Lin Birong, Ma Huaxi, Lin Yan, Lin Ting, Han Xiao, Lin Minghua, Gao Haibing
Department of Infectious Diseases, Mengchao Hepatobiliary Hospital of Fujian Medical University, Fuzhou, China.
College of Biological Science and Engineering, Fuzhou University, Fuzhou, China.
Tob Induc Dis. 2025 Jul 26;23. doi: 10.18332/tid/204511. eCollection 2025.
Viral hepatitis, caused by various hepatitis viruses, is a global health threat leading to chronic liver disease, hepatic cirrhosis, hepatic failure, and hepatocellular carcinoma. Smoking, a known risk factor for numerous chronic diseases, has been implicated in the pathogenesis of viral hepatitis. However, understanding the relationship between smoking and viral hepatitis is complex due to the presence of confounding factors and the potential for reverse associations.
We utilized Mendelian randomization (MR) analysis to explore the potential association between smoking behavior and viral hepatitis. In this study, SNPs were utilized as instrumental variables in a Mendelian randomization framework to examine the relationship between smoking behavior and viral hepatitis risk. To ensure the accuracy of the experiment, our data were sourced from large-scale genome-wide association studies (GWAS) and analyzed using a series of methods, such as inverse variance weighting (IVW) and leave-one-out analysis.
The MR analysis revealed significant positive associations between SNPs related to smoking initiation, status, and cessation, and the risk of viral hepatitis. The IVW method demonstrated a consistent rightward shift of the effect estimates, indicating a potential increase in viral hepatitis risk associated with smoking exposure. Smoking initiation, status, and cessation were associated with increased odds of viral hepatitis by 2.17-fold (95% CI: 1.45-3.24, p=0.00015), 2.93-fold (95% CI: 1.58-5.41, p=0.00061), and 5.30-fold (95% CI: 2.05-13.70, p=0.00057), respectively. The leave-one-out analysis further validated the robustness of our model, with minor SNP-specific deviations observed.
Our study presents strong associations between smoking behavior and an elevated risk of viral hepatitis, highlighting the need for further investigation into this potential connection. These findings underscore the importance of smoking cessation in liver disease management and inform public health strategies aimed at reducing the burden of viral hepatitis.
由多种肝炎病毒引起的病毒性肝炎是一种全球性的健康威胁,可导致慢性肝病、肝硬化、肝衰竭和肝细胞癌。吸烟是许多慢性疾病的已知风险因素,已被认为与病毒性肝炎的发病机制有关。然而,由于存在混杂因素和反向关联的可能性,理解吸烟与病毒性肝炎之间的关系较为复杂。
我们利用孟德尔随机化(MR)分析来探讨吸烟行为与病毒性肝炎之间的潜在关联。在本研究中,单核苷酸多态性(SNPs)在孟德尔随机化框架中用作工具变量,以检验吸烟行为与病毒性肝炎风险之间的关系。为确保实验的准确性,我们的数据来源于大规模全基因组关联研究(GWAS),并使用一系列方法进行分析,如逆方差加权(IVW)和留一法分析。
MR分析显示,与吸烟起始、现状和戒烟相关的SNPs与病毒性肝炎风险之间存在显著正相关。IVW方法表明效应估计值一致向右偏移,表明与吸烟暴露相关的病毒性肝炎风险可能增加。吸烟起始、现状和戒烟与病毒性肝炎发生几率增加分别相关2.17倍(95%置信区间:1.45 - 3.24,p = 0.00015)、2.93倍(95%置信区间:1.58 - 5.41,p = 0.00061)和5.30倍(95%置信区间:2.05 - 13.70,p = 0.00057)。留一法分析进一步验证了我们模型的稳健性,观察到轻微的SNP特异性偏差。
我们的研究表明吸烟行为与病毒性肝炎风险升高之间存在密切关联,突出了对这一潜在联系进行进一步研究的必要性。这些发现强调了戒烟在肝病管理中的重要性,并为旨在减轻病毒性肝炎负担的公共卫生策略提供了依据。