The beneficial impact of nutritional treatment in non-cirrhotic patients with acute liver decompensation after bariatric surgery

Vande Berg, Perrine [UCL] Ulaj, Artida [UCL] de Broqueville, Graziella [UCL] de Vos, Marie Delire, Bénédicte [UCL] Hainaut, Philippe [UCL] Thissen, Jean-Paul [UCL] Starkel, Peter [UCL] Komuta, Mina [UCL] Henry, Paulina [UCL] Lanthier, Nicolas [UCL]

Rationale: Hepatic decompensation can occur in the absence of cirrhosis after bariatric surgery (BS), sometimes leading to death, despite “rescue” transplant treatments. The clinical presentation and management of these patients is poorly understood. Methods: We describe the clinical characteristics, histological findings and clinical management of patients without cirrhosis who developed acute hepatic decompensation after BS in our single tertiary-care hospital. Results: From 2014 to 2019, 6 patients (mean age 44 years) underwent a transvenous liver biopsy for acute liver decompensation after BS. The time between BS and the onset of symptoms varied widely (min. 8 months, max. 17 years). Mean percentage of weight loss was high (43%) with an excess body weight loss of 98%. The clinical presentation was: fatigue and jaundice (5/6), leg edema (3/6) and ascites (1/6). Blood test showed increased transaminases (ALAT 53 UI/L, ASAT 130 UI/L), bilirubin (6 mg/dL) and INR (1.5) with a low albumin level (27 mg/dL). Histology revealed steatosis, hepatocyte ballooning but also portal inflammation with polymorphonuclear cells and bile duct alterations. Mean fibrosis score was 2. Due to the prominent malnutrition among the patients, nutritional treatment was started in all patients (parenteral nutrition only in 2 patients, parenteral and enteral feeding in 3 patients and only oral supplements in 1 patient). Three patients had diuretics and two patients had intravenous albumin supplementation. The clinical course was favorable in all patients with a mean follow-up of 36 months. Conclusion: Acute liver decompensation in the absence of cirrhosis can occur after BS with a highly variable delay. A special histological signature is present with the coexistence of steatosis and bile duct alterations with portal inflammation. Substantial clinical improvement with appropriate refeeding seems to be effective.