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Association of the Missense Glu298Asp Variant of the Endothelial Nitric Oxide Syntahse Gene With Severe Preeclampsia

Departments of Ostetrics and Gynecology and Cardiovascular Medicine, Kumamoto University School of Medicine, Kumamoto; and Department of Medicine and Clinical Scinece, Kyoto University Graduate School of Medicine, Kyoto, Japan; yoshimur{at}kaju.medic.kumamoto-u.ac.jp

Michihiro Yoshimura, MD

Ai Tabatal, MD

Yukio Shimasaki, MD

Masafumi Nakayama, MD

Yoshihiro Miyamoto, MD

Yoshihiko Saito, MD

Kazuwa Nakao, MD

Hirofumi Yasue, MD

Hitoshi Okamura, MD

Departments of Ostetrics and Gynecology and Cardiovascular Medicine, Kumamoto University School of Medicine, Kumamoto; and Department of Medicine and Clinical Scinece, Kyoto University Graduate School of Medicine, Kyoto, Japan

Objective: A large number of studies suggest that abnormalities in nitric oxide (NO) synthesis may contribute to the development of preelampsia. We recently identified a variant within exon 7 of the endothelial NO synthase (eNOS) gene: G to T conversion at nucleotide position 894 resulting in replacement of glutamic acid with aspartic acid at codon 298 (Glu298Asp). We analyzed the association between the Glu298Asp eNOS gene variant and preeclampsia.

Study design: The study included 152 preeclampsia patients (35 mild, 80 severe, and 37 superimposed) and 170 control subjects. Screeing for the Glu298Asp eNOS gene variant was carried out by analysis of polymerase chain reaction-restriction fragment length polymorphism.

Results: The frequency of the Glu298Asp variant was significantly higher in the severe preclampsia group (28.8%) than in the control (14.1%; p < .01), superimposed preeclampsia (8.1%; p < .01), and mild preeclampsia (11.4%; p < .01) groups.

Conclusions: We conclude that the presence of the Glu298Asp eNOS gene could be a marker of increased risk of developing severe preeclampsia.

Key Words: Nitric oxide • endothelial nitric oxide synthase • preeclampsia • genetics • polymorphism

Journal of the Society for Gynecologic Investigation, Vol. 7, No. 4, 238-241 (2000)
DOI: 10.1177/107155760000700408


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