Fatal fetal outcome with the combined use of valsartan and atenolol

Citation
Gg. Briggs et Mp. Nageotte, Fatal fetal outcome with the combined use of valsartan and atenolol, ANN PHARMAC, 35(7-8), 2001, pp. 859-861
Citations number
15
Categorie Soggetti
Pharmacology
Journal title
ANNALS OF PHARMACOTHERAPY
ISSN journal
10600280 → ACNP
Volume
35
Issue
7-8
Year of publication
2001
Pages
859 - 861
Database
ISI
SICI code
1060-0280(200107/08)35:7-8<859:FFOWTC>2.0.ZU;2-P
Abstract
OBJECTIVE: To report a case of anhydramnios, pulmonary hypoplasia, very sma ll placenta, and fetal death in a pregnancy omplicated by chronic hypertens ion and diabetes mellitus that had been treated through the first 24 weeks of gestation with valsartan and atenolol. CASE SUMMARY: A 40-year-old Hispanic woman with well-controlled chronic hyp ertension and diet-controlled type 2 diabetes mellitus was treated with val sartan and atenolol until pregnancy was diagnosed at 24 weeks' gestation. A n ultrasound examination revealed normal fetal growth and anatomy but anhyd ramnios (amniotic fluid index 0). Valsartan was discontinued, and amniotic fluid volume normalized within two weeks. Intrauterine fetal death was docu mented at 33 weeks' gestation. Labor was induced, with the delivery of a st illborn female fetus with small, hypoplastic lungs (weight 41% of expected) and an extremely small, 148-g placenta (weight 48% of the 10th percentile for gestational age). DISCUSSION: The use of valsartan, a selective angiotensin II receptor antag onist (ARA), in human pregnancy has not been reported, but this class of ag ents would be expected to cause fetal toxicity similar to that observed wit h angiotensin-converting enzyme inhibitors. This toxicity includes reduced perfusion of the fetal kidneys, resulting in anuria, oligohydramnios, and s ubsequent pulmonary hypoplasia. The small hypoplastic lungs and very small placenta were probably a consequence of valsartan and atenolol combination therapy. CONCLUSIONS: Resolution of anhydramnios after discontinuing valsartan is ev idence for ARA-induced fetal toxicity. The pulmonary hypoplasia observed in the stillborn infant was a direct result of the severe oligohydramnios. Th e cause of fetal death nine weeks later is uncertain, but because the woman 's chronic hypertension and diabetes were well controlled, we believe the p rimary cause was chronic placental insufficiency resulting from the previou s combination of valsartan and atenolol.