Perrine Vande Berg1, Artida Ulaj2, Graziella de Broqueville1, Marie de Vos3, Bénédicte Delire1, Philippe Hainaut2, Jean-Paul Thissen4, Peter Stärkel1, Mina Komuta5, Paulina Henry5, Nicolas Lanthier6. 1. Service d'Hépato-Gastroentérologie, Cliniques Universitaires Saint-Luc, UCLouvain, Brussels, Belgium. 2. Service de Médecine Interne Générale, Cliniques Universitaires Saint-Luc, UCLouvain, Brussels, Belgium. 3. Service d'Hépato-Gastroentérologie, Hôpital de Jolimont, Haine-Saint-Paul, Belgium. 4. Service d'Endocrinologie et de Nutrition, Cliniques Universitaires Saint-Luc, UCLouvain, Brussels, Belgium. 5. Service d'Anatomie Pathologique, Cliniques Universitaires Saint-Luc, UCLouvain, Brussels, Belgium. 6. Service d'Hépato-Gastroentérologie, Cliniques Universitaires Saint-Luc, UCLouvain, Brussels, Belgium. nicolas.lanthier@saintluc.uclouvain.be.
Abstract
PURPOSE: Metabolic dysfunction-associated fatty liver disease-related cirrhosis is possible at the time of bariatric surgery, complicated by further liver decompensation. Hepatic decompensation can also occur in the absence of cirrhosis but the presentation is less clear. METHODS: We analyze the clinical characteristics, histological findings, and management of patients without cirrhosis who developed hepatic decompensation after bariatric surgery in our single tertiary-care hospital. RESULTS: From 2014 to 2019, 6 patients underwent a transvenous liver biopsy for liver decompensation after bariatric surgery. Mean age at diagnosis was 44 years. The time between bariatric surgery and the onset of symptoms varied widely (min. 8 months, max. 17 years). Mean % of weight loss was high at 43%. The clinical presentation was as follows: fatigue and jaundice (5/6), leg edema (3/6), and ascites (1/6). Blood test showed increased transaminases (mean ALT 53 UI/L, mean AST 130 UI/L), bilirubin (mean 6 mg/dL), and INR (mean 1.5) with a low albumin level (mean 27 mg/dL). The hepatic venous pressure gradient was high (mean 10 mmHg). Histology revealed steatosis, hepatocyte ballooning but also portal inflammation with polymorphonuclear cells, and bile duct alterations. Mean fibrosis score was 2. The clinical course was favorable with nutritional support with a mean follow-up of 36 months. CONCLUSION: Liver decompensation in the absence of cirrhosis can occur after bariatric surgery with a highly variable delay. A special histological signature is present with the coexistence of steatosis, bile duct alterations, and portal inflammation. Substantial clinical improvement with appropriate nutritional support seems to be effective.
PURPOSE: Metabolic dysfunction-associated fatty liver disease-related cirrhosis is possible at the time of bariatric surgery, complicated by further liver decompensation. Hepatic decompensation can also occur in the absence of cirrhosis but the presentation is less clear. METHODS: We analyze the clinical characteristics, histological findings, and management of patients without cirrhosis who developed hepatic decompensation after bariatric surgery in our single tertiary-care hospital. RESULTS: From 2014 to 2019, 6 patients underwent a transvenous liver biopsy for liver decompensation after bariatric surgery. Mean age at diagnosis was 44 years. The time between bariatric surgery and the onset of symptoms varied widely (min. 8 months, max. 17 years). Mean % of weight loss was high at 43%. The clinical presentation was as follows: fatigue and jaundice (5/6), leg edema (3/6), and ascites (1/6). Blood test showed increased transaminases (mean ALT 53 UI/L, mean AST 130 UI/L), bilirubin (mean 6 mg/dL), and INR (mean 1.5) with a low albumin level (mean 27 mg/dL). The hepatic venous pressure gradient was high (mean 10 mmHg). Histology revealed steatosis, hepatocyte ballooning but also portal inflammation with polymorphonuclear cells, and bile duct alterations. Mean fibrosis score was 2. The clinical course was favorable with nutritional support with a mean follow-up of 36 months. CONCLUSION: Liver decompensation in the absence of cirrhosis can occur after bariatric surgery with a highly variable delay. A special histological signature is present with the coexistence of steatosis, bile duct alterations, and portal inflammation. Substantial clinical improvement with appropriate nutritional support seems to be effective.
Authors: Masahiro Takeuchi; Paula T Vidigal; Mateus T Guerra; Melanie A Hundt; Marie E Robert; Maria Olave-Martinez; Satoshi Aoki; Tanaporn Khamphaya; Remco Kersten; Emma Kruglov; Randolph de la Rosa Rodriguez; Jesus M Banales; Michael H Nathanson; Jittima Weerachayaphorn Journal: Gut Date: 2020-11-19 Impact factor: 23.059