Iron-deficiency anemia may be a clinical presenting sign of pouchitis. Hemoglobin levels may be considered as surveillance tools for pouchitis in patients with IPAA.

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INTRODUCTION: Autoimmune hepatitis (AIH) has a variety of clinical phenotypes. AIH presenting with acute liver failure (AFL) and jaundice is generally uncommon, however, other possible liver etiologies may confuse and delay diagnosis. Prompt recognition of AIH as possible cause of ALF is crucial in order to prevent morbidity and mortality associated with ALF. We present an atypical presentation that may help future clinicians in the early recognition and diagnosis of this condition despite possible confounders. CASE DESCRIPTION/METHODS: This is the case of a 39-year-old female (G2P1A0) with no history of systemic illness with intrauterine pregnancy of 32 5/7 weeks gestational age that was consulted to our service due to elevated transaminase and bilirubin levels. Patient had originally arrived at OB/GYN Emergency Department with complaints of nausea, vomits, jaundice and dark urine; no acholia, fever, or change in mental status noted. Additionally, patient reported recent use of oral antibiotics for UTI. On arrival patient presented hyperbilirubinemia (11.86) with direct predominance, elevated AST/ALT (251/134) and coagulopathy (INR 1.76). Patient with sudden clinical deterioration including altered mental status. Differential diagnoses included Acute Fatty Liver of Pregnancy (AFLP), Drug Induced Liver Injury, and preeclampsia with severe features. Due to suspected AFLP she was provided with IV steroid for fetal lung maturation and emergent C-Section preformed. MRCP reported no intra or extra hepatic bile duct dilation and liver US with Doppler noted with patent vasculature. Labs remarkable for negative ANA, ASMA, AMA, Anti DS DNA among other work up. After delivery patient had slow improvement of AST/ALT and bilirubin until 5 days later when AST/ALT and bilirubin levels began to increase steadily. Patient transferred to liver transplant center and empiric steroids started. Liver biopsy preformed and findings compatible with AIH but not diagnostic. After starting steroids patient began with slow improvement and was discharged on oral steroids. At post-hospitalization clinic visit, AST/ALT and bilirubin continued to improve and patient started on Azathioprine. DISCUSSION: It is suspected that initial brief improvement of liver function was secondary to steroids provided for fetal lung maturation, which lead us preemptively classify the ALF secondary to AFLP instead of AIH. This case is a prime example of pregnancy as a possible confounding factor that may delay the recognition and diagnosis of AIH.