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DGDispatch
Switch to Atazanavir Normalizes Aberrant Cholesterol Values: Presented at IDSA
By Ed Susman
SAN FRANCISCO, CA -- October 13, 2005 -- In a small study, doctors demonstrated that by switching from 1 protease inhibitor to a second-generation drug it is possible to correct the dyslipidemia seen in patients with HIV receiving antiretroviral therapy.
"The switch does not affect high density lipoprotein (HDL) cholesterol levels significantly but may normalize total cholesterol, non-HDL cholesterol, low density lipoprotein cholesterol, and triglyceride levels," said Nicolas de la Pena, MD, research scientist, Associates in Infectious Diseases and Tropical Medicine, Pittsburgh, Pennsylvania.
In addition, the switch does not seem to compromise virologic and immunologic outcomes, he said in his poster presentation here on October 8th at the 43rd Annual Meeting of the Infectious Diseases Society of America (IDSA).
The use of highly active antiretroviral therapy (HAART) has led to increased life expectancy among patients infected with HIV. However, patients on such regimens can develop metabolic changes such as dyslipidemia that cannot always be corrected with dietary or lifestyle changes, he explained. On the other hand, some cholesterol-lowering agents in themselves sometimes interact adversely with the HAART regimen.
To determine whether a switch of therapy to antiretrovirals with fewer effects on lipid levels can help reduce lipid levels, Dr. de la Pena and colleagues identified 10 patients in their Pittsburgh practice who had developed lipid abnormalities while on protease inhibitor-based HAART regimens.
The study subjects had undetectable viral loads and mean CD4 counts greater than 550 cells/mL while on a HAART regimen that included protease inhibitors - nelfinavir, amprenavir, indinavir, or lopinavir boosted by ritonavir. All failed to see significant improvements in their cholesterol and triglyceride levels after following a diet and exercise regimen for 6 months.
All patients were switched from the protease inhibitor to atazanavir, a second-generation protease inhibitor that was designed to prevent unwanted lipid level changes. At 12 weeks, 24 weeks, 36 weeks, and 48 weeks of treatment, patients were monitored for fasting cholesterol, non-HDL cholesterol, low-density lipoprotein (LDL) cholesterol, and triglyceride levels as well as viral load and CD4 counts.
The average age of the patients was 43 years; 6 were men; half were African-American and half were Caucasian. The fasting total cholesterol averaged about 232 mg/dL and triglycerides averaged 343 mg/dL.
Results showed a decrease of 20% in total cholesterol after 24 weeks and by 29% after 48 weeks, a 20% decrease in non-HDL cholesterol after 24 weeks and 24% after 48 weeks, a 21% decrease in LDL cholesterol after 24 weeks and 24% after 48 weeks, a 40% decrease in triglycerides after 24 weeks and 64% after 48 weeks. There was no significant change in HDL cholesterol levels.
"This study shows that in HIV-infected patients who develop hyperlipidemia as a result of the protease inhibitor component in their HAART regimen, a simple switch to atazanavir may restore their cholesterol and triglyceride levels to near normal," Dr. de la Pena concluded.
The normalization often occurs within 6 months of treatment and is fully normalized after a year, he said. Using ritonavir-boosted atazanavir does not seem to affect lipid levels adversely.
He acknowledged that the small numbers of patients in the study limit its findings.
[Presentation title: Treatment of Hyperlipidemia With Switch Therapy to Boosted Atazanavir Among HIV Patients on Protease-Inhibitor-Based Antiretroviral Regimens. Abstract 813]
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