Curtis L Cooper1, Edward Mills, Jonathan B Angel. 1. Division of Infectious Diseases, The Ottawa Hospital, University of Ottawa, Ottawa, Ontario, Canada. ccooper@ottawahospital.on.ca
Abstract
BACKGROUND: Hyperlipidemia is a recognized complication of HIV antiretroviral therapy. The interactions between HIV, hepatitis C virus (HCV), antiretroviral agents and lipids are not well understood. METHODS: We evaluated the lipid data of patients receiving antiretroviral therapy at the Ottawa Hospital Immunodeficiency Clinic between January 1996 and June 2005 using a clinic database. RESULTS: A total of 357 HIV-mono-infected and 115 HIV/HCV-co-infected patients were evaluated. The mean changes in total cholesterol (mmol/l) from baseline to months 6 and 12 were 1.00 and 1.24 in HIV mono-infection, and 0.19 (P < 0.001) and 0.01 (P < 0.001) in HIV/HCV, respectively. Metabolic complications including hypercholesterolemia resulted in the interruption of HAART in HIV mono-infection (8%), but not in those with HIV/HCV (< 1%; P < 0.001). Eight per cent of HIV-mono-infected and no co-infected patients initiated lipid-lowering therapy while on their initial course of HAART (P < 0.001). Total cholesterol increased by 0.85 mmol/l in HIV/HCV-co-infected recipients of interferon-based HCV treatment achieving a sustained virological response (SVR), but did not change in those who did not achieve a SVR. CONCLUSION: HCV co-infection appears to confer a degree of protection from HAART-related lipid complications. The mechanism of this finding deserves evaluation. The implications of this observation for long-term cardiovascular disease risk remains a pressing issue.
BACKGROUND:Hyperlipidemia is a recognized complication of HIV antiretroviral therapy. The interactions between HIV, hepatitis C virus (HCV), antiretroviral agents and lipids are not well understood. METHODS: We evaluated the lipid data of patients receiving antiretroviral therapy at the Ottawa Hospital Immunodeficiency Clinic between January 1996 and June 2005 using a clinic database. RESULTS: A total of 357 HIV-mono-infected and 115 HIV/HCV-co-infectedpatients were evaluated. The mean changes in total cholesterol (mmol/l) from baseline to months 6 and 12 were 1.00 and 1.24 in HIV mono-infection, and 0.19 (P < 0.001) and 0.01 (P < 0.001) in HIV/HCV, respectively. Metabolic complications including hypercholesterolemia resulted in the interruption of HAART in HIV mono-infection (8%), but not in those with HIV/HCV (< 1%; P < 0.001). Eight per cent of HIV-mono-infected and no co-infected patients initiated lipid-lowering therapy while on their initial course of HAART (P < 0.001). Total cholesterol increased by 0.85 mmol/l in HIV/HCV-co-infected recipients of interferon-based HCV treatment achieving a sustained virological response (SVR), but did not change in those who did not achieve a SVR. CONCLUSION:HCV co-infection appears to confer a degree of protection from HAART-related lipid complications. The mechanism of this finding deserves evaluation. The implications of this observation for long-term cardiovascular disease risk remains a pressing issue.
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