Additive interaction between hepatitis B virus infection and tobacco smoking on the risk of gastric cancer in a Chinese population.

IF 3.1 2区医学 Q3 IMMUNOLOGY

Infectious Agents and Cancer Pub Date : 2025-03-20 DOI:10.1186/s13027-025-00648-0

Danjing Chen, Rong Yu, Yongfeng Cai, He Zhang, Yijun Jiang, Yunli Wu, Xian-E Peng

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引用次数: 0

Abstract

Objective: Although hepatitis B virus (HBV) infection was regarded as a risk factor for liver cancer, the association of HBV infection with gastric cancer (GC) is unclear. In this study, we aim to assess the association of HBV infection with the risk of GC and explore the interaction between HBV infection and other risk factors.

Methods: A case-control study was conducted and 409 GC cases and 1275 healthy controls were enrolled in Fujian province, China. Serum hepatitis B surface antigen (HBsAg) was measured and epidemiological data were collected. The association between HBV infection and GC risk was analyzed using logistic regression and meta-analysis method was employed to make estimates more conservative. Meanwhile, multiplicative and additive models were used to explore the interaction between HBV infection and other risk factors.

Results: The prevalence of serum HBsAg positivity was 13.20% among GC cases and 6.20% among controls. Compared to HBsAg-negative subjects, the adjusted odds ratios (OR) for HBsAg positive were 3.30 [95% confidence interval (CI): (1.84-5.91)]. Compared to HBsAg-negative never smokers, the adjusted OR was 2.00 (95%CI: 1.19-3.34) for HBsAg-negative ever smokers,4.27 (95%CI: 1.97-9.26) for HBsAg-positive never smokers, and 4.73 (95%CI: 1.85-12.08) for HBsAg-positive ever smokers. These evidences indicated super-additive [API (95%CI): 0.78 (0.67-0.90), S (95%CI): 5.45 (3.26-9.08)] between HBV infection and tobacco smoking. No interaction between HBV infection and alcohol drinking was found on the risk of GC.

Conclusions: HBV infection increased the risk of GC, and tobacco smoking and HBV infection may positively interact in the development of GC.

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乙型肝炎病毒感染与吸烟对中国人群胃癌发生风险的加性相互作用

目的：虽然乙型肝炎病毒（HBV）感染被认为是肝癌的危险因素，但HBV感染与胃癌（GC）的关系尚不清楚。在本研究中，我们旨在评估HBV感染与GC风险的相关性，并探讨HBV感染与其他危险因素之间的相互作用。方法：采用病例-对照研究方法，在福建省选取409例胃癌患者和1275名健康对照者。测定血清乙型肝炎表面抗原（HBsAg）并收集流行病学资料。采用logistic回归分析HBV感染与GC风险的相关性，并采用meta分析方法使估计更加保守。同时，采用乘法和加性模型探讨HBV感染与其他危险因素的相互作用。结果：胃癌患者血清HBsAg阳性率为13.20%，对照组为6.20%。与HBsAg阴性受试者相比，HBsAg阳性的校正优势比（OR）为3.30[95%可信区间（CI）：（1.84-5.91）]。与hbsag阴性的从未吸烟者相比，hbsag阴性的从未吸烟者的调整OR为2.00 (95%CI: 1.19-3.34)， hbsag阳性的从未吸烟者的调整OR为4.27 (95%CI: 1.97-9.26)， hbsag阳性的从未吸烟者的调整OR为4.73 （95%CI: 1.85-12.08）。这些证据表明HBV感染与吸烟之间存在超加性[API (95%CI): 0.78 (0.67 ~ 0.90), S (95%CI): 5.45(3.26 ~ 9.08)]。未发现HBV感染与饮酒对胃癌的风险有相互作用。结论：HBV感染可增加胃癌的发生风险，吸烟与HBV感染在胃癌的发生发展中可能存在正相互作用。

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.