Key result
Maternal homozygosity for the angiotensinogen T allele was associated with significantly elevated mean systolic and diastolic blood pressures in the third trimester (118.4/71.5 vs 116.9/70.4 mmHg; P<0.05).
Why the study?
Are maternal angiotensinogen M235T and ACE insertion/deletion polymorphisms associated with hypertensive disorders in pregnancy?
Observational (n=1,068)
No
Are maternal angiotensinogen M235T and ACE insertion/deletion polymorphisms associated with hypertensive disorders in pregnancy?
The maternal angiotensinogen M235T polymorphism is associated with increased blood pressure during the third trimester of pregnancy, suggesting a genetic contribution to gestational hypertension.
Answers are grounded in this paper and cite their sources.
Should not prompt genetic testing in pregnancy; leaves open predictive value for hypertensive disorders.
OBJECTIVE: To test the hypothesis that genetically determined alterations of the renin-angiotensin system are associated with hypertensive disorders in pregnancy. METHODS: A genetic association study was conducted at the obstetrics department of the Charité university hospital, Berlin, Germany. A total of 1068 Caucasian women were consecutively included after delivery and genotyped for the angiotensinogen M235T polymorphism and the angiotensin-converting enzyme (ACE) insertion/deletion polymorphism. RESULTS: Women homozygous for the angiotensinogen T allele have significantly elevated mean systolic and diastolic blood pressures in the third trimester (118.4 +/- 1.1/71.5 +/- 0.7 versus 116.9 +/- 0.3/70.4 +/- 0.2 mmHg, n = 128 versus 940; P < 0.05). This finding is especially pronounced in the subgroup of primigravid women. The ACE polymorphism is not associated with blood pressure during pregnancy. None of the polymorphisms is associated with urinary protein excretion or oedema during pregnancy. Maternal polymorphisms do not influence fetal growth and birth weight. There is, however, an interesting trend towards an increased incidence of circulatory system malformations in newborns carrying alleles that are known to be associated with decreased intrinsic renin-angiotensin system activity. CONCLUSION: We demonstrate for the first time in a large Caucasian population that a common maternal polymorphism of the angiotensinogen gene is related to a blood pressure increase during pregnancy. The angiotensinogen M235T polymorphism might contribute to the multifactorial pathogenesis of gestational hypertension and pre-eclampsia.
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Pfab et al. (2007) conducted an observational in Pregnancy (n=1,068). Angiotensinogen M235T polymorphism (homozygous T allele) vs. Non-homozygous T allele carriers was evaluated on Mean systolic and diastolic blood pressures in the third trimester (p=< 0.05). Maternal homozygosity for the angiotensinogen T allele was associated with significantly elevated mean systolic and diastolic blood pressures in the third trimester (118.4/71.5 vs 116.9/70.4 mmHg; P<0.05).
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