Hyperlipidemia is an unwelcome complication of protease inhibitor (PI)-based antiretroviral regimens and a risk for cardiovascular disease. At present, atazanavir is the only PI that is not associated with hyperlipidemia.

The objective of the BMS AI424067 study, which was presented at the 12^th CROI meeting, was to demonstrate that HIV PI-associated hyperlipidemia can be reversed when the patient’s PI is switched to atazanavir. Since lipid reduction is associated with a reduction in cardiovascular disease risk in non-HIV-infected patients, the assumption is that there will be a similar effect in patients with HIV disease.

Managing HIV PI–associated hyperlipidemia is a significant challenge for clinicians. Nonetheless, clinicians are often reluctant to change PI-based regimens in patients who have achieved viral control.

This study demonstrated that switching the PI in a "successful" regimen to unboosted atazanavir greatly improves lipid profiles. Furthermore, viral suppression was maintained at least through the 12 weeks of the study.

Although the use of unboosted atazanavir may be an efficient strategy in avoiding PI-associated hyperlipidemia, I doubt that most physicians are comfortable in "playing the PI card" with an unboosted PI.

Will the lipid neutrality of atazanavir be lost when boosted with ritonavir? Will the viral suppression seen in ritonavir-boosted regimens also be seen with unboosted atazanavir long term? Until these questions are answered, most clinicians will almost always be comfortable using boosted atazanavir.