Aa
HEPATITIS RESEARCHER or JIM
I'm seroiously contemplating re-treating with Infergen/riba and Alinia. The clinical trial which took place in Egypt with Alinia was it tested on type 4 only and if so is type 4 similiar to type 1A in regards to its toughness as a strain of the virus? Also, HR do you think my doc will prescribe the Alinia and if not do you beleive the stuff from the Mexican pharms would be the legitimate product? One more thing do you think I would have to only treat with the Alinia for the fisrt three monthes to get the desired effect from it?
HRs analogy above is enough to get me to pull my covers over my head and be REAL still:) OK, just trying to get my somewhat short mental arms 'round all this and come up with some kind of plan. As a 3/1 my time is running short. My hepotologist is offering me 4 choices(earlier post) soc, albu. int.(4weeks tween doses) 950 phase 3, alania + soc. My answer to these choices is YES, only I don't have THAT choice right now. SO, what about something like this. Go for the alinia/soc/ppc and hope for the best. If it were to fail there is hope that being that there were 00 relaspers, and this might mean that "NTZ reduces the invisable residue...because there is no real resistance"hr, I could aviod making NTZ super bugs. If I were lucky the treatment time might even improve or at least mark time for my liver. Do the anti-fibrotic thing for awhile and when hard hitting telaprevir can be used w/ rescues, and maybe albumin with its' reduced sx along with alinia again, well wham bam thank you mam!! This is why I am so interested in the alinia failures as to how, non-responce/breakthru also evr rvr. jerry
Your son is blessed to have you as an advocate. There is no reason for this "gap" in care, but hopefully his new doctor will come up with the right plan. That said, if you're more comfortable with the "well-published Hep C specialist", you might try calling that offfice directly and make the same case. My heart goes out to you and your son.
-- Jim
-- Jim
Therefore you suggest:
"If you want to play it perfect, you would have to stop SOC once you know you are responding, let your quasispecies return to "wild type" and then hit it with simulstart to optimize the SVRupping effect of Tela".
So in this case, once response was established, one would wait for what in Jack London terms might be "The Call of the Wild" -- then jump to #3 (above) with more confidence to obliterate any emerging mutants with SOC before they can hide like the sissies they are behind the skirt of still too imperfect TMAs.
Still, even by your language, i.e. "If you want to play it perfect" aren't we talking shades of grey that could be quantified via trial and then correlated with degrees of interferon response? It may turn out that the difference between "perfect" and reality may not be a lot, at least with the stronger interferon responders. Or are they going to skip this step altogether and just add another antiviral to the mix. And where is the FDA in all this? Would they have a concern in treating interferon non-responders with a single antiviral and SOC? Hopefully, there will be a lot of good reading out of all this in the months to come. Just hope they are more attentive than the audience in your Hep B auditorium example :)
-- Jim
"If you want to play it perfect, you would have to stop SOC once you know you are responding, let your quasispecies return to "wild type" and then hit it with simulstart to optimize the SVRupping effect of Tela".
So in this case, once response was established, one would wait for what in Jack London terms might be "The Call of the Wild" -- then jump to #3 (above) with more confidence to obliterate any emerging mutants with SOC before they can hide like the sissies they are behind the skirt of still too imperfect TMAs.
