S5897 Starvation in Silence: A Rare Case of Severe Hepatitis in Chronic Anorexia Nervosa

Introduction: Anorexia nervosa is a psychiatric disorder marked by extreme caloric restriction, fear of weight gain, and body image distortion, often resulting in multisystem complications. Mild transaminitis is common, typically due to hepatic steatosis in malnutrition. However, aminotransferase levels exceeding 1,000 IU/L are rare and suggest alternative or additional liver injury. We describe a case of a 42-year-old woman with longstanding anorexia nervosa who presented with severe acute hepatitis, manifesting only as fatigue and weakness. Case Description/Methods: The patient, with a body mass index of 13.17 and history of obsessive compulsive disorder (status post deep brain stimulator placement), depression, and thyroid disease, was referred from clinic for markedly abnormal liver enzymes. She reported 2–4 weeks of weakness, fatigue, and nausea, with one episode of confusion and slurred speech. Labs revealed aspartate aminotransferase (AST) 8,924, alanine aminotransferase (ALT) 5,960, alkaline phosphatase (ALP) 1,055, total bilirubin 2.2, international normalized ratio 1.2, and lipase 262. She denied alcohol, drug, or supplement use. Hospitalization was notable for intermittent hypotension and hypothermia. Workup for infectious, autoimmune, metabolic, and vascular etiologies was negative. Imaging revealed preserved liver architecture and vasculature, though echocardiogram showed dilated chambers with septal dyssynergia. Right heart catheterization showed normal pressures, ruling out true cardiac hepatopathy. Liver biopsy demonstrated chronic congestive hepatopathy with pericellular and central venular fibrosis. With nutritional support and weight gain, liver enzymes improved: AST 68, ALT 208, ALP 239, and total bilirubin 0.5. She was discharged to a residential eating disorder facility. Discussion: While mild liver enzyme elevation is common in anorexia nervosa, extreme transaminase levels prior to refeeding are rare. Starvation hepatitis is thought to arise from autophagy, apoptosis, and hypoperfusion in the context of severe malnutrition. This case underscores the importance of considering starvation hepatitis in the differential for acute hepatitis in patients with eating disorders. Diagnosis remains one of exclusion, and management relies primarily on careful nutritional rehabilitation, which can lead to marked biochemical recovery.