Case Presentation: 25-year-old pregnant female was transferred to a tertiary care center at 15 weeks gestation for further work-up of abnormal LFTs. Her pre-pregnancy medical history was limited, at 8 weeks gestation she suffered a large MCA stroke, and pregnancy had been complicated by hyperemesis gravidarum (HG). Hypercoagulability workup revealed positive antiphospholipid antibodies and was otherwise negative. While recovering from her stroke in an inpatient rehabilitation center, she was found to have elevated transaminases (AST 278, ALT 748), with normal alkaline phosphatase and bilirubin 2.1. She reported intractable nausea with greater than 20 episodes of emesis per day and a 40 pound weight loss. She denied abdominal pain, diarrhea, recent fever, chills, joint pains or rashes. She had no recent unusual exposures, recent illnesses, or sick contacts. Medications included only enoxaparin, prenatal vitamins, phenergan, and ondansetron.Her vital signs were normal. She had normal bowel sounds, mild tenderness to palpation in the right upper quadrant without guarding or rebound. She also had residual muscle weakness and hyperreflexia in her left extremities from her recent stroke. Her LFTs peaked on the day after transfer, with AST 363, ALT 1053, and total bilirubin 2.6. Her coagulation studies were normal (INR 1.0) and abdominal US with doppler was unremarkable. An extensive workup done for viral hepatitis, auto-immune hepatitis, Wilson’s Disease, hemochromatosis, and A1AT deficiency were all negative. Maternal Fetal Medicine was consulted regarding her hyperemesis, and they felt that her lab abnormalities could all be from her severe hyperemesis. Patient was counseled on her options and elected to terminate pregnancy, which resulted in nearly immediate cessation of vomiting and her liver enzymes normalized within 3 days.
Discussion: Hyperemesis gravidarum presents as a spectrum of nausea and vomiting in early pregnancy that is typically self-limited with resolution by the 20th week of gestation. It has been associated with elevation in liver enzymes, most often due to cholestasis of pregnancy with mild elevations in transaminases (1000 U /L) posing challenges to diagnosis within a timely manner. Hospitalists often care for pregnant women, particularly early in pregnancy. It is important to recognize that hyperemesis gravidarum should remain in the differential diagnosis for a pregnant patient presenting with severe transaminitis in a hepatocellular pattern. Failure to recognize this as a likely cause can lead to an extensive workup, as well as a delay in diagnosis. A literature review on marked transaminitis during pregnancy reveals few cases with this level of liver enzyme elevation, and even fewer are available to demonstrate the rapid resolution of this transaminitis.
Conclusions: Recognition that marked transaminitis may be due to hyperemesis gravidarum will prevent delays in treatment and diagnosis, as well as decrease the cost of extensive workup.