THE ANGIOTENSIN-CONVERTING ENZYME GENE POLYMORPHISM IS ASSOCIATED WITH PREGNANCY MISCARRIAGE AND PLACENTAL INSUFFICIENCY
Bespalova ON, Ivashchenko TE, Tarasenko OA, Demin GS, Ajlamazjan EK, Baranov VS*
*Corresponding Author: Professor Vladislav S. Baranov, Laboratory for Prenatal Diagnostics, Scientific Research Institute of Obstetrics and Gynecology D.O. Otta, Russian Academy of Medical Science, Mendeleev­skaya line 3, 199034 Saint Petersburg, Russia; Tel.: +7-812-328-0487; Fax: +7-812-328-0487; E-mail: Baranov@vb2475.spb.edu
page: 3

INTRODUCTION

Numerous studies have shown that pregnancy miscarriage (PM) and placental insufficiency (PI) underlie many kinds of severe obstetric pathology that result in complications of pregnancy and of fetal development. The occurrence of PI developed during previous PMs varied from 47.6 to 77.3% [1]. Pregnancy miscarriage can be considered to be the clinical manifestation of PI. Secondly, PI is a common complication in women with a former history of PM. Compensated and subcompensated forms of PI manifest as threatened spontaneous abortion or threatened premature birth, while decompensated PI may be complicated by early or late spontaneous abortion, delayed miscarriage and premature birth [2]. These clinical complications are considered to be forms of PM. Thus, PI and PM are closely interconnected, but they can also be treated as independent entities.

The etiology of PM and PI includes: hormonal insufficiency, abnormal vascularization of the uterus, endometrium lesions due to previous curettages, genital infantilism, detrimental inflammatory or vascular reactions and thrombophilic complications provoked by autoimmune processes. Consequently, PI in patients with PM is usually treated as a primary abnormality [3]. Placental insufficiency often occurs as a secondary consequence of uterine blood-flow abnormalities resulting from, for example, hypo- or hypertension, heart attack, partial detachment of the placenta or inflammatory reaction to genital infection in the mother [4,5]. Thus, abnormalities of placental blood circulation, including microcirculation failure that leads to defects of efficient metabolic exchange between maternal and fetal tissues, constitute the basic mechanism of PI etiology.

Recent clinical findings attribute a major role, in PI and in PM, to endothelial dysfunction in the mother, the fetoplacental complex and in umbilical cord arteries [6]. The angiotensin-converting enzyme (ACE) occupies a key position in maintenance of a proper balance between vasoconstriction and vasodilatation of blood vessels, and thus in blood pressure regulation. The enzyme converts angiotensin I into angiotensin II. Angiotensin II has vasoconstrictor properties, and consequently participates in regulation of vascular tone [7-10]. Changes in the concentration of angiotensin II may be very important in regulation of functions of the fetoplacental complex and of blood circulation in the placenta. Information on the association of the ACE gene polymorphisms and PM/PI is rather scanty [11,12]. The regulation of a vascular tone by ACE is mainly attributed to insertion/deletion (I/D) of a 287 bp Alu-repeat polymorphism in intron 16 of the ACE gene which affects expression of the ACE gene [6,13,14]. The presence of the D allele correlates with increase of ACE concentration in blood plasma. The I allele is functionally less active than the D allele [13,15]. The present study focuses on the analysis of allele and genotype frequencies of the I/D polymorphism of the ACE gene in placentae from parturient women with a history of PI and PM.




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