Still, even by your language, i.e. "If you want to play it perfect" aren't we talking shades of grey that could be quantified via trial and then correlated with degrees of interferon response? It may turn out that the difference between "perfect" and reality may not be a lot, at least with the stronger interferon responders. Or are they going to skip this step altogether and just add another antiviral to the mix. And where is the FDA in all this? Would they have a concern in treating interferon non-responders with a single antiviral and SOC? Hopefully, there will be a lot of good reading out of all this in the months to come. Just hope they are more attentive than the audience in your Hep B auditorium example :)
-- Jim
It's a sad story to be true. This is my H - probable cirrohsis dx by bx - I didn't push him to go 72 even though I knew he probably should. His doc freaked when his PCR came back 2 weeks after treatment and then the next week it was up to 28,000 so he told him to "start back up immediately" and H complied. He had effectively at this point a 3 week break in treatment. His doc is done with him, won't see him again and scheduled him at the big state U at week 12. He's getting blood draws only because we had blank lab slips and had an 8 week PCR (blank signed lab slips are wonderful) but I don't think the doc will call us unless his neuts fall or his Hemo falls drastically if they are even looking at the test results so he's "doctorless" until big state U appointment week 12. I'm getting copies of labs to bring to big State U (and to keep an eye on H since no one else is) and they have his file through week 48 of the original treatment. He's got meds that will last 'til the appointment, although I know that the doc who is really not his doc anymore will call in a refill if we call and demand. Our family doc tells my H it's a good thing he's got an "advocate" me, but has zip to add doctor-wise, he's shocked that H has this and that his liver is in such bad shape after knowing both of us for over 20 years (small town). It's a sad medical world we live in these days. Big State U called today at 4:45 and tried to move H's appointment 2 more months out and I lost it. I told them my H was injecting himself and pilling himself with no medical supervision and it was all begining to smell like medical malfesance albeit not theirs so they found "another" spot for him in 2 weeks with the head of the transplant unit - I told them we were trying to prevent a transplant, but they assured me "this doc" can help. Our prior apopintment was with a fairly well known, well published hep C specialist. Hopefully they all talk over the water coolers. I'm a smart, successful tough person, but I was in my office at 6:15 tonght crying my eyes out at this stupid medical system and we've got great insurance. All the way home I couldn't help but wonder what people with no insurance or no advocates do and wishing I would have gone to med school instead of the post graduate track I chose.
All is well, just moving forward and trying to understand as with the rest.
jasper
jasper
MEDICAL PROFESSIONAL
Just look at your scenario it in terms of molecular events:
1. introduce Tela later: There sits this one hepatocyte with an HCV strain, that already contains the Telaresmut. The increased T cell response under IFN and the enhanced innate "inside "the liver response both now have a chance to kill that very hepatocyte. When Tela starts, this strain is gone and cannot participate in the HCV run for survival. Hence Tela keeps working longer better, deeper. Good.
But another hepatocyte contains that very low key, low replication efficiency HCV mutant that shows no more epitopes, the cell looks perfectly clean to the patrolling cytotoxic class 1 T-cells, it replicates so slowly that it really does not use any riba to mess up its genome. After 4 weeks on SOC it has come from one rat in the US to 40000 rats in the US. Still not very remarkable. But now when the Tela hits, it also gets hit, reducing its stock from 40000 to a meager 500 at the end of Tela, but has meanwhile developed a few children that wear a thorny belt where the oh so cuddly Tela molecule always wants to attach and hinder their magnificent selfcutting and cleaning process , and because it is still a very silent, careful mutant that has learned not to make much noise, a con artist really, to the immune system, while grimly, grimassing with pain ( but no sound!) it puts its paw in the grinding machine of the host cell where its halts that silly thing like James Bond holding a rocket start with his finger , it will now sit out the remaining hard times under IFN and Riba (together with its depressed host) , getting reduced to a truly paltry 120 at EOT, laughing at even the most sensitive PCR, but already licking its mouth at the thought of repopulating this huge now almost fully uninhabited liver. It was worth the wait and the duress and the modesty and the constant hiding and the voluntary limitation of replication. Surely to get up to speed with this taunting task to repopulate the empty liver with its offspring, some sacrifices will need to be made to all this traits that helped it to survive. But after all, in its speech to the small family '"we are one of the most successful molecular machines in the history of evolution and adaptivity was always our strength, so let us swallow the pride of the spartanic survivors and get up to speed with our breeding power". So 12 weeks later, the pupulation has grown to 800000 per liver and the sensitive blood tests are just picking it up. And something a trillions time bigger with a white coat says: " you got a relapse John, maybe we should have started the Telaprevir right away to prevent those ill defined SOC mutants to grow even a little bit".
2. Introduce Tela before SOC - you know how that story would go.
3. Introduce both at the same time. Still a chance for the virus, by similar thoughts, always some roulette game for both virus and host but maybe?? the best. SVR rates of about 65%....So the next member of the combo is eagerly awaited, even for naive treaters.
