Clinical progression of hepatitis C virus-related chronic liver disease in human immunodeficiency virus-infected patients undergoing highly active antiretroviral therapy

Abstract

Little is known about the natural history of liver disease in human immunodeficiency virus (HIV)/hepatitis C virus (HCV)-coinfected subjects under highly active antiretroviral therapy (HAART). The objectives of this study were to obtain information about the mortality, the incidence of hepatic decompensations, and the predictors thereof in this population. In a multicenter cohort study, the time to the first hepatic decompensation and the survival of 1,011 antiretroviral naïve, HIV/HCV-coinfected patients who started HAART and who were followed prospectively were analyzed. After a median ( Abbreviations: AIDS, acquired immune deficiency syndrome; HAART, highly active antiretroviral therapy; HCC, hepatocellular carcinoma; HCV, hepatitis C virus; HDV, hepatitis D virus; HE, hepatic encephalopathy; HIV, human immunodeficiency virus; PHGB, portal hypertensive gastrointestinal bleeding; PI, protease inhibitor; RNA, ribonucleic acid. From the

Fast fibrosis progression between repeated liver biopsies in patients coinfected with human immunodeficiency virus/hepatitis C virus

“…25 The impact of immunosuppression on liver mortality is one reason for this recommendation. [2][3][4][5] In the present study, lack of control of HIV replication was a risk factor for progression. This is an additional reason to consider earlier ART initiation.…”

“…[12][13][14] On the contrary, in a prospective cohort of ART-naïve patients, HAART-mediated control of HIV RNA was a protective factor for liver-related death. 5 We found that fibrosis progression between liver biopsies was independently related with HIV RNA suppression both in the global study group and in the patients without anti-HCV treatment. A possible mechanism underlying the association of HIV suppression and fibrosis progression is the effect of HIV on fibrogenesis.…”

“…One of the cohorts was a collaboration of 11 centers, and the other cohort recruited patients from five centers from January 1997. 4,5 All individuals were evaluated at clinical visits scheduled every 3 months. Nine university hospitals participating in these cohorts followed 9,257 HIV/HCV-coinfected individuals from January 1986 to January 2008.…”

“…1 Low CD4 cell counts, lack of exposure to antiretroviral therapy (ART), and advanced liver disease are risk factors for liver events and mortality in cohort studies. [1][2][3][4][5] Particularly, CD4 cell recovery and suppression of HIV replication after starting highly active antiretroviral therapy (HAART) are predictors of survival free of complications of cirrhosis. 5 Most data on liver fibrosis progression in HIV and HCV coinfection come from cross-sectional studies that relied on a single liver biopsy.…”

“…[1][2][3][4][5] Particularly, CD4 cell recovery and suppression of HIV replication after starting highly active antiretroviral therapy (HAART) are predictors of survival free of complications of cirrhosis. 5 Most data on liver fibrosis progression in HIV and HCV coinfection come from cross-sectional studies that relied on a single liver biopsy. [6][7][8][9][10][11] In those studies, the date of HCV infection is usually estimated as the date of the first use of injection drugs.…”