Incidence of and factors associated with hepatocellular carcinoma among hepatitis C virus and human immunodeficiency virus coinfected patients with decompensated cirrhosis
Incidence of and factors associated with hepatocellular carcinoma among hepatitis C virus and human immunodeficiency virus coinfected patients with decompensated cirrhosis
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DOI：
10.1089/aid.2006.22.1236
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发表时间：
2006-12-01
影响因子：
1.5
通讯作者：
Pineda, Juan A.
中科院分区：
文献类型：
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作者：
Garcia-Garcia, Jose A.;Romero-Gomez, Manuel;Pineda, Juan A.
我们比较了丙型肝炎病毒(丙型肝炎病毒)单一感染者和人类免疫缺陷病毒(HIV)/丙型肝炎病毒混合感染者(均为失代偿期肝硬变)的肝细胞癌的发生率和相关因素。在一项回顾性研究中，对来自西班牙八个中心的180名HIV合并感染患者和1037名单一感染丙型肝炎病毒的失代偿期丙型肝炎相关性肝硬变患者进行了分析。肝细胞癌发生在234例(23%)丙型肝炎病毒单一感染者和4例(2%)艾滋病病毒混合感染者(p<；0.001)。在第一次肝脏失代偿时，前者和后者分别有188例(17%)和4例(2%)(p<；0.001)出现了肝细胞癌。在随访期间，54名(11%)无肝细胞癌的患者在随访期间发生了这种疾病。在艾滋病毒共同感染人群中没有发生病例。HIV/丙型肝炎病毒混合感染者和丙型肝炎病毒单独感染者的肝癌发病率密度(95%IC)分别为0(0~1.7)例/百人年(P&0.001)和3.31(2.7~4.64)例/百人年(p<；无HIV感染[调整优势比(AOR)(95%IC)=16.7(3.9-71.1)]和高丙氨酸氨基转移酶水平[AOR(95%IC)=2.5(1.1-5)]是仅有的两个独立预测肝癌发生的因素。在可以估计出丙型肝炎病毒感染日期的患者组中，在HIV感染的受试者中，被诊断为肝癌的时间较短。丙型肝炎病毒相关性肝硬变患者首次肝脏失代偿后肝细胞癌的发生率低于HIV感染患者。这可能是由于HIV感染缩短了合并有终末期肝病的丙型肝炎病毒感染患者的生存时间，以至于肝细胞癌没有机会出现。
We compared the incidence of and factors associated with hepatocellular carcinoma (HCC) among hepatitis C virus (HCV)-monoinfected subjects and human immunodeficiency virus (HIV)/HCV-coinfected individuals, both with decompensated cirrhosis. In a retrospective study, a cohort of 180 individuals with HIV coinfection and 1037 HCV-monoinfected patients with decompensated HCV-related cirrhosis from eight centres in Spain were analyzed. HCC was found in 234 (23%) HCV-monoinfected subjects and in four (2%) HIV-coinfected subjects (p < 0.001). At the time of the first hepatic decompensation, 188 (17%) and 4 (2%) (p < 0.001) patients in the former and in the latter group, respectively, showed HCC. Fifty-four (11%) patients without HCC at baseline developed such a disease during follow-up. There were no incident cases among the HIV-coinfected population. The density of incidence (95% IC) of HCC in HIV/HCV-coinfected and HCV-monoinfected patients was 0 (0-1.70) and 3.31 (2.70-4.64) cases per 100 person-years (p < 0.001), respectively. Lack of HIV infection [ adjusted odds risk (AOR) (95% IC) = 16.7 (3.9-71.1)] and high alanine aminotransferase levels [AOR ( 95% IC) = 2.5 (1.1-5)] were the only two independent predictors of the emergence of HCC. In the group of patients in whom the date of HCV infection could be estimated, the time elapsed until HCC diagnosis was shorter among HIV-coinfected subjects. The incidence of HCC in patients with HCV-related cirrhosis after the first hepatic decompensation is lower in HIV-coinfected patients. This is probably due to the fact that HIV infection shortens the survival of HCV-coinfected patients with end-stage liver disease to such an extent that HCC not had a chance to emerge.