1. introduce Tela later: There sits this one hepatocyte with an HCV strain, that already contains the Telaresmut. The increased T cell response under IFN and the enhanced innate "inside "the liver response both now have a chance to kill that very hepatocyte. When Tela starts, this strain is gone and cannot participate in the HCV run for survival. Hence Tela keeps working longer better, deeper. Good.
But another hepatocyte contains that very low key, low replication efficiency HCV mutant that shows no more epitopes, the cell looks perfectly clean to the patrolling cytotoxic class 1 T-cells, it replicates so slowly that it really does not use any riba to mess up its genome. After 4 weeks on SOC it has come from one rat in the US to 40000 rats in the US. Still not very remarkable. But now when the Tela hits, it also gets hit, reducing its stock from 40000 to a meager 500 at the end of Tela, but has meanwhile developed a few children that wear a thorny belt where the oh so cuddly Tela molecule always wants to attach and hinder their magnificent selfcutting and cleaning process , and because it is still a very silent, careful mutant that has learned not to make much noise, a con artist really, to the immune system, while grimly, grimassing with pain ( but no sound!) it puts its paw in the grinding machine of the host cell where its halts that silly thing like James Bond holding a rocket start with his finger , it will now sit out the remaining hard times under IFN and Riba (together with its depressed host) , getting reduced to a truly paltry 120 at EOT, laughing at even the most sensitive PCR, but already licking its mouth at the thought of repopulating this huge now almost fully uninhabited liver. It was worth the wait and the duress and the modesty and the constant hiding and the voluntary limitation of replication. Surely to get up to speed with this taunting task to repopulate the empty liver with its offspring, some sacrifices will need to be made to all this traits that helped it to survive. But after all, in its speech to the small family '"we are one of the most successful molecular machines in the history of evolution and adaptivity was always our strength, so let us swallow the pride of the spartanic survivors and get up to speed with our breeding power". So 12 weeks later, the pupulation has grown to 800000 per liver and the sensitive blood tests are just picking it up. And something a trillions time bigger with a white coat says: " you got a relapse John, maybe we should have started the Telaprevir right away to prevent those ill defined SOC mutants to grow even a little bit".
2. Introduce Tela before SOC - you know how that story would go.
3. Introduce both at the same time. Still a chance for the virus, by similar thoughts, always some roulette game for both virus and host but maybe?? the best. SVR rates of about 65%....So the next member of the combo is eagerly awaited, even for naive treaters.
Honestly, not all that up on what the future Teleprevir studies will be doing. But it looks from what is posted, that Telaprevir will be in the mix from the beginning, as it was in the earlier Telaprevir trials. Then SOC will kick in (without Telaprevir) in some arms for various lengths of time.
To oversimplify, what I believe HR was suggesting in previous posts, is that if someone is an interferon non-responder, then starting triple therapy (telaprevir plus SOC) all at once, would be similar to treating with Telaprevir Mono, which we know doesn't work. And the result, therefore, possibly might be the development of resistant mutants that would make future treatments more difficult, if not impossible, with the same class of drugs. Hope I got that right but I'm sure someone will correct me if wrong.
What was discussed in the last couple of posts, was a strategy to identify non-responders prior to the introduction of Telaprevir, basically by starting with SOC. Then if the patient didn't respond, treatment would then either stop, or perhaps continue with some sort of amped up SOC, therefore not exposing the non-responding patient to the risks of developing a resistant mutant.
I should add that a lot here is speculation, cause new stuff seems to be coming out every day now.
Hope you're doing OK these days,
-- Jim
To oversimplify, what I believe HR was suggesting in previous posts, is that if someone is an interferon non-responder, then starting triple therapy (telaprevir plus SOC) all at once, would be similar to treating with Telaprevir Mono, which we know doesn't work. And the result, therefore, possibly might be the development of resistant mutants that would make future treatments more difficult, if not impossible, with the same class of drugs. Hope I got that right but I'm sure someone will correct me if wrong.
