HCV protects against abnormal blood lipids in HAART-treated HIV patients
HIV-positive patients treated with HAART who are also coinfected with hepatitis C virus (HCV) are less likely to have abnormally high levels of cholesterol or triglycerides according to a small Spanish study published as a research letter in the April 2003 edition of AIDS.
Investigators looked for the prevalence of hyperlipidemia and its risk factors among 197 HIV-positive men attending an outpatient clinic in Vizcaya, Spain. Patients had an average age of 36.8 years, most had injecting drug use as their risk factor for HIV and all were clinically stable.
Blood samples were obtained after an overnight fast. Hyperlipidemia was defined as total cholesterol or triglyceride levels greater than 200mg/dl.
In total, 29.9% of patients were found to have hyperlipidemia. Patients who had been receiving HAART for longer (average 26.7 months versus 24.4 months) were found to have a higher risk of abnormal lipid levels. Changes in body fat distribution were found more often in patients with high blood lipids (38.8%) compared to those with normal lipids (27.7%).
When investigators looked at the anti-HIV drugs that their patients had been treated with, they found that ‘patients treated with efavirenz had higher rates of hyperlipidemia than patients treated with nevirapine (49% versus 20.7%, respectively), and than those treated with PI (31.5%)’.
However, the most interesting finding of the study was ‘the appreciably lower rate of hyperlipidemia’ seen in HIV/HCV coinfected patients. The difference could not be attributed to viral load, as the proportion of HIV/HCV and HIV monoinfected patients with undetectable viral load was almost identical (66% versus 67%). Rather, the investigators attributed the difference to ‘HCV-induced hepatic dysfunction’.
The protective effect of HCV infection on lipids was only seen when a patient was treated with HAART, leading the investigators to theorise that ‘the interactions of HAART on lipidic metabolism seem to be neutralised by the HCV infection’. However, higher rates of body fat redistribution were found in patients coinfected with HIV/HCV (27% versus 11.8%).
It is difficult to know what to make of this study, and the article title is premature until confirmed by further research.
HCV/HIV-coinfection is a marker for iv-drug use which is associated with malnutrition (social reasons, lack of appetite due to opoids/constipation). This may result in lower lipids, which has been shown previously. In contrast, high triglycerides have been observed in a minority of HCV-monoinfected patients which are thought to be the result of high endogenous interferon levels. In addition, lipodystrophy is usually associated at least with higher triglycerides.