Association of Angiotensin-Converting Enzyme Intron 16 Insertion/Deletion and Angiotensin II Type 1 Receptor A1166C Gene Polymorphisms with Preeclampsia in South East of Iran

Saeedeh Salimi,Minoo Yaghmaei,Mojgan Mokhtari,Mohammad Jamshidi,Anoosh Naghavi

doi:10.1155/2011/941515

Abstract

Some evidence suggests that a variety of genetic factors contributed in pathogenesis of the preeclampsia. The aim of this study was to assess the association between the angiotensin-converting enzyme (ACE) I/D and angiotensin II type1 receptor A1166C polymorphisms with preeclampsia. This study was performed in 125 preeclamptic pregnant women and 132 controls. The I/D Polymorphism of the ACE gene was assessed by polymerase chain reaction and the A1166C Polymorphism of the AT1R gene was determined by restriction fragment length polymorphism. The genotype and allele frequencies of I/D polymorphism differed between two groups. The risk of preeclampsia was 3.2-fold in pregnant women with D allele (OR, 3.2 [95% CI, 1.1 to 3.8]; P = 0.01). The distribution of the AT1R gene A1166C polymorphism was similar in affected and control groups. Our results supported that presence of the I/D polymorphism of ACE gene is a marker for the increased risk of preeclampsia.

Highlights

Preeclampsia is a potentially serious condition of pregnancy that covers almost 10% of pregnancies in the developing countries
The I/D Polymorphism of the angiotensin-converting enzyme (ACE) gene was assessed by polymerase chain reaction and the A1166C Polymorphism of the angiotensin I variant (II) type-1 receptor (AT1R) gene was determined by restriction fragment length polymorphism
Preeclampsia is a multifactorial disorder that results from the interaction of multiple environmental and genetic factors

Summary

Introduction

Preeclampsia is a potentially serious condition of pregnancy that covers almost 10% of pregnancies in the developing countries. It has a severe morbidity and mortality risk for both mother and child [1]. The exact etiology of this disease is still unknown but several pathophysiological mechanisms have been suggested for preeclampsia. These include endothelial dysfunction, inflammatory pathway, oxidative stress, activation of thrombosis, and the renin-angiotensin system [2]. Several studies have tried to demonstrate or refute the role of rennin angiotensin system genes as candidates for the development of preeclampsia. The circulating renin-angiotensin system (RAS) is an important pathway that regulates blood pressure and electrolyte balance [1]

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