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Biomedical subjects

G G Briggs

Publications and source records attributed to G G Briggs.

24 records · Page 2Linked to original sources
PubMedDate not supplied

Medication use during the perinatal period.

OBJECTIVE: To briefly describe the drug therapy administered during the perinatal period of pregnancy for common maternal and fetal complications, and to identify those agents that should not be used for these conditions. DATA SOURCES: References were obtained from an ongoing literature search of peer-reviewed obstetric and gynecologic journals and other selected medical and pharmacy journals available in the English language. Primary search vehicle was a weekly review of the tables of contents of nearly 1,300 medical journals provided by Reference Update (Institute of Scientific Information, Philadelphia). MEDLINE searches were also conducted using key terms for each subtopic. STUDY SELECTION: Specific references were selected for each topic based on the adequacy of their study design, patient population, and a recent publication date. Reviews were used if a large number of primary references would have been required to adequately describe the topic. DATA EXTRACTION: Most references reflected the current opinions expressed in the Educational (Technical) Bulletin and Committee Opinion series published by the American College of Obstetricians and Gynecologists. Recent, well-conducted studies that arrived at different conclusions were also included. DATA SYNTHESIS: Data obtained from each reference reflected the conclusions of the authors based on their research or an analysis of the research on others on the appropriate use of the drug(s) for the specific condition being treated. CONCLUSION: Drug therapy during the perinatal period is frequently required and can be beneficial for the mother, fetus, and newborn. Many complications previously associated with severe morbidity and mortality, such as infections, premature rupture of membranes, preterm labor, hypertension, maternal pain during labor, and postpartum hemorrhage, are now controlled with appropriate pharmacologic therapy. All health professionals who provide services to pregnant women should be knowledgeable in this drug therapy.

Adult↗
PubMedDate not supplied

Fatal fetal outcome with the combined use of valsartan and atenolol.

OBJECTIVE: To report a case of anhydramnios, pulmonary hypoplasia, very small placenta, and fetal death in a pregnancy complicated by chronic hypertension 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 hypertension and diet-controlled type 2 diabetes mellitus was treated with valsartan and atenolol until pregnancy was diagnosed at 24 weeks' gestation. An ultrasound examination revealed normal fetal growth and anatomy but anhydramnios (amniotic fluid index 0). Valsartan was discontinued, and amniotic fluid volume normalized within two weeks. Intrauterine fetal death was documented at 33 weeks' gestation. Labor was induced, with the delivery of a stillbom 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 antagonist (ARA), in human pregnancy has not been reported, but this class of agents would be expected to cause fetal toxicity similar to that observed with angiotensin-converting enzyme inhibitors. This toxicity includes reduced perfusion of the fetal kidneys, resulting in anuria, oligohydramnios, and subsequent 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 evidence for ARA-induced fetal toxicity. The pulmonary hypoplasia observed in the stillbom infant was a direct result of the severe oligohydramnios. The cause of fetal death nine weeks later is uncertain, but because the woman's chronic hypertension and diabetes were well controlled, we believe the primary cause was chronic placental insufficiency resulting from the previous combination of valsartan and atenolol.

Adult↗