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.

INTRODUCTION: When a patient with inflammatory bowel disease (IBD) presents with respiratory complaints the differential diagnosis includes many conditions unrelated to IBD. Extra-intestinal manifestations (EIM) involving the lungs are relatively uncommon. Biologics for IBD can also have secondary effects including pulmonary toxicity and infectious complications. CASE DESCRIPTION/METHODS: A 48 y/o female nurse with history of bronchial asthma and hypertension was diagnosed with ulcerative pancolitis in 2005. In 2017, she was started on adalilumab (ADA) after repeated use of steroids and intolerance to azathioprine. ADA was discontinued after one year due to multiple subcutaneous nodules and fever that cleared on drug discontinuation. Differential diagnosis included erythema nodosum and hidradenitis. She was found with (+) quantiferon despite negative tuberculin (TB) skin test and chest x ray and was treated for latent TB with isoniazid for one year (04/18-04/19). Four months later (08/18), she was started on infliximab (IFX) with good response. On 01/19, an incidental left pleural effusion was found and she underwent thoracentesis. In 03/19, she developed night sweats and pleuritic chest pain. Chest x-ray demonstrated a large right pleural effusion. Bronchoscopy and pleural biopsy showed necrotizing granulomas negative for AFB and GMS. IFX was discontinued and she was started on high dose steroids with little improvement. Chest CT preformed on 05/19 demonstrated bilateral effusions and multiple upper lobe and centrilobar noncalcified opacities with tree in bud appearance. Bronchoscopy with lung biopsy showed multiple noncaseating granulomas negative for AFB and GMS. DISCUSSION: The differential diagnosis in this patient includes lung involvement of IBD, vasculitis, infections, drug reaction and concurrent primary sarcoidosis among others. Vasculitis and infections have been excluded, and the lack of improvement after IFX discontinuation and steroids suggests IFX is not the cause. However, several cases of sarcoidosis associated to anti-TNF drugs have been reported and drug-induced sarcoidosis remains a high probability. Pulmonary EIM is also still a possibility in spite of clinical remission of UC.This case report demonstrates the importance of remaining aware of possible rare EIM of IBD and also of other rarer complications in this new age of biologics. Early diagnosis and effective treatment are important to prevent complications and improve outcomes for these patients.