What was discussed in the last couple of posts, was a strategy to identify non-responders prior to the introduction of Telaprevir, basically by starting with SOC. Then if the patient didn't respond, treatment would then either stop, or perhaps continue with some sort of amped up SOC, therefore not exposing the non-responding patient to the risks of developing a resistant mutant.
I should add that a lot here is speculation, cause new stuff seems to be coming out every day now.
Hope you're doing OK these days,
-- Jim
Question here,
If I am reading this right the new telaprevir study will be treating the first 12 weeks with just telaprevir at different does and times and then the remaining 24 weeks with the two pegylated interferons alfa 2a and 2b with Ribavirin. Isn’t this what everyone has been discussing prior to the abstracts being released?
Would this not show what the telaprevir could do to the viral load and the baseline side effects of the drug before introducing the INF and Riba.
jasper
Telaprevir, Phase II
The purpose of the study is to explore the safety and effectiveness of each treatment combination and to study the amount of telaprevir in the blood. Two different doses of telaprevir (750 mg every 8 hours, and 1125 mg every 12 hours) will be studied in combination with the two standard therapies commercially available for chronic Hepatitis C Virus infection. Telaprevir will be administered for 12 weeks in combination with 24 weeks of standard therapy. In case of sub-optimal response, standard therapy will be extended to 48 weeks.
The study involves frequent visits to the clinic to assess the safety and effectiveness of the treatment (daily visits until Day 4 of treatment; then weekly until Week 4; then every 2 weeks until Week 16; and then every 4 weeks until Week 24). After the end of treatment, all patiens will be followed for 24 weeks to assess the safety and effectiveness of the treatment and to study the virus in the blood. If no virus can be detected in the blood at the end of the treatment.
There will be 4 treatment groups:
12 weeks of telaprevir 750 mg every 8 hours + 24 weeks of Pegylated interferon alfa 2a + ribavirin;
12 weeks of telaprevir 750 mg every 8 hours + 24 weeks of Pegylated interferon alfa 2b + ribavirin;
12 weeks of telaprevir 1125 mg every 12 hours + 24 weeks of Pegylated interferon alfa 2a + ribavirin;
12 weeks of telaprevir 1125 mg every 12 hours + 24 weeks Pegylated interferon alfa 2b + ribavirin.
http://www.clinicaltrials.gov/ct2/show/NCT00528528?term=telaprevir&rank=1
If I am reading this right the new telaprevir study will be treating the first 12 weeks with just telaprevir at different does and times and then the remaining 24 weeks with the two pegylated interferons alfa 2a and 2b with Ribavirin. Isn’t this what everyone has been discussing prior to the abstracts being released?
Would this not show what the telaprevir could do to the viral load and the baseline side effects of the drug before introducing the INF and Riba.
jasper
Telaprevir, Phase II
The purpose of the study is to explore the safety and effectiveness of each treatment combination and to study the amount of telaprevir in the blood. Two different doses of telaprevir (750 mg every 8 hours, and 1125 mg every 12 hours) will be studied in combination with the two standard therapies commercially available for chronic Hepatitis C Virus infection. Telaprevir will be administered for 12 weeks in combination with 24 weeks of standard therapy. In case of sub-optimal response, standard therapy will be extended to 48 weeks.
The study involves frequent visits to the clinic to assess the safety and effectiveness of the treatment (daily visits until Day 4 of treatment; then weekly until Week 4; then every 2 weeks until Week 16; and then every 4 weeks until Week 24). After the end of treatment, all patiens will be followed for 24 weeks to assess the safety and effectiveness of the treatment and to study the virus in the blood. If no virus can be detected in the blood at the end of the treatment.
There will be 4 treatment groups:
12 weeks of telaprevir 750 mg every 8 hours + 24 weeks of Pegylated interferon alfa 2a + ribavirin;
12 weeks of telaprevir 750 mg every 8 hours + 24 weeks of Pegylated interferon alfa 2b + ribavirin;
12 weeks of telaprevir 1125 mg every 12 hours + 24 weeks of Pegylated interferon alfa 2a + ribavirin;
12 weeks of telaprevir 1125 mg every 12 hours + 24 weeks Pegylated interferon alfa 2b + ribavirin.
http://www.clinicaltrials.gov/ct2/show/NCT00528528?term=telaprevir&rank=1
While the "great minds" are a dinner, or whatever, I'll take a crack. Don't know enough bout Alinia to comment, but if you're saying the first time that you became UND between weeks 12 and 24, then the 48 week course probably wasn't long enough -- as studies now suggest 72 weeks would have been a better number.
