The Angiotensin-Converting Enzyme Gene Polymorphism is Associated with Pregnancy Miscarriage and Placental Insufficiency

Abstract

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 mis carriage 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 vaso constriction and vasodilatation of blood vessels, and thus, in blood pressure regulation. DNA samples were geno typed 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.

Acetylcholinesterase gene polymorphism and recurrent pregnancy loss

“…If the I allele is found to be homozygous it could decrease the concentration of ACHE and hence decrease the rate of bradykinin inactivation in the placenta. This is crucial for vessel permeability and modulation of inflammatory reaction, thus provoking premature pregnancy loss [6]. On the other hand, the DD genotype increases acetylcholinesterase plasma concentration (more angiotensin I is converted into angiotensin II) and inactivation of bradykinin, and plays a key role in the origin and progression of endothelial dysfunction and vasoconstriction [2,7].…”