Impact of chronic hepatitis C infection on outcomes of patients with an advanced stage of HIV-1 infection in an area of low prevalence of co-infection

Author:

Hung C-C1,Chen M Y2,Hsieh S M2,Hsiao C F3,Sheng W H2,Chang S C2

Affiliation:

1. Department of Internal Medicine, National Taiwan University Hospital, 7 Chung-Shan South Road, Taipei and Department of Parasitology, National Taiwan University College of Medicine, Taipei, Taiwan

2. Department of Internal Medicine, National Taiwan University Hospital, 7 Chung-Shan South Road, Taipei, Taiwan

3. Division of Biostatistics and Bioinformatics, National Health Research Institutes, Taipei, Taiwan

Abstract

To ascertain whether hepatitis C (HCV) co-infection affects the progression of HIV infection, we initiated an eight-year prospective observational study at a university hospital in Taiwan where seroprevalences of HCV antibody and HIV antibody were low. Fifty-three (12.0%) consecutive non-haemophiliac HIV1-infected patients with HCV co-infection and 387 (88.0%) patients without HCV and hepatitis B co-infection were enrolled between June 1994 and June 2002 and observed until December 2002. Outcomes evaluated included the risk for acute hepatitis, hepatic decompensation, HIV disease progression and mortality, and changes of CD4+ count and plasma viral load (PVL) after initiation of highly active antiretroviral therapy (HAART) at the end of the study. The baseline CD4+ count, PVL and proportion of patients with AIDS-defining opportunistic illnesses (OI) at study entry were similar between patients with HCV co-infection and those without co-infection, but HCV-co-infected patients were older (39 versus 35 years, P = 0.01) and had a higher proportion of intravenous drug use (17.0% versus 0.8%, P < 0.001). After a total observation duration of 1137 patient-years (PY) (median, 791 days; range, 3–3053 days), the incidence of acute hepatitis in HCV-co-infected patients was 13.89 per 100 PY (95% confidence interval [CI], 13.31–14.49) and that in patients without co-infection was 6.39 per 100 PY (95% CI, 6.24–6.55 per 100 PY), with an adjusted odds ratio (OR) of 2.769 (95% CI, 1.652–4.640). At the end of the study, CD4+ count increased by 137 × 106 and 157 × 106/L in patients with and without HCV co-infection, respectively, ( P = 0.47). The proportions of achieving undetectable PVL (<400 copies/mL) after HAART was similar (76.7% versus 74.9%, P = 0.79). The adjusted OR for development of new AIDS-defining OI was 1.826 (95% CI, 0.738–4.522) in HCV-co-infected patients as compared with HCV- uninfected patients. The adjusted hazards ratio for death of HCV-co-infected patients when compared with those without co-infection was 0.781 (95% CI, 0.426–1.432). Our findings suggested that HCV co-infection was associated with a significantly higher risk for acute hepatitis in HIV-infected patients receiving antiretroviral therapy, but it had no adverse impact on virological, immunological and clinical responses to HAART and survival when compared with patients without HCV and HBV co-infection.

Publisher

SAGE Publications

Subject

Infectious Diseases,Pharmacology (medical),Public Health, Environmental and Occupational Health,Dermatology

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