Stribild® as Achille's Heel
This paper was originally published here, in French. We provide this translation for your convenience. Some practical aspects may differ where you live.
A patient at Clinique l'Actuel, screwed by Stribild ®
Development of a G118R mutation in HIV-1 integrase Following a switch to monotherapy dolutegravir ...
Montreal: another victim of Achille's Heel:
A 42-year-old Quebec man having sex with men was diagnosed with HIV-1 infection in 1999. He remained asymptomatic and ART-naive until 2013 with viral loads ,6000 copies/mL and CD4 cell counts > 500 cells/mL. Initiation of ART was considered in August 2014, when he presented with a CD4 cell count < 350 cells/mL and a viral load of 4000 copies/mL. Genotypic analysis revealed a subtype B infection and CXCR4 tropism. He tested
HLA-*5701 positive, contraindicative for abacavir.
In September 2014, he initiated a once-daily Stribild® regimen of elvitegravir/cobicistat/tenofovir disoproxil fumarate/emtricitabine and was virally suppressed for 5 months. In February 2015, the patient’s viral load was undetectable (< 40 copies/mL) and his CD4 cell count had increased to > 500 cells/mm3. The patient,
aware of the existence of so-called ‘light’ therapy prescribed elsewhere, requested a switch to dolutegravir monotherapy to minimize side effects. After discussion with the physician about potential problems involving monotherapy [Ch-E: so the doctor says ...], the patient was switched from Stribild® to dolutegravir monotherapy (Tivicay®) at that time.[Ch-E: Who writes the Rx ? The Doc, No ? ...]
The patient had detectable viral escape (< 50 copies/mL) in August 2015. Drug resistance testing on his plasma viral RNA on two occasions in August (300–800 copies/mL) revealed the acquisition of the G118R in viral integrase Analysis of the patient’s proviral cDNA revealed an absence of G118R in archived virus. Sequencing of
RT and protease revealed an absence of any acquired resistance mutations or polymorphisms. The integrase, RT and protease genes were all of subtype B origin.
In August 2015, the patient’s ART regimen was changed to darunavir/cobicistat/tenofovir/emtricitabine and his viral load returned to undetectable by September 2015. The patient has remained virally suppressed to date, indicative of treatment adherence.
Poor patient ... HLA * 5701 positive ... This may have helped him be asymptomatic for so long. Why enter the treatment on the basis of a single reading of CD4 < 350? Ah ... Yes ... The new US recommendations, with, as first choice, Stribild ®. Why start so early with the Tivicay® mono-therapy, whereas a Dual Therapy Tivicay® + Lamivudine could have made a reasonable step? See how the Doctor (Dr Thomas?), puts the blame on the patient? He would have learned about the mono Tivicay ®? Where so? On the internet probably. Oh ... Naughty boy! ... And he is pushing, despite admonitions by his doctor ... Yes ... But without prescription, the patient can do nothing ...
In the discussion, the authors note:
Bad luck, the marketing teams from their Southern neighbors had already managed to position the
You read, here, and nowhere else, about the Achilles heel, the Mono Tivicay as first Line, the extraordinary success of ANRS-4D, the negative recommendation by the HAS for Genvoya ®, the Montreal patient (another exclusive ...), then you begin to see the broad picture. That's it, you think you have it all!
Not so fast! You do not know yet the Munich patient, DoluMono, Domono (later, this October!), how the snowman melts, suicides during the START trial ... I have more! And the best!
The
Hop! (as Achille Talon would say) Good weekend and good fuck!
This paper was originally published here, in French. We provide this translation for your convenience. Some practical aspects may differ where you live.
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