INTRODUCTION: Pregnancy-related liver disease is seen in up to 3% of all pregnancies. Pregnancy-related etiologies include hyperemesis gravidarum, pre-eclampsia, HELLP, intrahepatic cholestasis of pregnancy, and acute fatty liver of pregnancy (AFLP). Given the significant morbidity and mortality associated with these conditions, there is a need for early recognition. Here we present a unique case of pregnancy-related liver disease in an asymptomatic patient. Despite a thorough evaluation for liver and non-liver related causes, her lack of symptomatology and associated laboratory findings made establishing a definitive diagnosis difficult. CASE DESCRIPTION/METHODS: 30 year-old woman G1P0 at 29 weeks gestation with dichorionic triamniotic triplets presented with generalized weakness. Her past medical and surgical histories were otherwise non-contributory and her only medication included prenatal vitamins. The physical exam was unremarkable except for a gravid uterus. Throughout her hospital course, she remained normotensive. Admission labs were significant for an abnormal liver profile: AST 200 U/L, ALT 349 U/L, ALP 121 U/L, and total bilirubin 0.5 mg/dL, compared to a previous normal baseline. Complete blood count and renal function were normal. Abdominal ultrasound (US) showed increased liver echogenicity consistent with fatty liver disease. Additional work-up revealed a normal coagulation profile, fibrinogen, lactate dehydrogenase, and haptoglobin. Urinalysis was negative for proteinuria. Serologies for viral and autoimmune hepatitis were negative. Total bile acids were mildly elevated at 9.3 umol/L (normal < 6.8umol/L) and 24-hour urinary copper was normal. Though she remained asymptomatic, liver enzymes continued to uptrend. On day 16 she underwent urgent C-section due to rising liver enzymes and evidence of fetal distress. Liver enzymes continued to rise until POD1 before rapidly declining. DISCUSSION: This was a unique case of pregnancy-related liver disease of unknown etiology, but most consistent with an early manifestation of AFLP. We suspected AFLP based on the steatosis noted on US, however, since we could not check her children for LCHAD deficiency a definitive diagnosis could not be made. Surveillance US showing resolution of steatosis would have helped confirm the diagnosis however the patient was lost to follow up. This was an interesting presentation of AFLP as most cases are discovered in women presenting with acute liver failure; this case was unique in that it was discovered unexpectedly.