A 38-year-old woman, gravida 2 para 1, at 28 weeks gestation comes to the office for a routine prenatal visit. The patient has had no abdominal pain, vaginal bleeding, or leakage of fluid. She reports active fetal movement. The patient has been on antiretroviral therapy since being diagnosed with HIV 3 years ago, and her last viral load was undetectable. She had negative syphilis and hepatitis C screening at her initial prenatal visit. Blood pressure is 122/74 mm Hg, and pulse is 86/min. The abdomen is nontender, and fundal height is 28 cm. Fetal heart tones are 140/min. The rest of the examination is normal. Laboratory results are as follows:
| Complete blood count | |
| Hemoglobin | 10 g/dL |
| Platelets | 180,000/mm3 |
| Leukocytes | 4,100/mm3 |
| Liver function studies | |
| Alkaline phosphatase | 220 U/L (normal: 38-229 in 3rd trimester) |
| Aspartate aminotransferase (SGOT) | 300 U/L |
| Alanine aminotransferase (SGPT) | 254 U/L |
Ultrasound of the right upper quadrant shows no stones or dilation of the common bile duct. Which of the following is the best next step in management of this patient?
The differential for abnormal liver enzymes in pregnant patients is broad and includes diseases specific to pregnancy (eg, preeclampsia, acute fatty liver of pregnancy) and those that affect the general population (eg, viral hepatitis, autoimmune hepatitis). This patient has a hepatocellular pattern of liver injury (ie, elevated transaminases, normal alkaline phosphatase). In association with the normal vital signs and otherwise normal laboratory values, this presentation is most concerning for viral hepatitis, likely hepatitis C.
Viral hepatitis should remain on the differential for any patient with hepatocellular liver injury, even in those with negative screening tests at their initial prenatal visit because the disease can be contracted at any time and antibody testing may not detect those with very recent exposure. Patients with a history of other blood-borne or sexually transmitted disease (eg, HIV) may be at elevated risk. Most patients are asymptomatic, although acute disease can cause pain in the right upper quadrant, nausea, and jaundice. Acute hepatitis often causes markedly elevated aminotransferases (>10-20× the upper limit of normal); however, most patients develop chronic hepatitis C in the following weeks to months and have less significant aminotransferase elevations. A viral hepatitis panel confirms the diagnosis.
(Choice A) A 24-hour urine protein collection evaluates for preeclampsia, which can occur in the third trimester and cause elevated aminotransferases. However, this patient does not have hypertension, making this diagnosis unlikely.
(Choices B and D) Antinuclear antibody is elevated in autoimmune hepatitis, whereas serum ceruloplasmin is used to evaluate for Wilson disease. Although both diseases can also cause a hepatocellular pattern of injury, they are much less common than viral hepatitis. Furthermore, Wilson disease typically causes extrahepatic manifestations (eg, Kayser-Fleischer rings, neuropsychiatric symptoms). However, an expanded workup (including testing for these diseases) can be considered if the viral hepatitis panel is negative.
(Choice C) Immediate delivery is a management option for acute fatty liver of pregnancy, which can present in the third trimester with elevated aminotransferases. However, patients typically are symptomatic (eg, nausea, malaise, right upper quadrant pain) and have additional laboratory abnormalities, including leukocytosis and thrombocytopenia, making this diagnosis unlikely.
Educational objective:
Viral hepatitis should be considered in pregnant patients with a hepatocellular pattern of liver injury (eg, elevated aminotransferases), even in those with negative screening tests at initial prenatal visits.