can be considered to be the clinical manifestation of PI, which is a common complication in women with a previous history of PM. Endothelial dysfunction in the mother and in the fetoplacental complex are basic causes of PI. The angiotensin-converting enzyme (ACE) plays a key role in maintenance of proper balance between vasoconstriction and vasodilatation of blood vessels, and thus, in blood pressure regulation. DNA samples were genotyped for insertion/deletion (I/D) polymorphism of the ACE gene by polymerase chain reaction (PCR) assay. This study shows that the frequency of allele I of the ACE gene in DNA samples from placentae of the women with PM and PI (group 4) is twice as high than in the placentae of women with a PM history but without PI in the current pregnancy (group 3) (64.6 and 30.4%, respectively, p <0.001). Odds ratio (OR) analyses showed that the D/D genotype in placentae increases by 3-fold the risk of PI in women negative for PM history. The presence of the I/I genotype in patients positive for PM history increases the risk of PI 2.6-fold. It is concluded that the D/D genotype in placentae correlates with increased risk of PI in women negative for PM history, whereas the I/I genotype is a risk factor for PI in patients positive for PM history.

Key words: Pregnancy miscarriage (PM); Placental insufficiency (PI); ACE gene; Angiotensin-converting enzyme (ACE)