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Clinical posts from members and guests of the Australasian Society for HIV, Viral Hepatitis and Sexual Health Medicine (ASHM) from various international medical and scientific conferences on HIV, AIDS, viral hepatitis, and sexual health.
Drugs and therapies
Drugs and therapeutic challenges were the themes of this morning’s session.
The plenary started with some excellent overview talks, especially one detailing the various attempts to induce activation of latently infected cells. Current strategies still in vogue are to use IL-7, (Eramune studies), or the HDACi inhibitor vorinostat. Studies using disulfiram or IFN-alpha have not been successful to date.
The next session was a series of important pharma-sponsored studies. First up Mills from Los Angeles presented 96 weeks data on maraviroc 150mg od with ritonavir boosted atazanavir, compared to truvada boosted atazanavir. It was a phase 2b study, so not many stats were presented. At 96 weeks 82% of the truvada arm were 50 copies/ml compared to 67.8% of the maraviroc arm. Most of the detectable VL in the maraviroc arm were in the 50-400 range, and the presenters focussed on this, and the lack of resistance and rather avoided discussing the primary outcome. I thought it was disappointing they appeared to gloss over this; surprisingly tese results have been taken as encouraging and a further study is planned, this time using ritonavir boosted darunavir and maraviroc.
Next up J Gallant presented the 48 weeks results of a ritonavir vs cobcistat booster comparison study. When used with truvada and atazanavir cobcicistat was non-inferior to ritonavir, in fact there was little to choose between them, except for the known rise in creatinine with cobicistat as it blocks creatinine active secretion in the tubules. Although non-significant, 5/6 who had renal dysfunction with cobicistat had proximal tubular disease, compared to 2/5 of renal dysfunction cases on ritonavir. Lipids were the same.
Pallela then presented the SPRIT study, which is a switch study from 2NRTIs plus a boosted PI to Eviplera. Patients were 50/ml prior to switching. Results showed switching did not compromise virological control, and lipids improved a bit. Thy did not stratify lipid changes by which PI was used. Interestingly, all 17 patients who were known to harbour the K103N mutation successfuly suppressed on a rilpivirine based regimen.
Finally Elion et al presented the 96 weeks data on study 145, a raltegravir versus elvitegravir double blind double dummy study in treatment experienced patients. I think all patients had a boosted PI in their regimen already, which makes interpreting differential lipid and GI toxicity difficult. Results were pretty equal between the arms with around 55-60% 50copies/ml, a CD4 rise of 200 cells, and about 40% discontinuations. Each arm developed resistance mutations to integrase inhibitors in 7% of cases. The resistance pattern was different however, with less N155H mutations in the elvitegravir arm, and a broader range of mutations seen. How this will impact on sequencing IIs and the role of dolutegravir aftr either raltegravir or elvitegravir failure was unfortunately not discussed.