Vande Berg Perrine, Ulaj Artida, de Broqueville Graziella, de Vos Marie, Delire Bénédicte, Hainaut Philippe, Thissen Jean-Paul, Stärkel Peter, Komuta Mina, Henry Paulina, Lanthier Nicolas
Service d'Hépato-Gastroentérologie, Cliniques Universitaires Saint-Luc, UCLouvain, Brussels, Belgium.
Service de Médecine Interne Générale, Cliniques Universitaires Saint-Luc, UCLouvain, Brussels, Belgium.
Obes Surg. 2022 Apr;32(4):1227-1235. doi: 10.1007/s11695-022-05930-3. Epub 2022 Feb 9.
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.
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.
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.
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.
在进行减肥手术时,代谢功能障碍相关脂肪性肝病相关的肝硬化是有可能出现的,且会并发进一步的肝失代偿。肝失代偿也可能在无肝硬化的情况下发生,但表现不太明确。
我们分析了在我们这所单一的三级医疗中心医院接受减肥手术后出现肝失代偿但无肝硬化的患者的临床特征、组织学发现及治疗情况。
2014年至2019年期间,6例患者在减肥手术后因肝失代偿接受了经静脉肝活检。诊断时的平均年龄为44岁。减肥手术与症状出现之间的时间差异很大(最短8个月,最长17年)。平均体重减轻百分比高达43%。临床表现如下:疲劳和黄疸(5/6)、腿部水肿(3/6)和腹水(1/6)。血液检查显示转氨酶升高(平均谷丙转氨酶53 UI/L,平均谷草转氨酶130 UI/L)、胆红素升高(平均6 mg/dL)、国际标准化比值升高(平均1.5)且白蛋白水平较低(平均27 mg/dL)。肝静脉压力梯度较高(平均10 mmHg)。组织学检查显示有脂肪变性、肝细胞气球样变,还有伴有多形核细胞的门管区炎症以及胆管改变。平均纤维化评分为2分。通过营养支持,临床病程良好,平均随访36个月。
减肥手术后无肝硬化的情况下也可能发生肝失代偿,延迟时间差异很大。存在一种特殊的组织学特征,即脂肪变性、胆管改变和门管区炎症并存。适当的营养支持带来的显著临床改善似乎是有效的。