It`s very useful stuff, Malcolm, interesting and informative as always. Many thanks for taking the time to share this.
Wishing you, and everyone else here, all the very best of luck in achieving SVR, goodness knows you deserve it! ~ Jill xx
mallani said
Aug 22, 2012
Hi guys, Glad you're interested. It's sometimes hard to know if anyone other than me, finds this stuff useful. The SVR figures for Inc. and Vict. are virtually identical, unlike the trials, and my doc gets the impression Vict. is being prescribed more. Maybe patients are researching, and don't like the rash or anorectal issues. I still find the high pill burden of Vict. to be a pain.
Alan, you have probably healed yourself to an F2 now, so will be fine!
Tim, who knows. Maybe you're done enough.
JoAnne, I'm also happy with >70% although I was told 80% based on my early VL's.
Dave and Karen, Thanks for the kind words. Cheers.
hrsetrdr said
Aug 22, 2012
JoAnneh wrote:
I am excited I have 70 percent chance! Do glad to have hope at F4 but 48 weeks is frightening So I will just get thru today. Having to rest more than I want to. Week 14 of 48 Hail to new discoveries JoAnne
JoAnne, wishing you low sx and high SVR!
-Tim
JoAnneh said
Aug 21, 2012
I am excited I have 70 percent chance! Do glad to have hope at F4 but 48 weeks is frightening So I will just get thru today. Having to rest more than I want to. Week 14 of 48 Hail to new discoveries JoAnne
davesf said
Aug 21, 2012
Tim/Alan, If we don't hit SVR we'll try some of those upcoming cushy drugs next.
Malcolm, thanks again for bringing greater understanding and clarity of our disease. It's a blessing to have a medically educated cotraveler on this forum.
All the best, Dave
Karen said
Aug 21, 2012
Hi Malcolm...
Read your post, very informative.
My doc basically explained the same story. He also mentioned that there are issues w/SOME of the new drug trials-mutation of the virus. Currently, they are seeing this mainly with patients who are unable to complete treatment.
Mutation is currently my main concern. If your doctor is not talking about this point you need to ask the question before starting any treatment.
Ps..nice new photo
hrsetrdr said
Aug 21, 2012
Malcolm,
Thanks for yet another informative post that helps to put our 'situation' in a reality-based perspective.
I know that in my case, having only 16 weeks of tx that my chances of SVR are low; however, I'll be interested in seeing my next VL, week after next.
It will be a long 3 or 4+ year wait until any 'oral-only' treatments are available...'tis my only hope.
LUV2RYDE said
Aug 21, 2012
Wow the chances are pretty good. And with a little time the chances are going to get even better. Wish I had a wand to take everyone's away or good period.
mallani said
Aug 21, 2012
Hi Alan, all this came from my doc who's just been to Meetings in the USA. I asked about reducing to 36 weeks in view of my sRVR, and got a firm 'no'. The 36-48 weeks for F3's has come about from clinical experience, but I haven't seen anything in print. Cheers.
news said
Aug 21, 2012
It is ironic that this thread has been started right now. I came across an article recently that said many physicians are going to 48 week triples for Stage 3-4 fibrosis patients. That's me. And I only did 36 weeks. I approached the doctor about this. he responded that they extended from 24 to 36 weeks because I was not completely UND at 4 weeks, and decided to balance the bad effects of treatment with the efficacy of a 48 week treatment. they arrived at a 36 week protocol for me. I believe in my doctor, and am confident that we made the right choice. But it seems many doctors and patients have decided that the additional 12 weeks of discomfort and exposure to risk is justified by the increase in SVR odds. I just hope I didn't make a mistake. After the Incivek triple, I think I am seriously limited on what I can do next.