Hard to tell what's happening now since your new pre-tx viral load (28,000) appears tobe an extension of your post tx relapse viral load on the way up. You did then drop a log during the first four weeks but since it's a treatment on top of a treatment I'm at a loss what to make of the drop, or for that matter how long to treat this time.
Do you give yourself credit for the 48 weeks done and add another another 24 weeks (to 72), or do you add 48 weeks, or do you do another 72 weeks. Uncharted waters I think, and part of the decision might have to do with how much liver damage you have, and how therefore you weigh the risks of all that treatment time against the rewards of a possible SVR. How long is your doc suggesting you treat?
Given all, I can certainly see why you're considering injecting another element like Alinia at this point. I know I'd be looking for every edge possible. How is your hemoglobin? If you're handling things OK, you might talk to the doc about upping the riba until you're UND.
All the best,
-- Jim
Hard to tell what's happening now since your new pre-tx viral load (28,000) appears tobe an extension of your post tx relapse viral load on the way up. You did then drop a log during the first four weeks but since it's a treatment on top of a treatment I'm at a loss what to make of the drop, or for that matter how long to treat this time.
Do you give yourself credit for the 48 weeks done and add another another 24 weeks (to 72), or do you add 48 weeks, or do you do another 72 weeks. Uncharted waters I think, and part of the decision might have to do with how much liver damage you have, and how therefore you weigh the risks of all that treatment time against the rewards of a possible SVR. How long is your doc suggesting you treat?
Given all, I can certainly see why you're considering injecting another element like Alinia at this point. I know I'd be looking for every edge possible. How is your hemoglobin? If you're handling things OK, you might talk to the doc about upping the riba until you're UND.
All the best,
-- Jim
So great minds, what if you are week 8, round 2 of treatment w/same drugs, same dosage. Round 1 responder w/greater than 2 log drop at 8 weeks, but very slow to clear to undetectable by TMA. but no spikes or breakthroughs like slow, slow decline post week 12. Relapsed 2 weeks post 48 wk treatment, started again 1 week later per docs orders. Does it make any sense at all to add Alinia at this point instead of "leading" with it to take a chance at knocking this thing out once and for all. Waiting for 8 week PCR results, but expectation is to either be non detectable or very, very low viral load. Round two pre-treatment viral load at 28,000, 4 wk at 2300. H is headed for big state U week 12 looking for answers hopefully.
I suppose they could trial it both ways -- stop SOC once you know you're responding -- let quasispecies return to "wild type" and then hit with triple; or just introduce triple at whatever point the patient is deemed a responder. The latter seems more efficient, if results proved similar. I thought there was one PI trial where they started SOC first in one of the arms, but I'm probably mistaken.
-- Jim
-- Jim
MEDICAL PROFESSIONAL
Your scenario of pretesting superhort "mono" SOC while PCRing along to reduce the danger of introducing a later unmendable Telaprevir resistant mutation to SOC nonresponders is certainly a useful and good idea. If you want to play it perfect, you would have to stop SOC once you know you are responding, let your quasispecies return to "wild type" and then hit it with simulstart to optimize the SVRupping effect of Tela.
MEDICAL PROFESSIONAL
The data on this thing" were just presented at the AASLD ( see below), and the midstream aspect is also correct.But thank xxx they went from arrogance to reason.
I came across what I think was the beginning of the Egyptian trial and it started as a 24 week mono trial, had a disappointing 1 log vl drop and was changed mid- stream and soc was added. Is this correct? Man I want to see the data on this thing! I asked my hepatologist WHY EGYPT? Was it less stringent or something? He said no, Eygpt has one of the largest hep c populations on the planet, around 24%. jm
While we've got you in this thread (taser extended :) ) -- wanted to run a thought I had last night by you. On the null-responder thing.
