Department of Biostatistics, Epidemiology, and Informatics, Center for Clinical Epidemiology and Biostatistics, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA.
Department of Biostatistics, Epidemiology, and Informatics, Center for Pharmacoepidemiology Research and Training, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA.
J Acquir Immune Defic Syndr. 2019 Sep 1;82(1):71-80. doi: 10.1097/QAI.0000000000002094.
Hepatitis B virus (HBV) infection is a leading cause of end-stage liver disease (ESLD) and hepatocellular carcinoma (HCC) in HIV. Factors contributing to the high rates of liver complications among HIV/HBV-coinfected individuals remain unknown.
North American AIDS Cohort Collaboration on Research and Design.
We performed a retrospective cohort study among HIV/HBV-coinfected patients in 10 US and Canadian cohorts of the North American AIDS Cohort Collaboration on Research and Design that validated ESLD (ascites, spontaneous bacterial peritonitis, variceal hemorrhage, and/or hepatic encephalopathy) and HCC diagnoses from 1996 to 2010. Multivariable Cox regression was used to examine adjusted hazard ratios [aHRs with 95% confidence interval (CIs)] of liver complications (first occurrence of ESLD or HCC) associated with hypothesized determinants and with increasing durations of HIV suppression (≤500 copies/mL).
Among 3573 HIV/HBV patients with 13,790 person-years of follow-up, 111 liver complications occurred (incidence rate = 8.0 [95% CI: 6.6 to 9.7] events/1000 person-years). Rates of liver complication were increased with non-black/non-Hispanic race [aHR = 1.76 (1.13-2.74)], diabetes mellitus [aHR = 2.07 (1.20-3.57)], lower time-updated CD4 cell count [<200 cells/mm: aHR = 2.59 (1.36-4.91); 201-499 cells/mm: aHR = 1.75 (1.01-3.06) versus ≥500 cells/mm], heavy alcohol use [aHR = 1.58 (1.04-2.39)], and higher FIB-4 at start of follow-up [>3.25: aHR = 9.79 (5.73-16.74); 1.45-3.25: aHR = 3.20 (1.87-5.47) versus FIB-4 <1.45]. HIV suppression for ≥6 months was associated with lower liver complication rates compared with those with unsuppressed HIV [aHR = 0.56 (0.35-0.91)].
Non-black/non-Hispanic race, diabetes, lower CD4 cell count, heavy alcohol use, and advanced liver fibrosis were determinants of liver complications among HIV/HBV patients. Sustained HIV suppression should be a focus for HIV/HBV-coinfected patients to reduce the risks of ESLD/HCC.
乙型肝炎病毒 (HBV) 感染是导致艾滋病毒感染者发生终末期肝病 (ESLD) 和肝细胞癌 (HCC) 的主要原因。导致 HIV/HBV 合并感染个体中肝脏并发症发生率高的因素仍不清楚。
北美艾滋病队列协作研究与设计。
我们对北美艾滋病队列协作研究与设计中的 10 个美国和加拿大队列中的 HIV/HBV 合并感染患者进行了回顾性队列研究，验证了 1996 年至 2010 年 ESLD（腹水、自发性细菌性腹膜炎、静脉曲张出血和/或肝性脑病）和 HCC 的诊断。多变量 Cox 回归用于检查与假设决定因素相关的调整后风险比（aHR，95%置信区间 [CI]）和 HIV 抑制持续时间增加（≤500 拷贝/mL）的肝脏并发症（首次发生 ESLD 或 HCC）的风险。
在 3573 名 HIV/HBV 患者中，有 13790 人年的随访时间，发生了 111 例肝脏并发症（发生率=8.0 [95%CI：6.6 至 9.7]例/1000 人年）。非黑人和非西班牙裔种族[aHR=1.76（1.13-2.74）]、糖尿病[aHR=2.07（1.20-3.57）]、较低的时间更新 CD4 细胞计数[<200 个细胞/mm：aHR=2.59（1.36-4.91）；201-499 个细胞/mm：aHR=1.75（1.01-3.06）与≥500 个细胞/mm]、大量饮酒[aHR=1.58（1.04-2.39）]和较高的 FIB-4 起始随访时[aHR=9.79（5.73-16.74）；1.45-3.25：aHR=3.20（1.87-5.47）与 FIB-4<1.45]，与较高的肝脏并发症发生率相关。与未抑制的 HIV 相比，HIV 抑制时间≥6 个月与较低的肝脏并发症发生率相关[aHR=0.56（0.35-0.91）]。
非黑人和非西班牙裔种族、糖尿病、较低的 CD4 细胞计数、大量饮酒和晚期肝纤维化是 HIV/HBV 患者发生肝脏并发症的决定因素。持续抑制 HIV 应成为 HIV/HBV 合并感染患者的重点，以降低 ESLD/HCC 的风险。
