Survival in patients with HIV infection and viral hepatitis B or C

Bonacini, Maurizio; Louie, Stan G.; Bzowej, Natalie; Wohl, Amy Rock

doi:10.1097/00002030-200410210-00008

Cited by 244 publications

(191 citation statements)

References 21 publications

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“…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.…”

Section: Discussionmentioning

confidence: 49%

“…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.…”

mentioning

confidence: 99%

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

et al. 2009

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Section: Discussionmentioning

confidence: 49%

mentioning

confidence: 99%

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

et al. 2009

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“…The levels of HBV replication are increased in HIV-infected patients. A more rapid progression of liver fibrosis and a higher rate of hepatic decompensation on cirrhosis (but not HCC) have been demonstrated in concurrently infected patients [25,26]. The risk of HBV-associated end-stage liver disease and liver-related mortality may be increased in HIV concurrent infection [26,27].…”

Section: Hbv and Hdvmentioning

confidence: 99%

Current therapy for hepatitis C or D or immunodeficiency virus concurrent infection with chronic hepatitis B

Chien

2008

Hepatol Int

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Concurrent hepatitis C virus (HCV), hepatitis delta virus (HDV), or human immunodeficiency virus (HIV) infection with chronic hepatitis B virus (HBV) appears to increase the risk of progressive liver disease including liver cirrhosis and hepatocellular carcinoma. There is a 10% prevalence of HCV infection in chronic HBV or HDV infection. Serological evidence of previous exposure to HBV is found in more than 80% of HIVpositive patients in the high risk group. Notably, the most recently acquired virus tends to suppress the pre-existing virus. In chronic HBV infection acquired perinatally or in early childhood, usually HCV is dominant and may suppress or even displace HBV and HDV. Less frequently, HBV or HDV suppresses HCV. It is generally agreed that the dominant virus should be identified in order to make appropriate treatment decisions. Studies with standard interferon (IFN) to treat patients with HCV dominantly dual HBV/HCV infection have showed only limited virological response. But high dose of IFN has been demonstrated with better response rate. Combined ribavirin with standard or pegylated IFN therapy could achieve a sustained HCV clearance rate comparable with those infected with HCV alone. On the contrary, patients with HBV dominantly dual viral infection might indicate more appropriate addition of lamivudine to IFN than ribavirin. Additionally, patients with concurrent infection of HBV and HDV, IFN seems to be the only effective agent. However, the efficacy of IFN is related to the dose. High dose of IFN [9 MU tiw (thrice per week)] and longer treatment duration (at least 2 years) have been shown to achieve adequate virological response. In patients with concurrently infected HBV and HIV, anti-HBV therapy should be considered for all patients with evidence of liver disease, irrespective of the CD4 cell count. In patients not requiring antiretroviral therapy, HBV therapy should be preferentially based on IFN, adefovir, or telbivudine. In contrast, in patients with CD4 cell counts \350 cells/ll or those already on antiretroviral therapy, agents with double anti-HBV and anti-HIV activity are preferred. At present, the evidence of therapeutic efficacy is not sufficient to make a recommendation in treating patients with dual HBV/HCV or HBV/HDV or HBV/HIV infection. Further studies of the well-designed, larger scale are needed to elucidate the role of different regimens or combination in the treatment of dual viral infection.

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“…HIV increases the risk of cirrhosis and end-stage liver disease in HBV coinfection [36]. In some studies, the risk of liver related mortality has been found to be 2-3 times higher in HIV/HBV co-infected patients than in HIV-mono-infected patients [37]. HIV co-infection with HBV is associated with more frequent flares of hepatic transaminases, which can occur with immune reconstitution inflammatory syndrome (IRIS) owing to ART, interruption of HIV/HBV treatment, or the development of resistance to HIV/HBV treatment.…”

Section: Hiv/hbv Co-infectionmentioning

confidence: 99%

HIV Co-Infection with Hepatotropic Viruses and Mycobacterial Tuberculosis

BU¹

2013

J AIDS Clin Res

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Survival in patients with HIV infection and viral hepatitis B or C

Cited by 244 publications

References 21 publications

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

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

Current therapy for hepatitis C or D or immunodeficiency virus concurrent infection with chronic hepatitis B

HIV Co-Infection with Hepatotropic Viruses and Mycobacterial Tuberculosis

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