Dataset Information

Prenatal hypocalvaria after prolonged intrauterine exposure to angiotensin II receptor antagonists.

ABSTRACT: We report a case of prenatal exposure to angiotensin II receptor antagonists (ARA II) from the beginning of pregnancy in a patient with a hypokinetic dilated cardiomyopathy. This case report emphasizes the fetal renal impact of prolonged intrauterine exposure to renin-angiotensin system (RAS) blockers, and highlights that this exposure can cause severe prenatal hypocalvaria. This delayed ossification can be reversible after birth, but the presence of anhydramnios indicates an early and irreversible block of RAS blockers in the fetus that is responsible for fetal kidney development abnormalities. This association carries a high risk of neonatal death. Prolonged exposure to ARA II or other RAS blockers remains prohibited throughout pregnancy.

SUBMITTER: Lallemant M

PROVIDER: S-EPMC6243420 | biostudies-literature | 2018 Oct-Dec

REPOSITORIES: biostudies-literature

ACCESS DATA

Publications

Prenatal hypocalvaria after prolonged intrauterine exposure to angiotensin II receptor antagonists.

Lallemant Marine M Prévost Sarah S Nobili François F Riethmuller Didier D Ramanah Rajeev R Seronde Marie-France MF Mottet Nicolas N

Journal of the renin-angiotensin-aldosterone system : JRAAS 20181001 4

We report a case of prenatal exposure to angiotensin II receptor antagonists (ARA II) from the beginning of pregnancy in a patient with a hypokinetic dilated cardiomyopathy. This case report emphasizes the fetal renal impact of prolonged intrauterine exposure to renin-angiotensin system (RAS) blockers, and highlights that this exposure can cause severe prenatal hypocalvaria. This delayed ossification can be reversible after birth, but the presence of anhydramnios indicates an early and irreversi ...[more]

PMID: 30394825

Similar Datasets

Project description:BackgroundImpaired in utero fetal growth trajectory may have long term health consequences of the newborns and increase risk of adulthood metabolic diseases. Prenatal exposure to air pollution has been linked to fetal development restriction; however, the impact of exposure to ambient air pollutants on the entire course of intrauterine fetal development has not been comprehensively investigated.MethodsDuring 2015-2018, two cohorts of mother-infant dyads (N = 678 and 227) were recruited in Shanghai China, from which three categories of data were systematically collected: (1) daily exposure to six air pollutants during pregnancy, (2) fetal biometry in the 2nd (gestational week 24, [GW24]) and 3rd trimester (GW36), and (3) neonatal outcomes at birth. We investigated the impact of prenatal exposure to air pollutant mixture on the trajectory of fetal development during the course of gestation, adjusting for a broad set of potential confounds.ResultsPrenatal exposure to PM2.5, PM10, SO2 and O3 significantly reduced fetal biometry at GW24, where SO2 had the most potent effect. For every 10 μg/m3 increment increase of daily SO2 exposure during the 1st trimester shortened femur length by 2.20 mm (p = 6.7E-21) translating to 5.3% reduction from the average of the study cohort. Prenatal air pollution exposure also decreased fetal biometry at GW36 with attenuated effect size. Comparing to the lowest exposed quartile, fetus in the highest exposed quartile had 6.3% (p = 3.5E-5) and 2.1% (p = 2.4E-3) lower estimated intrauterine weight in GW24 and GW36, respectively; however, no difference in birth weight was observed, indicating a rapid catch-up growth in the 3rd trimester.ConclusionsTo our knowledge, for the first time, we demonstrated the impact of prenatal exposure to ambient air pollutants on the course of intrauterine fetal development. The altered growth trajectory and rapid catch-up growth in associated with high prenatal exposure may lead to long-term predisposition for adulthood metabolic disorders.

Dataset Information

Prenatal hypocalvaria after prolonged intrauterine exposure to angiotensin II receptor antagonists.

Publications

Prenatal hypocalvaria after prolonged intrauterine exposure to angiotensin II receptor antagonists.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets