HCV antiviral recipients, diabetics and those on lipid-lowering drugs at baseline were excluded from the study. Factors associated with a decreased risk of grade 3 or 4 hyperlipidaemia or lipid-lowering drug use were assessed by multivariate logistic regression. A total of 1587 HIV-monoinfected, 190 HIV/HBV-coinfected and 255 HIV/HCV-coinfected patients were evaluated. Most were male (85–92% for the 3 groups evaluated: HIV, HIV/HBV, HIV/HCV). The median

[interquartile range (IQR)] age at HAART initiation was 48 (44–56) years and was similar between groups. The median (IQR) CD4 count at HAART initiation was 245 (120–370) cells/μL in HIV-monoinfected participants, 195 (110–330) cells/μL in HIV/HBV-coinfected participants and 268 (140–409) selleck products cells/μL in HIV/HCV-coinfected participants. Factors associated with a decreased risk of grade 3 or 4 hyperlipidaemia or lipid-lowering drug use included HIV/HCV coinfection [odds ratio (OR) 0.46; 95% confidence interval (CI) 0.34, 0.61; P<0.0001], HIV/HBV coinfection (OR

0.74; 95% CI 0.55, 0.99; P=0.04), year of starting HAART after 2004 vs. 1997 or earlier (OR 0.37; 95% CI 0.29, 0.48; P<0.0001) and year of starting HAART between 1998 and 2003 vs. 1997 or earlier (OR 0.75; 95% CI 0.61, 0.92; P<0.01). Factors http://www.selleckchem.com/products/ly2157299.html associated with increased risk included age (OR 1.55; 95% CI 1.39, 1.72; per 10 years, P<0.0001) and male gender (OR 1.84; 95% CI 1.36, 2.48; P<0.0001). HIV/HCV and IMP dehydrogenase to a lesser extent HIV/HBV coinfections are protective against HAART-related hyperlipidaemia. HIV, hepatitis B virus (HBV) and/or hepatitis C virus (HCV) infections frequently co-exist because of common risk factors for exposure

[1,2]. A negative interaction results in many instances. On average, HCV viral loads are increased and liver fibrosis rates are accelerated in the presence of HIV [3,4] and mortality rates are increased [5]. CD4 T-lymphocyte recovery following the initiation of combination antiretroviral therapy is blunted in HIV/HCV coinfection, although the causative role of HCV remains debatable [3]. Also, the occurrence of liver-specific adverse events related to antiretroviral therapy is increased and the efficacy of HBV and HCV antiviral therapy is diminished [4–6]. In contrast to the prevailing negative relationship between HIV and HCV infections in terms of the effect on the coinfected individual, there is evidence that the abnormal lipid profile observed in many patients following the initiation of highly active antiretroviral therapy (HAART) may be less pronounced in those with HIV/HCV coinfection [7]. Lower total cholesterol and low-density lipoprotein (LDL) cholesterol levels have been reported in those with HCV infection, with and without advanced liver disease [8–13].