食道静脉曲张可预测代偿性晚期非酒精性脂肪肝疾病的并发症。
Oesophageal varices predict complications in compensated advanced non-alcoholic fatty liver disease.
发表日期：2023 Sep
作者：
Grazia Pennisi, Marco Enea, Mauro Viganò, Filippo Schepis, Victor de Ledinghen, Annalisa Berzigotti, Vincent Wai-Sun Wong, Anna Ludovica Fracanzani, Giada Sebastiani, Carmen Lara-Romero, Elisabetta Bugianesi, Gianluca Svegliati-Baroni, Fabio Marra, Alessio Aghemo, Luca Valenti, Vincenza Calvaruso, Antonio Colecchia, Gabriele Di Maria, Claudia La Mantia, Huapeng Lin, Yuly P Mendoza, Nicola Pugliese, Federico Ravaioli, Manuel Romero-Gomez, Dario Saltini, Antonio Craxì, Vito Di Marco, Calogero Cammà, Salvatore Petta
来源：
BIOMEDICINE & PHARMACOTHERAPY
摘要：
我们的目标是评估食管静脉曲张（OV）及其发展对由非酒精性脂肪性肝病（NAFLD）引起的代偿性晚期慢性肝病（cACLD）并发症风险的影响。我们还评估了非侵入性评分用于预测并发症发展和识别低危高危OV患者的准确性。我们对629例有基线和随访食管胃十二指肠镜检查和临床随访记录失代偿、门静脉血栓形成（PVT）及肝细胞癌的NAFLD相关cACLD患者进行了回顾性评估。
在患者中，30％和15.9％分别在基线观察到小型OV和大型OV。从基线起，OV的4年发生率为16.3％，从小型OV进展到大型OV的发生率为22.4％. 糖尿病和体重指数（BMI）≥5％的增加与OV进展相关。多变量Cox回归分析显示，小（危险比[HR] 2.24，95% CI 1.47-3.41）和大（HR 3.86，95％CI 2.34-6.39）OV与失代偿独立相关。考虑OV状态和变化情况时，与基线和/或随访中无OV相比，基线和/或随访中存在的小（HR 2.65，95％CI 1.39-5.05）和大（HR 4.90, 95％CI 2.49-9.63）OV与失代偿独立相关。小（HR 2.8，95％CI 1.16-6.74）或大（HR 5.29，95％CI 1.96-14.2）OV的存在也与新发PVT独立相关。
在NAFLD相关cACLD中，OV的存在、严重程度和发展可分层患者发生失代偿和PVT的风险。门脉高压是慢性肝病失代偿的主要驱动因素，其非侵入性标志物有助于风险预测。食管静脉曲张的存在、严重程度和进展分层了非酒精性脂肪性肝病并发症的风险。易于获得的实验室指标和肝脏刚度测量可以识别低风险患者，无需进行内窥镜检查，并能分层肝相关并发症的风险。© 2023 The Authors.
We aimed to evaluate the impact of oesophageal varices (OV) and their evolution on the risk of complications of compensated advanced chronic liver disease (cACLD) caused by non-alcoholic fatty liver disease (NAFLD). We also assessed the accuracy of non-invasive scores for predicting the development of complications and for identifying patients at low risk of high-risk OV.We performed a retrospective assessment of 629 patients with NAFLD-related cACLD who had baseline and follow-up oesophagogastroduodenoscopy and clinical follow-up to record decompensation, portal vein thrombosis (PVT), and hepatocellular carcinoma.Small and large OV were observed at baseline in 30 and 15.9% of patients, respectively. The 4-year incidence of OV from absence at baseline, and that of progression from small to large OV were 16.3 and 22.4%, respectively. Diabetes and a ≥5% increase in BMI were associated with OV progression. Multivariate Cox regression revealed that small (hazard ratio [HR] 2.24, 95% CI 1.47-3.41) and large (HR 3.86, 95% CI 2.34-6.39) OV were independently associated with decompensation. When considering OV status and trajectories, small (HR 2.65, 95% CI 1.39-5.05) and large (HR 4.90, 95% CI 2.49-9.63) OV at baseline and/or follow-up were independently associated with decompensation compared with the absence of OV at baseline and/or follow-up. The presence of either small (HR 2.8, 95% CI 1.16-6.74) or large (HR 5.29, 95% CI 1.96-14.2) OV was also independently associated with incident PVT.In NAFLD-related cACLD, the presence, severity, and evolution of OV stratify the risk of developing decompensation and PVT.Portal hypertension is the main driver of liver decompensation in chronic liver diseases, and its non-invasive markers can help risk prediction. The presence, severity, and progression of oesophageal varices stratify the risk of complications of non-alcoholic fatty liver disease. Easily obtainable laboratory values and liver stiffness measurement can identify patients at low risk for whom endoscopy may be withheld, and can also stratify the risk of liver-related complications.© 2023 The Authors.