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Switching to Atazanavir (Reyataz) Lowers Cholesterol and Triglycerides, but No Improvement in Artery Function

SUMMARY: Switching from another protease inhibitor to boosted atazanavir (Reyataz) lowered blood cholesterol and triglyceride levels in people with suppressed HIV in a 24-week study, but did not improve endothelial (blood vessel) function or reduce inflammation biomarkers, according to a small study reported in the March 27, 2010 issue of AIDS.

By Liz Highleyman

People with HIV are at higher risk for cardiovascular disease compared with the HIV negative general population, but it is not clear whether this is due to long-term HIV infection itself, antiretroviral therapy (ART), or traditional risk factors.

Chronic HIV infection can lead to ongoing inflammation, and some antiretroviral drugs can cause metabolic changes including elevated total and low-density lipoprotein (LDL) "bad" cholesterol and reduced high-density lipoprotein (HDL) "good" cholesterol. Both inflammation and metabolic abnormalities contribute to atherosclerosis, or build-up of plaque in the arteries; dysfunction of the endothelial lining of the arteries is an early step in this process.

Robert Murphy and fellow investigators with the SABAR Study Team aimed to determine whether the protease inhibitor atazanavir -- which is known to be more "lipid-friendly" than other drugs in its class -- would have a beneficial effect on arterial function and other metabolic and inflammatory risk factors for cardiovascular disease.

This prospective multi-national trial included 50 HIV positive patients receiving stable protease inhibitor-based ART with plasma HIV RNA < 500 copies/mL. Inclusion criteria included elevated blood lipids at baseline, with either fasting LDL levels > 130 mg/dL or triglyceride levels > 200 mg/dL.

Most participants (85%) were men. The median CD4 cell count was high, at 499 cells/mm3. At baseline, the median total cholesterol level was 204 mg/dL, median LDL cholesterol was 122 mg/dL, and median triglyceride level was 244 mg/dL. People with uncontrolled diabetes, high blood pressure, and > 1 pack/day smokers were excluded (though nearly half smoked some).

Participants were randomly assigned to either continue on their current protease inhibitor -- usually lopinavir/ritonavir (Kaletra) -- or switch to atazanavir plus a boosting dose of ritonavir (Norvir) for 24 weeks; 26 patients switched and 24 stayed on their existing regimen.

The investigators measured blood lipid levels, inflammatory and metabolic biomarkers, and brachial artery (upper arm) flow-mediated dilation (how well an artery responds to changes in blood flow) at baseline, week 12, and week 24.

Results

At 24 weeks, participants who switched to atazanavir experienced significantly more favorable changes in blood lipid levels than those who remained on the old regimen:
 
Total cholesterol: -25 vs +1.5 mg/dL, respectively (P = 0.009);
Non-HDL cholesterol: -27 vs -0.5 mg/dL, respectively (P = 0.014);
Triglycerides: -58 vs +3.5 mg/dL, respectively (P = 0.013).
However, there were no significant changes in flow-mediated dilation in either treatment group after 12 or 24 weeks.

Based on these findings, the researchers concluded, "In dyslipidemic individuals with suppressed HIV RNA on stable therapy, changing the protease inhibitor to atazanavir/ritonavir for 24 weeks improved lipids; however, endothelial function, inflammatory, and metabolic markers did not change."

Northwestern University Center for Global Health, Northwestern University, Chicago, IL; ACLIRES Argentina SRL, Buenos Aires, Argentina; University of Cincinnati, Cincinnati, OH; University of Southern California Keck School of Medicine, Los Angeles, CA; University of Modena and Reggio Emilia, Modena, Italy; University of California-San Diego, San Diego, CA; SigmaClinical, Daglan, France; University of Wisconsin School of Medicine and Public Health, Madison, WI.

4/6/10

Reference

RL Murphy, B Berzins, C Zala, and others. Change to atazanavir/ritonavir treatment improves lipids but not endothelial function in patients on stable antiretroviral therapy. AIDS 24(6): 885-890 (Abstract). March 27, 2010.


 

 

 

 

 

 

 

 

 

 

 

 

 

 

 


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