Alan
Margo said
Aug 21, 2012
Very informative but scared me a bit...I am 1b, double therapy failed, hope triple works...
mallani said
Aug 21, 2012
It is an unfortunate fact that not all of us undergoing Rx will achieve SVR. To understand why, it is necessary to understand some features of our virus, and the effects of Rx. HCV first appeared in the early 1900's, and all genotypes and their subgroups are thought to have evolved from the original 1b genotype. As an RNA virus, it should be easy to obtain a vaccine eg. poliovirus is another RNA virus. A feature of our virus is it's ability to mutate. As it replicates, it makes mistakes, so we end up with a family of viruses with slightly different genetic material. This is why it is so difficult to culture and treat. Not all mutations are a problem- many cannot enter cells or replicate. However, some mutations have been identified that can replicate and have resistance to antiproteases. This is why we need triple therapy- the antiproteases knockout the original (in the wild) virus, and the Int. and Riba. control the mutations. Many of us will have a number of "undetecteds" in our VL. Why do some of us remain undetected after Rx stops?
Undetected means just that. The VL test can't detect any viral material. However, that doesn't mean we have zero circulating virus. After Rx stops, the virus is again free to replicate. Whether this is in the wild type virus or a resistant mutation is immaterial.
Hidden reservoirs of virus: Our virus relicates in hepatocytes, using our intracellular material. Whether the virus can replicate in other tissues has been the subject of much research. Blood monocytes, lymph tissue, brain, muscle have all been mentioned. It is still uncertain whether these can provide new virus, to cause SVR failure.
SVR is less likely in patients with liver fibrosis, particularly the F4's (cirrhotics) and the F3's., irrespective of sRVR. This suggests the rebound in virus comes from intrahepatic virus. Liver fibrosis decreases liver perfusion with blood, so some liver nodules may not receive adequate exposure to the drugs. This is why F4's need prolonged treatment ( F3's are now thought to need at least 36 weeks Rx).
So, with the early antiproteases, it is still a lottery. Good luck to all of us.
mallani said
Aug 21, 2012
Sorry Margo, didn't intend to scare anyone. SVR rates for F0-F2 patients is >90%, >80% for F3's and >70% for F4's. This is for Geno 1's. It would be wonderful if researchers could work out how to come up with a test to tell us who has zero viral material at end of Rx. Predictors of who will achieve SVR has been attempted, but have been unsuccessful (to my knowledge).
The newer drugs seem to be getting higher SVR's across the board, without the Sx of Peg. and Riba. No new research is being done on Incivek and Victrelis. All current research involves the antipolymerases ( part. GS7977), other antiproteases, other methods of blocking viral replication etc. It is amazing that Inciv. and Vict. are 'yesterday's' drugs, when they are yet to be approved or used in many countries. They have played their part, lifting SVR rates by 20-30% and showing researchers they are on the right track.
-- Edited by mallani on Tuesday 21st of August 2012 01:39:06 PM
It`s very useful stuff, Malcolm, interesting and informative as always. Many thanks for taking the time to share this.
Wishing you, and everyone else here, all the very best of luck in achieving SVR, goodness knows you deserve it!
~ Jill xx
Hi guys, Glad you're interested. It's sometimes hard to know if anyone other than me, finds this stuff useful. The SVR figures for Inc. and Vict. are virtually identical, unlike the trials, and my doc gets the impression Vict. is being prescribed more. Maybe patients are researching, and don't like the rash or anorectal issues. I still find the high pill burden of Vict. to be a pain.
Alan, you have probably healed yourself to an F2 now, so will be fine!
Tim, who knows. Maybe you're done enough.
JoAnne, I'm also happy with >70% although I was told 80% based on my early VL's.
Dave and Karen, Thanks for the kind words. Cheers.
JoAnne, wishing you low sx and high SVR!
-Tim
Do glad to have hope at F4 but 48 weeks is frightening
So I will just get thru today. Having to rest more than I want to.
Week 14 of 48
Hail to new discoveries
JoAnne
Tim/Alan, If we don't hit SVR we'll try some of those upcoming cushy drugs next.
Malcolm, thanks again for bringing greater understanding and clarity of our disease. It's a blessing to have a medically educated cotraveler on this forum.
All the best, Dave
Hi Malcolm...
Read your post, very informative.
My doc basically explained the same story. He also mentioned that there are issues w/SOME of the new drug trials-mutation of the virus. Currently, they are seeing this mainly with patients who are unable to complete treatment.
Mutation is currently my main concern. If your doctor is not talking about this point you need to ask the question before starting any treatment.
