Viramune and Reyataz questions
Apr 6, 2008
(1) Viramune (nevirapine) is listed as "alternative" regimen in the recently released DHHS guidelines (B2). Is this "simply because of the potential for hepatoxicity and the need for close monitoring for the first 18 weeks, OR is it because of nevirapine's lower efficacy/potency? (the 2NN study seems to indicate that nevirapine is as effective as efaivirenz, Sustiva.)
(2) The recent CASTLE study shows the non-inferiority of boosted Reyataz (atazanavir + a little ritonavir) to Kaletra (lopinavir + norvir). So why the A3 and A2 disparity in the strength of the recommendations?
(3) Most people seem to be taking boosted Reyataz with an NRTI backbone. I understand that that's necessary when the dual-NRTI is necessary. But if it's Epzicom (assuming the HLA-B*5701 test is negative), is unboosted Reyataz just as effective? Or are there general reasons for almost always using boosted 'taz?
Thank you very much.
Response from Dr. DeJesus
Loaded question...we could potentially discuss these in chapters, but here are a few quick answers:
1. You are correct, the reason why Viramune is recommended as an alternative regimen rather than a prefer regimen has to do mainly with the potential for toxicity, and not efficacy.
2. Before the results of Castle Study, presented at this year CROI, there were no large, randomized clinical trials comparing boosted atazanavir to another preferred PI regimen in nave patients. The new set of DHHS guidelines were released just a few days before CROI 08, when the Castle data were presented; so these Castle data were not considered in the revision of this last set of guidelines. It is possible that the strength of this recommendation will then change on the next set of revised guidelines later this year.
3. As a rule, boosted PI's are preferred over unboosted PI's due to the higher concentrations achieved by boosted PI's, increasing the IQ or viral inhibitory quotient and thus increasing the efficacy and the likelihood of virologic suppression; as well as decreasing the potential for the development of resistant mutations upon virologic failure. This was originally a theoretical mathematical calculation that have proven to be true in many studies including the original studies comparing Viracept (unboosted PI) to Kaletra, and most recently in a study comparing boosted vs unboosted atazanavir.
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