Case Presentation: A 22-year-old female with a history of biopsy-proven eosinophilic esophagitis, gastroparesis, multiple food allergies, and intermittent amenorrhea presented to the emergency room with weakness and lightheadedness. In the past month she experienced a 15lb weight loss, early satiety, and increasing fatigue. She was being followed outpatient by a gastroenterologist for several months of transaminitis (AST/ALT in the 100s) thought to be due to long-term use of over the counter supplements including curcumin and a prebiotic. Despite discontinuation of these supplements and a course of oral vitamin K, she continued to have worsening transaminitis and INR elevation. Her only medication at the time of presentation was Miralax. Vitals on presentation were notable for HR of 34, BP 103/78 with positive orthostatics, and a BMI of 11.6. Physical examination revealed a thin female with bitemporal wasting, right upper quadrant abdominal tenderness without rebound, and generalized pallor. No stigmata of liver disease was appreciated. Her workup was notable for marked sinus bradycardia on EKG and diffuse anasarca and bowel wall edema on CT abdomen/pelvis. Abdominal ultrasound was negative for cirrhosis or lesions. Serologic studies were notable for leukopenia (WBC 3.74 k/uL without eosinophilia), thrombocytopenia (platelets 76 k/uL), elevated BUN/Cr (37/1.1 mg/dL), lipase of 248 U/L, INR of 1.5, and severe transaminitis (ALT/AST 3285/3149 U/L). Gastroenterology was consulted and a liver biopsy was done, revealing no major histopathologic changes that would explain the degree of transaminitis. Serologic workup was negative for acute viral hepatitis, HIV, an extensive autoimmune antibody panel, and alpha-1 antitrypsin, with acetaminophen level <10 mcg/mL. This increased suspicion for acute liver injury secondary to malnutrition-induced liver autophagy. The patient was evaluated by an eating disorder specialist and diagnosed with anorexia nervosa-restricting type and was found to have had a drop in BMI from 16 to 11.6 over the past six months from food restriction. She was started on a high calorie diet with nasogastric feed supplementation and was monitored closely for refeeding syndrome. Her BMI improved to 15.1 and she was discharged to an intensive outpatient eating disorder rehabilitation facility. At her 6 month follow-up she maintained a normal BMI with complete normalization of liver function tests and blood count.
Discussion: Transaminitis in a hepatocellular pattern of injury is a common finding in anorexia nervosa. Up to 50% of patients having abnormalities to some degree. ALT is generally more elevated than AST, similar to the pattern of injury seen in nonalcoholic liver disease. As BMI approaches 12, AST and ALT can rise markedly from the low hundreds into the thousands as seen in this case. The mechanism of action is hypothesized to be due to starvation-induced autophagy – though this process leads to hepatocyte death, it actually does not result in major coagulopathy and synthetic impairment, and can actually serve a protective role. In most cases, biopsy contributes little to the work-up and should be deferred unless no clinical improvement is seen after optimizing nutrition.
Conclusions: This case highlights the importance of a broad differential diagnosis in cases of acute liver injury of unknown cause, particularly in patients with poor nutritional status and suspected eating disorders. Therapy is directed at nutritional and caloric repletion with close monitoring for refeeding syndrome.