摘要
AIM: To analyze the influence of human immunodeficiency virus (HIV) infection on the course of hepatitis C virus (HCV) infection. METHODS: We performed a meta-analysis to quantify the effect of HIV co-infection on progressive liver disease in patients with HCV infection. Published studies in the English or Chinese-language medical literature involving cohorts of HIV-negative and -positive patients coinfected with HCV were obtained by searching the PUBMED, EMBASE and CBM. Data were extracted independently from relevant studies by 2 investigators and used in a fixed-effect meta analysis to determine the difference in the course of HCV infection in the 2 groups. RESULTS: Twenty-nine trails involving 16 750 patients were identified including the outcome of histological fibrosis or cirrhosis or de-compensated liver disease or hepatocellular carcinoma or death. These studies yielded a combined adjusted odds ratio (OR) of 3.40 [95% confidence interval (CI) = 2.45 and 4.73]. Of note, studies that examined histological fibrosis/ cirrhosis, decompensated liver disease, hepatocellular carcinoma or death had a pooled OR of 1.47 (95% CI = 1.27 and 1.70), 5.45 (95% CI = 2.54 and 11.71), 0.76 (95% CI = 0.50 and 1.14), and 3.60 (95% CI = 3.12 and 4.15), respectively. CONCLUSION: Without highly active antiretroviral therapies (HAART), HIV accelerates HCV diseaseprogression, including death, histological fibrosis/ cirrhosis and decompensated liver disease. However, the rate of hepatocellular carcinoma is similar in persons who had HCV infection and were positive for HIV or negative for HIV.
AIM： TO analyze the influence of human immunodeficiency virus （HIV） infection on the course of hepatitis C virus （HCV） infection. METHODS： We performed a meta-analysis to quantify the effect of HIV co-infection on progressive liver disease in patients with HCV infection. Published studies in the English or Chinese-language medical literature involving cohorts of HIV-negative and -positive patients coinfected with HCV were obtained by searching the PUBMED, EMBASE and CBM. Data were extracted independently from relevant studies by 2 investigators and used in a fixed-effect meta analysis to determine the difference in the course of HCV infection in the 2 groups. RESULTS： Twenty-nine trails involving 16750 patients were identified including the outcome of histological fibrosis or cirrhosis or de-compensated liver disease or hepatocellular carcinoma or death. These studies yielded a combined adjusted odds ratio （OR） of 3.40 [95% confidence interval （CI） = 2.45 and 4.73]. Of note, studies that examined histological fibrosis/ cirrhosis, decompensated liver disease, hepatocellular carcinoma or death had a pooled OR of 1.47 （95% CI = 1.27 and 1.70）, 5.45 （95% CI = 2.54 and 11.71）, 0.76 （95% CI = 0.50 and 1.14）, and 3.60 （95% CI = 3.12 and 4.15）, respectively. CONCLUSION： Without highly active antiretroviral therapies （HAART）, HIV accelerates HCV disease progression, including death, histological fibrosis/ cirrhosis and decompensated liver disease. However, the rate of hepatocellular carcinoma is similar in persons who had HCV infection and were positive for HIV or negative for HIV.
