Aa
non rvr
hi all. as some of you know ive startedtreatment 8wks ago and am 3a, i done a viral test at 4 wks and got results when i meet doc 2day. i started with a vl of jus over 5.9m. my 4wk vl was jus over 1.1m. im on 180 peg and 800riba per day and i way 90kg, i have asked doc wat happens next as its not the vl he was looking 4 and said he`ll decide wat course of action 2 take hen he gets my 12wk vl. he said he might add a futher 16wks to my 26wks but depending on my vl.
if he`s not happy with vl he`l stop treatment.
i have tried 2 get him 2 entertain the opion off upping my riba but he`s not budging.
so if any 1 out there had same experiance or any1 can tell me what they think my chances of svr are.
thanx santa
if he`s not happy with vl he`l stop treatment.
i have tried 2 get him 2 entertain the opion off upping my riba but he`s not budging.
so if any 1 out there had same experiance or any1 can tell me what they think my chances of svr are.
thanx santa
I would read very carefully what **** Sparrow has posted above. I agree with him that the main problem is your poor response to interferon.
3a --- SVR no RVR --- weight based Riba 1200...
I didn't go UND until way late in the 24 week phase.
Had lousy sides - but I AM SVR.
Had significant damage - was seriously ill for 3 years prior to figuring out it was HCV.... Looked for everything ELSE but HCV
I think I'm a rare case.
Developed Fibromyalgia and Neuropathy after all was said and done. But worth it --- I'm human half the time - before I was a dying zombie ALL the time.
It is not impossible to get SVR if not RVR.
But I do think you're on too low of a dose of Riba --- dependent on your weight.
Much luck to ya!
Meki
I didn't go UND until way late in the 24 week phase.
Had lousy sides - but I AM SVR.
Had significant damage - was seriously ill for 3 years prior to figuring out it was HCV.... Looked for everything ELSE but HCV
I think I'm a rare case.
Developed Fibromyalgia and Neuropathy after all was said and done. But worth it --- I'm human half the time - before I was a dying zombie ALL the time.
It is not impossible to get SVR if not RVR.
But I do think you're on too low of a dose of Riba --- dependent on your weight.
Much luck to ya!
Meki
How can there be so much confussing information about this. Man.....I am geno3a also 55 yo male. Tried tx two times before was never able to handle the s/e's. And it always came back. This time I started tx Dec last year and finished in May and so am still undet! Go figure. Why this time? For some strange reason my vl before starting was low. In the past it was 3-5mil, this time it was under 100,000. I have no idea why. I wasn't doing anything different in fact I felt less healthy this time. Had been dumped by a girlfriend the year before wasn't over that, was taking pain pills because I hurt my neck.
So don't give up hope. But I think you need more riba and would just do it. If you need some I have some left over.
Red
So don't give up hope. But I think you need more riba and would just do it. If you need some I have some left over.
Red
Tailored Treatment for Hepatitis C
Thomas Berg, MD
Treatment guidelines recommend that patients infected with HCV genotype 2 or 3 infection can be treated for 24 weeks with the combination of peg-IFNa plus ribavirin at a dosage of 800 mg/d
If one is aware of the influence of viral and host factors with respect to the possible consequences of therapeutic response, it indeed seems rather illogical to treat all patients with the same fixed therapeutic regimen.
The rational background of any individualized therapy is based on the concept that rapid responders need less therapy as compared with those patients who are slow responders.
the article by Shiffman discussed how to identify the optimal doses in an individual-based strategy to influence the efficacy of the response. Perhaps even more important to solve the problem is to try to influence the therapeutic response by modifying treatment duration, thereby differentiating between slow and rapid virologic responders.
For instance, relapse rates were nearly three times higher in type 3–infected patients with a high viral load (gtr 600,000 IU/mL) as compared with those with low viremia (23% versus 8%) after a 24-week course of peg-IFNa-2b at a dose of 1.5 mg plus weight-based ribavirin (800–1400 mg).
Also in type 2 and 3 infection, viral kinetics (ie, time to HCV RNA negative status) are of increasing importance to optimize antiviral treatment individually.
Compared with type 1 infection, viral decline is more rapid in type 2 and 3 infection. Because most patients achieve an RVR at treatment week 4, this explains, analogous to the situation in type 1 infection, why most patients are sufficiently treated with a 24-week treatment course.
Extending treatment duration in those who are slow to respond
There are data from randomized prospective trials that show prolonging the duration of treatment increases SVR rates in genotype 1–infected patients who are slow to respond.
This raises the question of whether intensification of the therapeutic regimen could increase SVR rates in genotype 2– or 3–infected patients who do not achieve an RVR.
