Development and validation of a nomogram for assessing hepatocellular carcinoma risk after SVR in hepatitis C patients with advanced fibrosis and cirrhosis

IF 3.1 2区医学 Q3 IMMUNOLOGY

Infectious Agents and Cancer Pub Date : 2024-04-25 DOI:10.1186/s13027-024-00578-3

Shanshan Xu, Lixia Qiu, Liang Xu, Yali Liu, Jing Zhang

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引用次数: 0

Abstract

Hepatitis C patients with advanced fibrosis or cirrhosis are at high risk of developing hepatocellular carcinoma (HCC), even after sustained virological response (SVR). Clinical recommendations impose a significant burden on patients by recommending lifelong screening for HCC every six months. The goals of this study were to develop a nomogram that accurately stratifies risk of HCC and improve the screening approach that is currently in use. Risk factors for HCC were identified using univariate and multivariate analyses in this prospective study. We developed and validated a nomogram for assessing hepatocellular carcinoma risk after SVR in patients with advanced fibrosis and cirrhosis. During the median follow-up period of 61.00 (57.00–66.00) months in the derivation cohort, 37 patients (9.61%) developed HCC. Older age (HR = 1.08, 95% CI 1.02–1.14, p = 0.009), male gender (HR = 2.38, 95% CI 1.10–5.13, p = 0.027), low serum albumin levels (HR = 0.92, 95% CI 0.86–1.00, p = 0.037), and high liver stiffness measurement (LSM) (HR = 1.03, 95% CI 1.01–1.06, p = 0.001) were found to be independent predictors of HCC development. Harrell's C-index for the derivation cohort was 0.81. The nomogram’s 3-, 5- and 7-years time-dependent AUROCSs were 0.84 (95% CI 0.80–0.88), 0.83 (95% CI 0.79–0.87), and 0.81 (95% CI 0.77–0.85), respectively (all p > 0.05). According to the nomogram, patients are categorized as having low, intermediate, or high risk. The annual incidence rates of HCC in the three groups were 0.18%, 1.29%, and 4.45%, respectively (all p < 0.05). Older age, male gender, low serum albumin levels, and high LSM were risk factors for HCC after SVR in hepatitis C patients with advanced fibrosis and cirrhosis. We used these risk factors to establish a nomogram. The nomogram can identify a suitable screening plan by classifying hepatitis C patients according to their risk of HCC.

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开发并验证用于评估晚期纤维化和肝硬化丙型肝炎患者 SVR 后肝细胞癌风险的提名图

晚期纤维化或肝硬化的丙型肝炎患者即使在持续病毒学应答（SVR）后，也有罹患肝细胞癌（HCC）的高风险。临床建议每六个月进行一次终身肝细胞癌筛查，这给患者带来了沉重的负担。本研究的目的是开发一种能准确分层 HCC 风险的提名图，并改进目前使用的筛查方法。在这项前瞻性研究中，我们通过单变量和多变量分析确定了 HCC 的风险因素。我们开发并验证了一种提名图，用于评估晚期肝纤维化和肝硬化患者 SVR 后的肝细胞癌风险。在中位随访期 61.00 (57.00-66.00) 个月的衍生队列中，37 名患者（9.61%）发生了肝细胞癌。研究发现，高龄（HR = 1.08，95% CI 1.02-1.14，p = 0.009）、男性（HR = 2.38，95% CI 1.10-5.13，p = 0.027）、低血清白蛋白水平（HR = 0.92，95% CI 0.86-1.00，p = 0.037）和高肝硬度测量（LSM）（HR = 1.03，95% CI 1.01-1.06，p = 0.001）是HCC发展的独立预测因素。衍生队列的 Harrell C 指数为 0.81。提名图的 3 年、5 年和 7 年时间依赖性 AUROCS 分别为 0.84（95% CI 0.80-0.88）、0.83（95% CI 0.79-0.87）和 0.81（95% CI 0.77-0.85）（均 p > 0.05）。根据提名图，患者被分为低危、中危和高危。三组患者的 HCC 年发病率分别为 0.18%、1.29% 和 4.45%（均 p <0.05）。高龄、男性、低血清白蛋白水平和高 LSM 是晚期肝纤维化和肝硬化丙肝患者 SVR 后发生 HCC 的风险因素。我们利用这些风险因素建立了一个提名图。该提名图可以根据丙型肝炎患者罹患 HCC 的风险对其进行分类，从而确定合适的筛查方案。

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

Infectious Agents and Cancer ONCOLOGY-IMMUNOLOGY

CiteScore

5.80

自引率

2.70%

发文量

期刊介绍： Infectious Agents and Cancer is an open access, peer-reviewed online journal that encompasses all aspects of basic, clinical, epidemiological and translational research providing an insight into the association between chronic infections and cancer. The journal welcomes submissions in the pathogen-related cancer areas and other related topics, in particular: • HPV and anogenital cancers, as well as head and neck cancers; • EBV and Burkitt lymphoma; • HCV/HBV and hepatocellular carcinoma as well as lymphoproliferative diseases; • HHV8 and Kaposi sarcoma; • HTLV and leukemia; • Cancers in Low- and Middle-income countries. The link between infection and cancer has become well established over the past 50 years, and infection-associated cancer contribute up to 16% of cancers in developed countries and 33% in less developed countries. Preventive vaccines have been developed for only two cancer-causing viruses, highlighting both the opportunity to prevent infection-associated cancers by vaccination and the gaps that remain before vaccines can be developed for other cancer-causing agents. These gaps are due to incomplete understanding of the basic biology, natural history, epidemiology of many of the pathogens that cause cancer, the mechanisms they exploit to cause cancer, and how to interrupt progression to cancer in human populations. Early diagnosis or identification of lesions at high risk of progression represent the current most critical research area of the field supported by recent advances in genomics and proteomics technologies.