Ps..nice new photo
Malcolm,
Thanks for yet another informative post that helps to put our 'situation' in a reality-based perspective.
I know that in my case, having only 16 weeks of tx that my chances of SVR are low; however, I'll be interested in seeing my next VL, week after next.
It will be a long 3 or 4+ year wait until any 'oral-only' treatments are available...'tis my only hope.
Wow the chances are pretty good. And with a little time the chances are going to get even better. Wish I had a wand to take everyone's away or good period.
Hi Alan, all this came from my doc who's just been to Meetings in the USA. I asked about reducing to 36 weeks in view of my sRVR, and got a firm 'no'. The 36-48 weeks for F3's has come about from clinical experience, but I haven't seen anything in print. Cheers.
It is ironic that this thread has been started right now. I came across an article recently that said many physicians are going to 48 week triples for Stage 3-4 fibrosis patients. That's me. And I only did 36 weeks. I approached the doctor about this. he responded that they extended from 24 to 36 weeks because I was not completely UND at 4 weeks, and decided to balance the bad effects of treatment with the efficacy of a 48 week treatment. they arrived at a 36 week protocol for me. I believe in my doctor, and am confident that we made the right choice. But it seems many doctors and patients have decided that the additional 12 weeks of discomfort and exposure to risk is justified by the increase in SVR odds. I just hope I didn't make a mistake. After the Incivek triple, I think I am seriously limited on what I can do next.
Alan
It is an unfortunate fact that not all of us undergoing Rx will achieve SVR. To understand why, it is necessary to understand some features of our virus, and the effects of Rx. HCV first appeared in the early 1900's, and all genotypes and their subgroups are thought to have evolved from the original 1b genotype. As an RNA virus, it should be easy to obtain a vaccine eg. poliovirus is another RNA virus. A feature of our virus is it's ability to mutate. As it replicates, it makes mistakes, so we end up with a family of viruses with slightly different genetic material. This is why it is so difficult to culture and treat. Not all mutations are a problem- many cannot enter cells or replicate. However, some mutations have been identified that can replicate and have resistance to antiproteases. This is why we need triple therapy- the antiproteases knockout the original (in the wild) virus, and the Int. and Riba. control the mutations. Many of us will have a number of "undetecteds" in our VL. Why do some of us remain undetected after Rx stops?
Undetected means just that. The VL test can't detect any viral material. However, that doesn't mean we have zero circulating virus. After Rx stops, the virus is again free to replicate. Whether this is in the wild type virus or a resistant mutation is immaterial.
Hidden reservoirs of virus: Our virus relicates in hepatocytes, using our intracellular material. Whether the virus can replicate in other tissues has been the subject of much research. Blood monocytes, lymph tissue, brain, muscle have all been mentioned. It is still uncertain whether these can provide new virus, to cause SVR failure.
SVR is less likely in patients with liver fibrosis, particularly the F4's (cirrhotics) and the F3's., irrespective of sRVR. This suggests the rebound in virus comes from intrahepatic virus. Liver fibrosis decreases liver perfusion with blood, so some liver nodules may not receive adequate exposure to the drugs. This is why F4's need prolonged treatment ( F3's are now thought to need at least 36 weeks Rx).
So, with the early antiproteases, it is still a lottery. Good luck to all of us.
Sorry Margo, didn't intend to scare anyone. SVR rates for F0-F2 patients is >90%, >80% for F3's and >70% for F4's. This is for Geno 1's. It would be wonderful if researchers could work out how to come up with a test to tell us who has zero viral material at end of Rx. Predictors of who will achieve SVR has been attempted, but have been unsuccessful (to my knowledge).
The newer drugs seem to be getting higher SVR's across the board, without the Sx of Peg. and Riba. No new research is being done on Incivek and Victrelis. All current research involves the antipolymerases ( part. GS7977), other antiproteases, other methods of blocking viral replication etc. It is amazing that Inciv. and Vict. are 'yesterday's' drugs, when they are yet to be approved or used in many countries. They have played their part, lifting SVR rates by 20-30% and showing researchers they are on the right track.
-- Edited by mallani on Tuesday 21st of August 2012 01:39:06 PM