Abstract
Preeclampsia (PE) is the most serious complication of pregnancy that causes maternal and fetal morbidity and mortality. Although the exact pathophysiology of PE is unknown, a large number of studies have shown that abnormalities in nitric oxide (NO) synthesis may contribute to the development of this disorder. There are some evidences that polymorphisms of the endothelial nitric oxide synthase (eNOS) gene affect NO production and have been associated with hypertension and PE in some populations. Therefore the aim of this study was to assess the relation of the Glu298Asp eNOS polymorphism and PE in an Iranian population. We compared the frequency of the Glu298Asp polymorphism in 147 women with PE and 137 healthy pregnant control subjects by polymerase chain reaction- restriction fragment length polymorphism (PCR-RFLP) method. The frequencies of Glu298Asp genotypes were significantly different between PE women and controls (p < 0.001). The frequency of Asp allele was 0.32 in PE patients and 0.20 in controls and was significantly different (p < 0.001). The risk of PE was 2.4 fold in pregnant women with Asp allele. In conclusion, the Asp allele could be a risk factor for PE in South East of Iran. Key words: Nitric oxide synthase, polymorphism, preeclampsia, pregnancy.
Highlights
Preeclampsia (PE) is one of the most severe problems of pregnancy and has a familial predisposition
The exact pathophysiology of PE is unknown, a large number of studies have shown that abnormalities in nitric oxide (NO) synthesis may contribute to the development of this disorder
The endothelial nitric oxide synthase (eNOS) gene has a common polymorphism at position 298 (Glu298Asp) which has been associated with both altered NO production (Wang et al, 1997) and with vascular disorders including hypertension (Benjafield and Morris, 1999), myocardial infarction
Summary
Preeclampsia (PE) is one of the most severe problems of pregnancy and has a familial predisposition. Genetic factors and mutilation of nitric oxide (NO)–mediated vasodilation appear to have important roles in progress of PE (Salonen et al, 2000; Broughton et al, 2001). The role of endothelial nitric oxide synthase (eNOS) gene as a candidate gene for the development of PE has been investigated by many studies (Arngrimsson et al, 1997; Lade et al, 1999; Yoshimura et al, 2000; Tempfer et al, 2001). Some evidences demonstrated familial pregnancy-induced hypertension associated with a locus in the region of chromosome 7q36, which encodes the eNOS gene (Lade et al, 1999; Lewis et al, 1999). The eNOS gene has a common polymorphism at position 298 (Glu298Asp) which has been associated with both altered NO production (Wang et al, 1997) and with vascular disorders including hypertension (Benjafield and Morris, 1999), myocardial infarction
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