在长期随访中,肝脂肪变性并不增加慢性乙型肝炎患者发生肝细胞癌的风险

Microbiology insights Pub Date : 2020-05-13 eCollection Date: 2020-01-01 DOI:10.1177/1178636120918878
Chong Teik Lim, George Boon Bee Goh, Huihua Li, Tony Kiat-Hon Lim, Wei Qiang Leow, Wei Keat Wan, Rafay Azhar, Wan Cheng Chow, Rajneesh Kumar
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引用次数: 11

摘要

背景:慢性乙型肝炎(CHB)感染和非酒精性脂肪性肝病(NAFLD)是可能导致肝细胞癌(HCC)形成的肝脏疾病。这两种疾病实体都被独立地归因于HCC发展的风险增加。鉴于NAFLD患病率的增加,慢性乙型肝炎患者的肝脂肪变性变得越来越常见,但没有确凿的证据表明肝脂肪变性与慢性乙型肝炎感染患者HCC风险增加有关。本研究探讨chb感染个体中肝脏脂肪变性与HCC发展的关系。方法:对2000年1月至2014年12月期间接受肝活检的CHB患者进行回顾性研究。他们根据组织学证实的肝脂肪变性的存在和严重程度进行分层,随后随访以评估肝脂肪变性与HCC发展之间的关系。结果:289例患者中位随访111.1个月,185例(64.0%)存在肝脂肪变性。在随访中,27例患者发生HCC,其中21例发生肝脂肪变性。单因素Cox分析显示,年龄(风险比[HR] = 1.08, 95% CI = 1.042-1.12)、2型糖尿病(T2DM) (HR = 4.00, 95% CI = 1.622-9.863)和Ishak评分(HR = 1.221, 95% CI = 1.014-1.472)与HCC的发生有关,而多因素Cox分析显示,年龄和T2DM (HR = 2.69, 95% CI = 1.072-6.759)是HCC发生的重要危险因素。结论:慢性乙型肝炎感染患者并发肝脂肪变性不是肝细胞癌形成的危险因素。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Presence of Hepatic Steatosis Does Not Increase the Risk of Hepatocellular Carcinoma in Patients With Chronic Hepatitis B Over Long Follow-Up.

Presence of Hepatic Steatosis Does Not Increase the Risk of Hepatocellular Carcinoma in Patients With Chronic Hepatitis B Over Long Follow-Up.

Presence of Hepatic Steatosis Does Not Increase the Risk of Hepatocellular Carcinoma in Patients With Chronic Hepatitis B Over Long Follow-Up.

Presence of Hepatic Steatosis Does Not Increase the Risk of Hepatocellular Carcinoma in Patients With Chronic Hepatitis B Over Long Follow-Up.

Background: Chronic hepatitis B (CHB) infection and nonalcoholic fatty liver disease (NAFLD) are liver diseases which may lead to hepatocellular carcinoma (HCC) formation. Both disease entities have been attributed independently to increase risk of HCC development. While concomitant hepatic steatosis in patients with CHB are becoming more frequent in view of increasing NAFLD prevalence, there is no conclusive evidence linking presence of hepatic steatosis and increased HCC risk in patients with CHB infection. This study explores the association of hepatic steatosis among CHB-infected individuals in HCC development.

Methods: This is a retrospective study on a cohort of patients with CHB who underwent liver biopsy between January 2000 and December 2014. They were stratified according to presence and severity of histologically proven hepatic steatosis and subsequently followed up to evaluate the association between hepatic steatosis and HCC development.

Results: Among 289 patients with a median follow-up of 111.1 months, hepatic steatosis was present in 185 patients (64.0%). In all, 27 patients developed HCC on follow-up and 21 of them had hepatic steatosis. Univariate Cox analysis showed that age (hazard ratio [HR] = 1.08, 95% CI = 1.042-1.12), type 2 diabetes mellitus (T2DM) (HR = 4.00, 95% CI = 1.622-9.863), and Ishak score (HR = 1.221, 95% CI = 1.014-1.472) were associated with HCC development, whereas multivariate Cox analysis demonstrated that age and T2DM (HR = 2.69, 95% CI = 1.072-6.759) were significant risk factors for development of HCC.

Conclusions: Concurrent hepatic steatosis in patients with CHB infection is not a risk factor for hepatocellular carcinoma formation.

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