Hepatitis D Virus Infection Markedly Increases the Risk of Hepatocellular Carcinoma in Patients with Viral B Cirrhosis.

IF 11.6 1区医学 Q1 GASTROENTEROLOGY & HEPATOLOGY

Clinical Gastroenterology and Hepatology Pub Date : 2024-10-24 DOI:10.1016/j.cgh.2024.08.046

Dominique Roulot, Richard Layese, Ségolène Brichler, Nathalie Ganne, Tarik Asselah, Fabien Zoulim, Emmanuel Gordien, Pierre Nahon, Françoise Roudot-Thoraval

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引用次数: 0

Abstract

Background & aims: The specific causative role of hepatitis delta virus (HDV) infection in the development of hepatocellular carcinoma (HCC) remains debated and was not specifically demonstrated in patients with cirrhosis. Here we compared HCC incidence in hepatitis B virus (HBV)-HDV coinfected and HBV monoinfected patients with cirrhosis.

Methods: A total of 142 HBV-HDV and 271 HBV-infected patients with cirrhosis from the French ANRSCO12 CirVir and DeltaVir cohorts, with histologically proven cirrhosis and no history of decompensation, were included in the study.

Results: HBV-HDV patients were younger than HBV patients (37.2 vs 53.8 years), they were more often immigrants from sub-Saharan Africa, and displayed less comorbidities and more altered liver tests. After adjustment for age, cumulative incidences of HCC in coinfected and monoinfected patients at 1, 3, and 5 years were 5.2%, 11.8%, and 20.2% versus 1.1%, 2.5%, and 4.4%, respectively (P < .001). In multivariate analysis, HDV infection was an independent factor associated with the development of HCC (hazard ratio [HR], 2.94; 95% confidence interval [CI], 1.19-7.25; P = .019). Other independent factors were age (HR, 1.08; 95% CI, 1.05-1.11; P < .001), overweight (HR, 0.45; 95% CI, 0.22-0.93; P = .031), smoking (HR, 2.26; 95% CI, 1.23-4.16; P = .009), increased γ-glutamyltransferase (HR, 2.73; 95% CI, 1.24-6.00; P = .013), total bilirubin >17 μmol/L (HR, 2.68; 95% CI, 1.33-5.42; P = .006), and platelet count <150.000/mm³ (HR, 3.11; 95% CI, 1.51-6.41; P = .002). HDV coinfection was not an independent factor of liver decompensation, transplantation, or death.

Conclusions: The incidence of HCC seems significantly higher in HBV-HDV than in HBV-infected patients with cirrhosis. HDV infection emerges as an independent risk factor for HCC, indicating that in patients with cirrhosis, HDV plays a causative role for HCC independently of HBV.

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D 型肝炎病毒感染会显著增加病毒性 B 型肝硬化患者罹患肝细胞癌的风险。

背景和目的：HDV感染在肝细胞癌（HCC）发病中的具体致病作用仍存在争议，在肝硬化患者中也未得到具体证实。在此，我们比较了HBV-HDV合并感染和HBV单一感染肝硬化患者的HCC发病率：研究共纳入了来自法国 ANRSCO12 CirVir 和 DeltaVir 队列的 142 名 HBV-HDV 和 271 名 HBV 感染的肝硬化患者，这些患者均经组织学证实患有肝硬化且无失代偿史：HBV-HDV患者比HBV患者更年轻（37.2岁对53.8岁），他们更多是来自撒哈拉以南非洲的移民，并发症更少，肝脏检查变化更大。在对年龄进行调整后，合并感染和单一感染患者在1、3和5年内的HCC累积发病率分别为5.2%、11.8%和20.2% vs. 1.1%、2.5%和4.4%（P< .001）。在多变量分析中，HDV 感染是与 HCC 发展相关的独立因素（HR 2.94，95% CI 1.19-7.25；P= .019）。其他独立因素包括年龄（HR 1.08，1.05-1.11；P< .001）、超重（HR 0.45，0.22-0.93；P= .031）、吸烟（HR 2.26，1.23-4.16；P= .009）、GGT 增高（HR 2.73，1.24-6.00；P= .013）、总胆红素 >17 μmol/L （HR 2.68，1.33-5.42；P= .006）和血小板计数 3（HR 3.11，1.51-6.41；P= .002）。HDV合并感染不是肝脏失代偿、移植或死亡的独立因素：结论：HBV-HDV肝硬化患者的HCC发病率明显高于HBV感染者。HDV感染成为HCC的独立危险因素，表明在肝硬化患者中，HDV是HCC的致病因素，而非HBV。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Clinical Gastroenterology and Hepatology 医学-胃肠肝病学

CiteScore

16.90

自引率

4.80%

发文量

903

审稿时长

22 days

期刊介绍： Clinical Gastroenterology and Hepatology (CGH) is dedicated to offering readers a comprehensive exploration of themes in clinical gastroenterology and hepatology. Encompassing diagnostic, endoscopic, interventional, and therapeutic advances, the journal covers areas such as cancer, inflammatory diseases, functional gastrointestinal disorders, nutrition, absorption, and secretion. As a peer-reviewed publication, CGH features original articles and scholarly reviews, ensuring immediate relevance to the practice of gastroenterology and hepatology. Beyond peer-reviewed content, the journal includes invited key reviews and articles on endoscopy/practice-based technology, health-care policy, and practice management. Multimedia elements, including images, video abstracts, and podcasts, enhance the reader's experience. CGH remains actively engaged with its audience through updates and commentary shared via platforms such as Facebook and Twitter.