So, for discussions sake, let's assume that a null-responder should not be on a single viral like Telaprevir along with SOC.
For prior non-responders -- assuming there's enough info on file to label someone a non-responder -- then the answer is easy. Don't treat with a single anti-viral in combo with Peg because it would be like anti-viral monotherapy.
But what about a treatment naive. No prior history, so what do we do. And again, this question may end up being asked by many, assuming Telaprevir comes to market.
So how about this...
Why not start with the Peg with a tx naive and monitor viral loads as early as possible -- perhaps do a 24, 48 hour, and then weekly. We probably have enough studies in the vault already to tell by week 4 (if not quite earlier) how likely someone would be a non-responder based on early testing.
So then, if let's say by week 2, we can make a reasonable assessment that we have a responder. Then, the Telaprevir is started. Conversely, if the consensus is that we might have a non-responder. Then either SOC is continued with perhaps a more confirmatory test at week 4, with the bottom line being if the person appears to be an interferon non-responder, then treatment is stopped.
Assuming that starting Telaprevir (or any similar antiviral) a few weeks late, will not adversely affect SVR (I assume a trial might have to be done) this seems to address the issue of viral resistance you brought up in terms of screwing up the person's chances in the future. Love to hear your thoughts.
-- Jim
So, for discussions sake, let's assume that a null-responder should not be on a single viral like Telaprevir along with SOC.
For prior non-responders -- assuming there's enough info on file to label someone a non-responder -- then the answer is easy. Don't treat with a single anti-viral in combo with Peg because it would be like anti-viral monotherapy.
But what about a treatment naive. No prior history, so what do we do. And again, this question may end up being asked by many, assuming Telaprevir comes to market.
So how about this...
Why not start with the Peg with a tx naive and monitor viral loads as early as possible -- perhaps do a 24, 48 hour, and then weekly. We probably have enough studies in the vault already to tell by week 4 (if not quite earlier) how likely someone would be a non-responder based on early testing.
So then, if let's say by week 2, we can make a reasonable assessment that we have a responder. Then, the Telaprevir is started. Conversely, if the consensus is that we might have a non-responder. Then either SOC is continued with perhaps a more confirmatory test at week 4, with the bottom line being if the person appears to be an interferon non-responder, then treatment is stopped.
Assuming that starting Telaprevir (or any similar antiviral) a few weeks late, will not adversely affect SVR (I assume a trial might have to be done) this seems to address the issue of viral resistance you brought up in terms of screwing up the person's chances in the future. Love to hear your thoughts.
-- Jim
MEDICAL PROFESSIONAL
There is no aspect of Infergen that would lend itself to even a meaningful speculation as to whether it would work any different wit NTZ than Pegasys. Thats why there are all these trials...
George, again, how did that VL test come out??
Mimicking the US trials with NTZ is probably the safest thing, if your doc agrees with it. I personally do not like the 4week lead in, but would prefer simulstart.
The factoid about NTZ , thast I do not like, was its paltry monoperformance in terms of lowering VL in the Egyptian lead in phase. So it must have a fundamental kind of effect, like riba does, to explain the astounding effect on SVRs. It was barely stronger as riba as monoantiviral as already explained in the report re its Boston presentation.
George, again, how did that VL test come out??
Mimicking the US trials with NTZ is probably the safest thing, if your doc agrees with it. I personally do not like the 4week lead in, but would prefer simulstart.
The factoid about NTZ , thast I do not like, was its paltry monoperformance in terms of lowering VL in the Egyptian lead in phase. So it must have a fundamental kind of effect, like riba does, to explain the astounding effect on SVRs. It was barely stronger as riba as monoantiviral as already explained in the report re its Boston presentation.
Well, there is no stopping us now! The cat is "MEEEEOOOOWW" out of bag! Jim, Excellent post dude!
----------------------------------------------------------------------------------------
HR, What do think would be an optimal dose and duration?
----------------------------------------------------------------------------------------
HR, What do think would be an optimal dose and duration?
