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Aplastic anemia (AA) poses a significant threat to maternal and fetal health throughout the perinatal period. Diagnosis is based on complete blood count (CBC) and bone marrow biopsy with treatment varying based on severity of disease. This report highlights a case of AA incidentally identified by the third trimester CBC drawn in the outpatient office. Patient was referred for inpatient management to mobilize a multidisciplinary team of healthcare professionals including obstetricians, hematologists, and anesthesiologists to optimize maternal and fetal outcome. The patient received blood and platelet transfusions prior to delivering a healthy liveborn infant by cesarean section. This case highlights the importance for routine third trimester CBC screening to identify potential complications and decrease maternal and fetal morbidity and mortality.

Doxorubicin (DOX) is an anthracycline anticancer drug which unfortunately causes severe dose‐dependent dilated cardiomyopathy in some patients through poorly defined mechanisms. AMP‐activated protein kinase (AMPK) is an important cellular energy regulator which plays a protective role in conditions such as ischemic heart disease and diabetic cardiomyopathy when activated. AMPK activation is believed to be similarly protective against DOX‐induced cardiomyopathy. However, there has been little to no investigation into the role of the different subunits of AMPK or their individual isoforms in the cellular response to DOX. Previous studies have demonstrated subunit‐ and isoform‐specific differences in effect with other drugs that act on or via AMPK, suggesting the possibility that certain AMPK isoforms may either mediate or attenuate the cardiotoxic effects of DOX. In the present study, we investigated the effects of knocking down isoforms of the catalytic α subunit of AMPK on DOX‐induced cytotoxicity. H9c2 cardioblast cells were treated with siRNA to knock down the expression of α1, α2, or both and then exposed to DOX. Cell death was determined by propidium iodide (PI) staining that indicates necrosis and Western blot analysis of the expression levels of cleaved caspase 3 that signals apoptosis. Concurrent knockdown of both α1 and α2 isoforms dramatically reduced DOX‐induced H9c2 cell death as shown by the decreased number of PI positive cells and the amount of cleaved caspase 3. These data indicate that the AMPK signaling pathway may have contributed to DOX cardiotoxicity, in stark contrast to the predominant belief that AMPK is cardioprotective. More interestingly, whereas α1 knockdown decreased DOX‐induced cell death to the same degree as knocking down both α1 and α2 isoforms, α2 knockdown alone had minimal effect on DOX cytotoxicity. These results clearly demonstrate the isoform‐dependent differential effects of AMPK α on H9c2 cell response to DOX treatment. Further studies are warranted to elucidate the relative importance of AMPK α, β, and γ subunits and their isoforms in either mediating or attenuating DOX cardiotoxicity.

INTRODUCTION: In 2017, the American College of Cardiology (ACC) and the American Heart Association (AHA) redefined blood pressure (BP) categories in non-pregnant adults: Normal (140/90). In pregnancy, patients with BP>140/90 before 20 weeks gestation are considered to have chronic hypertension, correlating to S2. Unlike S2, pregnant women in Elevated and S1 cohorts receive no increased antepartum surveillance. The purpose of this study is to compare pregnancy outcomes between normal, elevated, and S1 cohorts to ascertain risk for hypertensive disorders of pregnancy (HDP), including gestational hypertension and pre-eclampsia. METHODS: This is a retrospective review of women who received prenatal care and delivered at our institution. Patients were classified according to the new guidelines based on BP readings prior to 20 weeks gestation. S2 patients were excluded, as these patients are already known to have increased risk for HDP. The primary outcome measure is incidence of HDP. IRB approval was obtained. RESULTS: 342 patients were included: normal (n=177), elevated (n=73), and S1 (n=76). Maternal characteristics were similar (P>.05). The incidence of HDP for patients with Elevated BP is 9.59% (P=.048) and S1 is 13.83% (P=.002), compared to normal (3.43%). The incidence of small for gestational age, preterm delivery, and NICU admissions were similar (P>.05). CONCLUSION: Women with S1 per the new guidelines are at increased risk for HDP of pregnancy. Further studies are warranted to determine if S1 patients will benefit from antepartum surveillance and prophylactic low dose aspirin.