RT @KirbyInstitute: David Cooper was a world-leading infectious diseases researcher & doctor. Sadly, he passed away in 2018. He believed ac…
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.
Yesterday afternoon climaxed with some exciting late breaker oral presentations.
CONSORT study- This study showed that isoniazid prophylaxis (vs placebo) reduced active Tuberculosis over a 4 year period. 1369 patients were given 12 months of INH. Participants were all HIV positive, and 50 on cART. Most benefit seemed to be in the first year, although an effect was seen over the full study course. The HR was 0.63 for active TB (95% CI 0.41-0.94) p=0.03. They didn’t screen for latent T, unlike in Australia, because the Cape Town setting of this study meant that TB is exposure is the norm, indeed 40% had a history of prior TB. Interestingly 70% of the participants were already on cART, and 30% started cART at the commencement of the study. Resistance to INH in the 95 who did manifest TB remains to be determined. In such a high exposure environment, is this prophylaxis of latent TB or prophylaxis against new acquisition?
SPRING-2- Double blind double dummy RCT of 2 NRTIs plus dolutegravir or raltegravir in 800 treatment naives. VL 50 in 88% and 85% at 48 weeks respectively, proving non-inferiority. Both drugs were really well tolerated, andthere was little to choose between them. No treatment emergent II resistance was seen in the dolutegravir arm, and just one case in the raltegravir arm. There was no difference for VL 100,000 nor between truvada and kivexa as the backbone. Dolutegravir inhibits creatinine tubular secretion, so the eGFR appeared to drop by 15mls/min, but this was not a true reflection of renal function.. it muddies the waters a bit though when trying to interpret creatinines on people on tenofovir.
HPTN 052- this analysis of the treatment as prevention study analysed clinic events in those starting immediately, or waiting to CD4 of 250. A combined endpoint of nonAIDS and AIDS did not show a difference, but there was a statistically significant reduction in AIDS evets. Questions from the audience focussed on the fact that this was all driven by diagnoses of extrapulmonary TB from just one clinical site, and that the average CD4 at commencement in the delayed arm was about 220-230, so much lower than we would ever wait in Australia.