S5906 Rising Enzymes: The Hepatic Fallout of Refeeding Syndrome

Introduction: Refeeding syndrome-associated hepatitis is liver inflammation that occurs when nutrition is reintroduced after prolonged starvation or severe malnutrition. This condition is driven by metabolic shifts and fat accumulation in the liver, leading to hepatocellular injury. Understanding this condition is important to prevent complications during hospitalization as this form of hepatitis is rare and often underrecognized in clinical practice. Case Description/Methods: A 23-year-old man with schizoaffective disorder was admitted for severe malnutrition with concern for refeeding syndrome. He had weight loss secondary to hallucinations that severely limited oral intake and caused extreme dietary restrictions. He lost approximately 128 lbs over 2 months. BMI decreased from 29.8 to 12.5. Upon initiating refeeding with a standard tube feed formula via nasogastric tube, the patient displayed signs of refeeding syndrome. Liver enzymes were normal on admission. These increased temporally with the up titration of tube feeds. On day 3 following initiation of tube feeds, alanine aminotransferase peaked at 542, aspartate aminotransferase at 464, and Alkaline phosphatase at 294. Bilirubin and international normalized ratio remained normal. Hepatology was consulted. Medications included mirtazapine, paliperidone, vitamin B1/B6 and vitamin D3. Ultrasound had findings of hyperechoic and heterogenous liver. Hepatitis panel, autoimmune hepatitis workup and celiac screen were negative. Vitamin C/E/K were normal. Vitamin A was low. Zinc and copper were normal. He continued treatment despite liver enzyme elevation. He received tube feed formula that provided 504 kcals, 26 grams protein, and 55 grams carbohydrates daily at 15 ml/hr. This was increased to 50 ml/hr over 10 days. The patient started to increase oral intake on his own with resolution of psychosis. Feeding was decreased gradually and discontinued. Liver enzymes declined to normal 20 days after the initial start of refeeding. He was restarted on oral antipsychotics and eventually returned to a weight of 165 lbs. No further imaging of his liver has been obtained. However, repeat testing does not show elevated liver enzymes as evidence of long-term liver injury. Discussion: This case emphasizes the importance of recognizing and understanding liver injury during refeeding syndrome. Liver enzyme elevations should not deter nutritional support, as treating the underlying malnutrition remains priority. With careful monitoring and gradual refeeding, this case illustrates that liver function often improves alongside nutritional status.