There are no data from prospective trials available on this topic. This question has been addressed through a retrospective analysis of data [36] from the trial by Hadziyannis and colleagues.
In patients who did not have RVRs, end-of-treatment response rates ranged from 65% to 76% across the four treatment groups.
Consistent with results observed in genotype 1-infected patients, relapse rates decreased in inverse proportion to the intensity of treatment and were lowest in those treated for 48 weeks with peg-IFNa- 2a plus ribavirin at a dosage of 1000/1200 mg/d (4%) and highest in those treated for 24 weeks with ribavirin at a dosage of 800 mg/d (26%).
Although these results must be confirmed in a prospective study, they suggest that intensification of therapy may be effective in increasing SVR rates in genotype 2– or 3–infected patients who do not achieve an RVR at week 4.
Summary: tailored treatment for hepatitis C virus type 2 and 3
It is no longer appropriate to generalize that patients who have HCV genotype 1 and 4 are ‘‘difficult to cure’’ because of viral kinetic evidence to the contrary.
Conversely, it is no longer appropriate to think of all patients who have HCV genotype 2 or 3 as ‘‘easy to cure.’’ Although genotype is an important driver of response and is useful in designing the initial treatment plan, it is clear that once treatment is initiated, RVR is the most important and powerful predictor of SVR.
In genotype 2– or 3–infected patients, response-guided therapy using measurement of the virologic response after 4 weeks of combination therapy allows the treatment regimen to be tailored to the individual.
CS
Thomas Berg, MD
Treatment guidelines recommend that patients infected with HCV genotype 2 or 3 infection can be treated for 24 weeks with the combination of peg-IFNa plus ribavirin at a dosage of 800 mg/d
If one is aware of the influence of viral and host factors with respect to the possible consequences of therapeutic response, it indeed seems rather illogical to treat all patients with the same fixed therapeutic regimen.
The rational background of any individualized therapy is based on the concept that rapid responders need less therapy as compared with those patients who are slow responders.
the article by Shiffman discussed how to identify the optimal doses in an individual-based strategy to influence the efficacy of the response. Perhaps even more important to solve the problem is to try to influence the therapeutic response by modifying treatment duration, thereby differentiating between slow and rapid virologic responders.
For instance, relapse rates were nearly three times higher in type 3–infected patients with a high viral load (gtr 600,000 IU/mL) as compared with those with low viremia (23% versus 8%) after a 24-week course of peg-IFNa-2b at a dose of 1.5 mg plus weight-based ribavirin (800–1400 mg).
Also in type 2 and 3 infection, viral kinetics (ie, time to HCV RNA negative status) are of increasing importance to optimize antiviral treatment individually.
Compared with type 1 infection, viral decline is more rapid in type 2 and 3 infection. Because most patients achieve an RVR at treatment week 4, this explains, analogous to the situation in type 1 infection, why most patients are sufficiently treated with a 24-week treatment course.
Extending treatment duration in those who are slow to respond
There are data from randomized prospective trials that show prolonging the duration of treatment increases SVR rates in genotype 1–infected patients who are slow to respond.
This raises the question of whether intensification of the therapeutic regimen could increase SVR rates in genotype 2– or 3–infected patients who do not achieve an RVR.
There are no data from prospective trials available on this topic. This question has been addressed through a retrospective analysis of data [36] from the trial by Hadziyannis and colleagues.
In patients who did not have RVRs, end-of-treatment response rates ranged from 65% to 76% across the four treatment groups.
Consistent with results observed in genotype 1-infected patients, relapse rates decreased in inverse proportion to the intensity of treatment and were lowest in those treated for 48 weeks with peg-IFNa- 2a plus ribavirin at a dosage of 1000/1200 mg/d (4%) and highest in those treated for 24 weeks with ribavirin at a dosage of 800 mg/d (26%).
Although these results must be confirmed in a prospective study, they suggest that intensification of therapy may be effective in increasing SVR rates in genotype 2– or 3–infected patients who do not achieve an RVR at week 4.
Summary: tailored treatment for hepatitis C virus type 2 and 3
It is no longer appropriate to generalize that patients who have HCV genotype 1 and 4 are ‘‘difficult to cure’’ because of viral kinetic evidence to the contrary.
Conversely, it is no longer appropriate to think of all patients who have HCV genotype 2 or 3 as ‘‘easy to cure.’’ Although genotype is an important driver of response and is useful in designing the initial treatment plan, it is clear that once treatment is initiated, RVR is the most important and powerful predictor of SVR.
