Division of Experimental Medicine, McGill University, Montreal, Quebec, Canada.
Lady Davis Institute for Medical Research, McGill University, Montreal, Quebec, Canada.
J Acquir Immune Defic Syndr. 2023 Nov 1;94(3):273-279. doi: 10.1097/QAI.0000000000003245.
People with HIV and hepatitis C virus (HCV) coinfection experience excess mortality because of multiple causes. Identification of biomarkers associated with mortality beyond that attributable to liver fibrosis may be relevant for prognostication. Fibroblast growth factor 23 (FGF23), a phosphotropic hormone, predicts adverse outcomes in several chronic conditions. We aimed to investigate whether elevated FGF23 predicts all-cause mortality in patients with HIV/HCV coinfection.
We included patients with HIV/HCV coinfection from the Canadian Coinfection Cohort with available serum FGF23, fibrosis biomarker fibrosis-4 (FIB-4), and at least 1-year follow-up. Elevated FGF23 and advanced liver fibrosis were defined as FGF23 > 241 reference unit/mL and FIB-4 > 3.25, respectively. All-cause mortality was analyzed using survival analysis. The effect of advanced liver fibrosis as a mediator on mortality was estimated by mediation analysis.
Three hundred twenty-one patients were included (24% with elevated FGF23, 19% with advanced liver fibrosis). During a mean follow-up period of 8.4 years, 34% of the cohort died. The incidence rate of all-cause mortality was higher in patients with elevated FGF23 (66.1 per 1000 person-years, 95% confidence interval 45.8 to 92.3) relative to patients without elevated FGF23 (37.5 per 1000 person-years, 95% confidence interval 29.6 to 46.9). After adjusting for potential confounders, elevated FGF23 was associated with significant direct and indirect effects (mediated through advanced liver fibrosis) on all-cause mortality, with 57% of deaths not mediated through advanced fibrosis.
In patients with HIV/HCV coinfection, FGF23 may be used as prognostic biomarker for risk stratification accounting also for death causes other than those attributable to liver fibrosis.
HIV 和丙型肝炎病毒(HCV)合并感染的患者由于多种原因而死亡率过高。识别与肝纤维化以外的死亡率相关的生物标志物可能与预后有关。成纤维细胞生长因子 23(FGF23)是一种磷酸化激素,可预测多种慢性疾病的不良结局。我们旨在研究升高的 FGF23 是否可预测 HIV/HCV 合并感染患者的全因死亡率。
我们纳入了加拿大合并感染队列中可获得血清 FGF23、纤维化生物标志物纤维化-4(FIB-4)和至少 1 年随访资料的 HIV/HCV 合并感染患者。升高的 FGF23 和晚期肝纤维化的定义分别为 FGF23>241 参考单位/mL 和 FIB-4>3.25。采用生存分析分析全因死亡率。通过中介分析估计晚期肝纤维化作为中介对死亡率的影响。
共纳入 321 例患者(24%的患者 FGF23 升高,19%的患者存在晚期肝纤维化)。在平均 8.4 年的随访期间,有 34%的患者死亡。FGF23 升高的患者全因死亡率(66.1/1000 人年,95%置信区间 45.8 至 92.3)高于 FGF23 不升高的患者(37.5/1000 人年,95%置信区间 29.6 至 46.9)。调整潜在混杂因素后,FGF23 升高与全因死亡率有显著的直接和间接影响(通过晚期肝纤维化介导),其中 57%的死亡未通过晚期纤维化介导。
在 HIV/HCV 合并感染患者中,FGF23 可作为预后生物标志物,用于风险分层,同时也考虑了与肝纤维化无关的死亡原因。