Ramier Clémence, Boyd Anders, Smit Colette, van Zoest Rosan, Claassen Mark A A, Pogány Katalin, Posthouwer Dirk, de Vries-Sluijs Theodora E M S, Carrieri Patrizia, Van der Valk Marc
Aix Marseille Univ, INSERM, IRD, SESSTIM, Sciences Économiques & Sociales de la Santé & Traitement de L'information Médicale, ISSPAM, Marseille, France.
Amsterdam UMC, Location University of Amsterdam, Amsterdam Institute for Immunology & Infectious Diseases, Infectious Diseases Program, Amsterdam, the Netherlands.
Liver Int. 2025 Jul;45(7):e70191. doi: 10.1111/liv.70191.
Little is known about the contribution of sociodemographic and behavioural factors to developing liver disease in individuals with an HIV and chronic hepatitis B virus (HBV) co-infection. We aimed to quantify the impact of these factors on incident liver disease in individuals with HIV/HBV receiving care in the Netherlands.
We used data from the Dutch observational ATHENA cohort combined with Statistics Netherlands. We included all hepatitis B surface antigen-positive individuals with HIV in care from 2008-2022. Severe liver disease (i.e., significant fibrosis (≥F2), cirrhosis, hepatocellular carcinoma, liver transplantation) was defined by physician diagnosis or a transient elastography result > 7 kPa. Determinants of incident liver disease were assessed using Cox proportional hazard models.
In the 1319 individuals included (12,277 person-years (PY); 93.3% HIV-RNA < 200 copies/ml), the incidence rate of severe liver disease was 0.59 per 100 PY [95% confidence interval (CI) = 0.47-0.75]. After adjustment for age and time since HBV diagnosis, tobacco smoking, HCV coinfection and body mass index > 25 kg/m increased the risk of liver disease [adjusted hazards ratio (aHR) = 2.33, 95% CI = 1.38-3.94; aHR = 4.00, 95% CI = 2.18-7.33, aHR = 1.75, 95% CI = 1.05-2.92, respectively]. Conversely, men who have sex with men (vs. other transmission routes, aHR = 0.54, 95% CI = 0.32-0.90), and individuals living in an urbanised municipality (aHR = 0.50, 95% CI = 0.30-0.85) had a reduced risk of liver disease.
Liver disease progression in people living with HIV/HBV appears to be linked to psychosocial/behavioural factors. More effective screening/management of coinfection and metabolic syndrome, as well as strategies for smoking cessation, should be included in clinical follow-up.
关于社会人口学和行为因素对人类免疫缺陷病毒（HIV）与慢性乙型肝炎病毒（HBV）合并感染个体发生肝病的影响，目前所知甚少。我们旨在量化这些因素对在荷兰接受治疗的HIV/HBV感染者发生肝病的影响。
我们使用了荷兰观察性ATHENA队列的数据，并结合荷兰统计局的数据。我们纳入了2008年至2022年期间接受治疗的所有乙肝表面抗原阳性的HIV感染者。严重肝病（即显著纤维化（≥F2）、肝硬化、肝细胞癌、肝移植）由医生诊断或瞬时弹性成像结果>7kPa定义。使用Cox比例风险模型评估肝病发生的决定因素。
在纳入的1319名个体中（12277人年（PY）；93.3%的HIV-RNA<200拷贝/ml），严重肝病的发病率为每100 PY 0.59例[95%置信区间（CI）=0.47-0.75]。在调整年龄和自HBV诊断以来的时间后，吸烟、丙型肝炎病毒（HCV）合并感染和体重指数>25kg/m²会增加肝病风险[调整后风险比（aHR）=2.33，95%CI=1.38-3.94；aHR=4.00，95%CI=2.18-7.33，aHR=1.75，95%CI=1.05-2.92]。相反，男男性行为者（与其他传播途径相比，aHR=0.54，95%CI=0.32-0.90）以及居住在城市化市镇的个体（aHR=0.50，95%CI=0.30-0.85）发生肝病的风险降低。
HIV/HBV感染者的肝病进展似乎与心理社会/行为因素有关。临床随访中应包括更有效的合并感染和代谢综合征筛查/管理，以及戒烟策略。