Do you think that Infergen will have the same synergy with the Alinia that the Pegs have with it?
Dont know how relevant some of my suggestions to your individual circumstance, but hopefully somewhat helpful.
I know you've treated several times in the past, and obviously you're looking to up the ante and ammo this time around. I'm assuming you're probably stage 3 or 4 by now, although sometimes the treatments can lower fibrosis.
While somewhat intutitive, I believe it was Dr. Jensen (or maybe Dieterich) over at the ClincalCareOptions web site, who made a point that step one in re-treatment is to identify as best as possible why the patient failed the first time. Were they a slow responder? Non-responder? Did they have a breakthrough? Was the dosing adequate? What about compliance? Etc, Etc.
Then once, a best guess is made as to what went wrong the first time, a plan can be put into action for better results the second time.
In other words, it's not necessarily just adding this or that, or extending here or there, but in fact analyzing the game film, so to speak, from the last game, so your chances of winning this time around are optimal.
Also, curious if you've had an outside consult (or two) since your last treatment. I had several during my single treatment course and found the different inputs very helpful in finally deciding on a plan. In my case, it was more about tx length and riba dose, but in your case an additional opinion or two could cover a lot more ground.
Please don't take the above with any disrespect, as you obviously have put a lot of time thinking about this, and seem to be developing a strong game plan, and as far as I know your're far ahead of any of us in terms of knowing what direction you should be going in -- I'm just throwing thoughts out in the hope that maybe one will be helpful, because I do want you to succeed. Whatever is not relevant please ignore.
All the best,
-- Jim
I know you've treated several times in the past, and obviously you're looking to up the ante and ammo this time around. I'm assuming you're probably stage 3 or 4 by now, although sometimes the treatments can lower fibrosis.
While somewhat intutitive, I believe it was Dr. Jensen (or maybe Dieterich) over at the ClincalCareOptions web site, who made a point that step one in re-treatment is to identify as best as possible why the patient failed the first time. Were they a slow responder? Non-responder? Did they have a breakthrough? Was the dosing adequate? What about compliance? Etc, Etc.
Then once, a best guess is made as to what went wrong the first time, a plan can be put into action for better results the second time.
In other words, it's not necessarily just adding this or that, or extending here or there, but in fact analyzing the game film, so to speak, from the last game, so your chances of winning this time around are optimal.
Also, curious if you've had an outside consult (or two) since your last treatment. I had several during my single treatment course and found the different inputs very helpful in finally deciding on a plan. In my case, it was more about tx length and riba dose, but in your case an additional opinion or two could cover a lot more ground.
Please don't take the above with any disrespect, as you obviously have put a lot of time thinking about this, and seem to be developing a strong game plan, and as far as I know your're far ahead of any of us in terms of knowing what direction you should be going in -- I'm just throwing thoughts out in the hope that maybe one will be helpful, because I do want you to succeed. Whatever is not relevant please ignore.
All the best,
-- Jim
MEDICAL PROFESSIONAL
I am trying to find out again if geno I studies on replicons have been done, comparing it with 4 .That is the best one con do at this point, other than speculating on the generality of the mechanism. You never told us how your retesting of the VL came out? The mex NTZ is produced under lic from Romark by a comany with a german name. Many docs sitting in the huge Hynes auditorium now have some expectations for NTZ, so chances are your doc will prescribe. NTZ was used for the full duration of the treatment together with SOC, except for a 12 week "lead" period. The new US NTZ/SOC trials shorten that lead period to 4 wks.
Have an Answer?
You are reading content posted in the Hepatitis C Community
Learn about this treatable virus.
Getting tested for this viral infection.
3 key steps to getting on treatment.
4 steps to getting on therapy.
What you need to know about Hep C drugs.
How the drugs might affect you.
These tips may up your chances of a cure.
A list of national and international resources and hotlines to help connect you to needed health and medical services.
Herpes sores blister, then burst, scab and heal.
Herpes spreads by oral, vaginal and anal sex.
STIs are the most common cause of genital sores.
Condoms are the most effective way to prevent HIV and STDs.
PrEP is used by people with high risk to prevent HIV infection.
