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Don’t take this the wrong way but……sometimes when I read this forum I think people could be forgiven for thinking the DAAs cause certain individuals to LOSE THEIR FUCKING MINDS!
Lighten up, Chester. I thought we agreed we would play the ball not the man.
Or does this restriction apply only to the critics of Prof Gane and not his defenders?
Male Geno 1a F3-4 Tx Naive
Contracted early 1970s Diagnosed 2012
Started 12 wks TWINVIR (Sof/Led) on 15 Nov 2015
Pre-treatment VL 1.8 million
UND at 8 Dec 2015; UND at 12 Jan 2016
Ended 12 wks TWINVIR on 6 Feb 2016
9 Feb 2016 EOT VL test <15 PCR Negative
UND at 3 May 2016 SVR12Thanks Lynne. It seems you are not much further ahead in treatment than I am. I will finish my 12-week course of Twinvir on Saturday. I will also post my results EOT. The best way to rebut Prof Gane is to show that that people using generics containing unlicensed Chinese-made ledipasvir (which seems to be the generic drug Prof Gane is most concerned about) can achieve SVR rates comparable to the equivalent branded medicines. People on the branded medicines, as well as people on generics (licensed and unlicensed), can relapse and no-one is expecting the generics to actually do better than the equivalent brand medicines. So stories of occasional relapse on generics do not call into question the efficacy of generics any more than occasional relapses on brands call into question the efficacy of the brands. What matters is to establish an overall picture of SVR rates for generics, particularly the unlicensed generics, which is comparable to the brand versions; that can only emerge if generic-users share their post-treatment results, whether as part of a formal study, as I understand Dr Freeman’s to be, or not.
Asif – thanks for your post. My on-treatment results have been fine. Pre-treatment my VL was 1.8 million with ALT 176 and AST 106 . By week 4 of treatment my VL was undetected and my ALT and AST were both back in the normal range. At week 8 of treatment I remained VL undetected. However, according to Prof Gane little reassurance can be obtained from on-treatment results. What matters is the post-treatment results. This is because where ledipasvir is combined with sofosbuvir, which it usually is, Prof Gane says the sofosbuvir may be effective while the ledipasvir is not. In this situation, according to Prof Gane, the sofosbuvir alone can maintain viral-suppression as long as treatment is maintained but when treatment is finished if the ledipasvir component of the medicine was ineffective the virus will then spring back causing relapse.
Chapel – thank you for posting the link. I agree with you that Prof Gane’s remarks seem to suggest that one way to respond to relapse – should it happen – is to go on permanent, lifelong sofosbuvir treatment, which alone should be enough to maintain viral suppression, if not cure – a bit like I understand that HIV patients take permanent, lifelong viral suppression medication. Is this correct? Could this be a way of dealing with relapse?
Male Geno 1a F3-4 Tx Naive
Contracted early 1970s Diagnosed 2012
Started 12 wks TWINVIR (Sof/Led) on 15 Nov 2015
Pre-treatment VL 1.8 million
UND at 8 Dec 2015; UND at 12 Jan 2016
Ended 12 wks TWINVIR on 6 Feb 2016
9 Feb 2016 EOT VL test <15 PCR Negative
UND at 3 May 2016 SVR12From Gilead Page:
HARVONI was administered once daily by mouth in these trials. Sustained virologic response (SVR12) was the primary endpoint and was defined as HCV RNA less than LLOQ at 12 weeks after the cessation of treatment.Thank you, Enkel, for pointing out (post#7415 on this thread and some other posts on other threads) that SVR12 is, apparently, not limited, as I had previously thought, to being HCV RNA undetected at 12 weeks after the last dose of treatment. Thanks also for backing this up with the quote above from a Gilead document which states that the definition of SVR12 used for the ION clinical trials into Harvoni (sof/led) was being below the LLOQ (Lowest Limit of Quantification) at 12 weeks post EOT (end of treatment). I assume that if this is the meaning of SVR12 used by Gilead in the ION trials it must be a meaning which is accepted not just by Gilead but also by the wider medical and scientific community.
It seems to me, if my understanding is correct, that, potentially at least, being below the LLOQ is not quite the same thing as being undetected at 12 weeks post-EOT (although clearly it includes being undetected at 12 weeks post-EOT). Is this correct? For example, does being below LLOQ for this purpose include being
LLOQ, which would constitute relapse and failure to attain SVR12. Another thing that puzzles me about this more lenient definition of SVR12 is that if someone achieves UND at EOT but then their VL test comes back
Male Geno 1a F3-4 Tx Naive
Contracted early 1970s Diagnosed 2012
Started 12 wks TWINVIR (Sof/Led) on 15 Nov 2015
Pre-treatment VL 1.8 million
UND at 8 Dec 2015; UND at 12 Jan 2016
Ended 12 wks TWINVIR on 6 Feb 2016
9 Feb 2016 EOT VL test <15 PCR Negative
UND at 3 May 2016 SVR12Hi Sonix, I am in the UK not Australia. I agree it can be helpful to see a poster’s country of origin in their signature but it can also be recorded in the profile.
Enkel, blood tests on the NHS (National Health Service – the UK public-funded health service) are free. Privately purchased blood tests in the UK can vary in price, but probably about £200 for HCV viral load qualitative; £150 for HCV viral load quantitative; and £80 for FBC and liver function test. So if you intended to have 3 sets of bloods, one at 4/52, one at EOT and finally one at SVR12, NHS monitoring could save you as much as £600 – £700.
Thanks, LG, for pointing out the significance of the cost and budgetary aspect. I think you may be right that this was a factor in my GP thinking it would be more appropriate for the hospital hepatology dept, rather than his GP practice, to do my VL monitoring. However, I’m grateful to my GP for interceding on my behalf with my hospital consultant: this may have been influential in securing my VL monitoring.
Perhaps the most significant thing to emerge from this thread is that of the 5 UK-based people who have broached the issue of generic-monitoring with NHS doctors – whether by GPs or consultants – all but Alsdad – perhaps because he was the first – have managed to get it. So maybe things are not now quite so grim for generic-using patients in the UK as is sometimes thought.
Male Geno 1a F3-4 Tx Naive
Contracted early 1970s Diagnosed 2012
Started 12 wks TWINVIR (Sof/Led) on 15 Nov 2015
Pre-treatment VL 1.8 million
UND at 8 Dec 2015; UND at 12 Jan 2016
Ended 12 wks TWINVIR on 6 Feb 2016
9 Feb 2016 EOT VL test <15 PCR Negative
UND at 3 May 2016 SVR12To my pleasant surprise, and to my NHS consultant’s credit, I am receiving NHS monitoring for my Twinvir (Sof/Led) treatment.
I wasn’t expecting this because I got short shrift from my consultant when I asked him for a script for generics. (I got my script from Dr Freeman at GP2U instead.)
I found my GP more receptive to my use of generics and he agreed to do a full blood test for me (ALT and AST came back normal – pretreatment both were raised) but said he didn’t have the authority to obtain a VL test for me. My consultant agreed to do VL tests for me but wrote to me that this was not to be taken as an endorsement either by him or by the NHS of my use of generics which was “entirely at my own risk” – something I was very happy to agree to.
Male Geno 1a F3-4 Tx Naive
Contracted early 1970s Diagnosed 2012
Started 12 wks TWINVIR (Sof/Led) on 15 Nov 2015
Pre-treatment VL 1.8 million
UND at 8 Dec 2015; UND at 12 Jan 2016
Ended 12 wks TWINVIR on 6 Feb 2016
9 Feb 2016 EOT VL test <15 PCR Negative
UND at 3 May 2016 SVR12 -
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