不符合抗病毒治疗标准的慢性乙型肝炎病毒感染者的肝细胞

StephenW

不符合抗病毒治疗标准的慢性乙型肝炎病毒感染者的肝细胞癌发病率
Omar Alshuwaykh 1 , Tami Daugherty 1 , Amanda Cheung 1 , Aparna Goel 1 , Renumathy Dhanasekaran 1 , T Tara Ghaziani 1 , Aijaz Ahmed 1 , Deepti Dronamraju 1 , Radhika Kumari 1 , Allison Kwong 1 , Mindie Nguyen 1 , W Ray Kim 1 , Paul Yien Kwo 1
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联系

    1
    美国加利福尼亚州斯坦福斯坦福大学医学中心胃肠病学和肝病学部。

    PMID：36004713 DOI：10.1002/hep4.2064

抽象的

慢性乙型肝炎病毒（HBV）感染是肝细胞癌（HCC）的主要危险因素。本研究的目的是探讨 HBV 患者队列中 HCC 的发生率，并与当前的 HBV 治疗指南相关。在研究期间，我们确定了 2846 名 HBV 受试者。 2846 名受试者中有 386 名（14%）被诊断为 HCC； 386 人中有 209 人（54%）在 HCC 诊断时接受了核苷（酸）类似物（NA）治疗，386 人中有 177 人（46%）未接受 NA 治疗。在随访期间未使用 NA 的 177 名受试者中，177 名中的 153 名（86%）患有肝硬化。在未使用 NA 的 177 名受试者中，177 名中有 158 名（89%）的 HBV DNA 检测不到，177 名中有 10 名（6%）的 HBV DNA < 2000 IU/L，177 名中有 9 名（5%）的 HBV DNA > 2000国际单位/升。在肝硬化和无法检测到 HBV DNA 的患者中，141 人中有 115 人患有代偿期肝硬化，141 人中有 26 人患有失代偿期肝硬化。事件发生时间分析中 HCC 的重要预测因子包括肝硬化（风险比 [HR] 10，95% 置信区间 [CI] 5.8-17.5；p < 0.001）、丙氨酸氨基转移酶水平（HR 1.004，95% CI 1.002-1.006；p < 0.001)、年龄 (HR 1.04, 95% CI 1.03-1.06; p < 0.001)、(HR 1.9, 95% CI 1.2-3.1; p 0.007) 和非酒精性脂肪肝 (HR 1.7, 95% CI 1.1- 2.8；p = 0.02）。 Kaplan-Meier 分析表明，接受 NA 治疗的代偿期肝硬化受试者的 HCC 累积发病率显着低于当前 HBV 治疗实践指南之外的代偿期肝硬化受试者（无法检测到 HBV DNA）（32% 对 51%；p < 0.001） .结论：未治疗HBV DNA检测不到的代偿期肝硬化不符合当前治疗指南的患者，其HCC发生率高于代偿期肝硬化且经NA治疗抑制HBV DNA的患者。这项研究强调了早期诊断和治疗 HBV 的必要性。

© 2022 作者。由 Wiley Periodicals LLC 代表美国肝病研究协会出版的 Hepatology Communications。

StephenW

Incidence of hepatocellular carcinoma in chronic hepatitis B virus infection in those not meeting criteria for antiviral therapy
Omar Alshuwaykh  1 , Tami Daugherty  1 , Amanda Cheung  1 , Aparna Goel  1 , Renumathy Dhanasekaran  1 , T Tara Ghaziani  1 , Aijaz Ahmed  1 , Deepti Dronamraju  1 , Radhika Kumari  1 , Allison Kwong  1 , Mindie Nguyen  1 , W Ray Kim  1 , Paul Yien Kwo  1
Affiliations
Affiliation

    1
    Division of Gastroenterology and Hepatology, Stanford University Medical Center, Stanford, California, USA.

    PMID: 36004713 DOI: 10.1002/hep4.2064

Abstract

Chronic hepatitis B virus (HBV) infection is the leading risk factor for hepatocellular carcinoma (HCC). The aim of this study was to explore the incidence of HCC in a cohort of subjects with HBV and correlate with HBV treatment current guidance. We identified 2846 subjects with HBV over the study period. HCC was diagnosed in 386 of 2846 (14%) subjects; 209 of 386 (54%) were on nucleos(t)ide analogue (NA) therapy at time of HCC diagnosis, and 177 of 386 (46%) were not on NA therapy. Of the 177 subjects not on NAs who developed HCC during follow-up, 153 of 177 (86%) had cirrhosis. Within the 177 subjects not on NAs, 158 of 177 (89%) had undetectable HBV DNA, 10 of 177 (6%) had detectable HBV DNA < 2000 IU/L, and 9 of 177 (5%) had HBV DNA > 2000 IU/L. Of those with cirrhosis and undetectable HBV DNA, 115 of 141 had compensated cirrhosis, and 26 of 141 had decompensated cirrhosis. Significant predictors of HCC on time to event analysis included cirrhosis (hazard ratio [HR] 10, 95% confidence interval [CI] 5.8-17.5; p < 0.001), alanine aminotransferase level (HR 1.004, 95% CI 1.002-1.006; p < 0.001), age (HR 1.04, 95% CI 1.03-1.06; p < 0.001), (HR 1.9, 95% CI 1.2-3.1; p 0.007), and nonalcoholic fatty liver disease (HR 1.7, 95% CI 1.1-2.8; p 0.02). Kaplan-Meier analysis demonstrated the cumulative incidence of HCC in subjects with compensated cirrhosis receiving NA therapy was significantly lower compared to subjects with compensated cirrhosis outside current HBV treatment practice guidance (undetectable HBV DNA) (32% vs. 51%; p < 0.001). Conclusion: Those with untreated compensated cirrhosis with undetectable HBV DNA who do not meet current guidance for treatment had higher rates of HCC than those with compensated cirrhosis and suppressed HBV DNA by NA therapy. This study highlights the need for earlier diagnosis and treatment of HBV.

© 2022 The Authors. Hepatology Communications published by Wiley Periodicals LLC on behalf of American Association for the Study of Liver Diseases.