In genotype 2– or 3–infected patients, response-guided therapy using measurement of the virologic response after 4 weeks of combination therapy allows the treatment regimen to be tailored to the individual.
CS
Merry Christmas Santa. -Sorry! Can’t help myself.
Well you have had a 0.73 log drop. Which aint that good.
Unlike most of the others I don’t think it’s the Riba dose that produced such a poor 4 week result.
Although, It could well impact your ability to EVR.
Its your poor response to Interferon that’s the problem, OK the Riba dose isn’t helping. But your main problem is that IFN isn’t working that well.
“Santa - any1 can tell me what they think my chances of svr are”
Without Increasing the IFN and Riba dose and extending to 48 weeks if you respond to the higher doses - Not Good.
In saying that there is always a G3 that breaks the rules. Here hoping you are 1 of them.
G3s are supposed to be easy to treat.
Like me, You seam to be trying to prove that aint necessarily always the case.
If you are not careful you will be joining me in the G3 NR club.
No offence but for now I am going to reject your application.
So what can you do about it.
Here is what ML Shiffman Thomas Berg have to say.
Ask why you cant do it this way. Get your Dr to disagree with Shiffman and Berg rather than you.
Optimizing the Current Therapy for Chronic Hepatitis C Virus: Peginterferon and Ribavirin Dosing and the Utility of Growth Factors.
Clin Liver Dis 12 (2008) 487–505
Mitchell L. Shiffman, MD
This article focuses on how altering the doses of peginterferon and ribavirin can affect the three milestones leading to SVR, namely, virologic response, breakthrough, and relapse.
Patterns of virologic response
The term early virologic response refers to a 2-log decline in HCV RNA from the pretreatment baseline or being HCV RNA undetectable within 12 weeks after the initiation of treatment.
Approximately 80% of patients who have genotype 1 and virtually all patients who have genotypes 2 and 3 achieve an EVR. Patients without an EVR rarely if ever achieve an SVR
Patients who have genotypes 2 and 3 who do not become HCV RNA undetectable after week 4 have an SVR of only 49% [4], and a recent retrospective analysis has suggested that prolonging treatment in these patients could also reduce relapse
Effect of interferon dosing on virologic response
It has long been recognized that the ability of interferon to reduce HCV RNA in serum is a dose-dependent process.
Studies conducted at the author’s center longer than a decade ago demonstrated that increasing the dosage of standard interferon from 3 to 5 to 10 mU and then to 20 mU three times weekly every 3 months in those patients who remained HCV RNA positive led to a stepwise increase in the overall percentage of patients becoming HCV RNA undetectable.
Up to 80% of patients treated with this approach eventually became HCV RNA undetectable.
High daily dosages of consensus interferon (9–15 mg/d) and higher dosages of peginterferon, up to a peginterferon alfa-2a dose of 360 mg/wk and a peginterferon alfa-2b dose of 3.0 mg/kg/wk, respectively, have been shown to lead to a virologic response in approximately 15% to 20% of patients who previously failed to become HCV RNA undetectable after treatment with standard doses of interferon or peginterferon
The major limitation to using higher doses of interferon or peginterferon is the adverse events of these agents, which increase with increasing dose and cause patients to discontinue treatment.
The current recommended starting doses for the two peginterferons were derived by balancing response and discontinuation rates to achieve the highest overall rates of SVR. Because most patients respond to the current starting dosages of peginterferon (180 mg/wk for peginterferon alfa-2a and 1.5 mg/kg/wk for peginterferon alfa-2b), it is not appropriate to initiate treatment with higher doses of these medications.
In contrast, it is quite rationale to consider escalating the dose of peginterferon or switching to high doses of daily interferon in patients with a suboptimal response who could tolerate such a treatment strategy.
It is therefore reasonable to consider escalating the interferon dose in patients with a partial virologic response as soon as this response pattern is recognized.
This typically occurs between treatment weeks 12 and 24 (Fig. 4). If patients do not have a further decline in HCV RNA and become virus RNA undetectable with 3 additional months of high-dose interferon therapy, it is highly unlikely that a virologic response is going to occur and treatment thereafter should be discontinued.
If such patients do not achieve an EVR or become HCV RNA undetectable within 12 to 24 weeks of treatment, however, this approach should also be abandoned. In either situation, a higher dose of peginterferon or high doses of daily consensus interferon can be used.
Effect of ribavirin dosing on virologic response
Ribavirin is an essential ingredient in the treatment of chronic HCV and affects all three of the milestones required to achieve an SVR (see Table 1).
Ribavirin is a weak antiviral agent and does not cause a reduction in serum HCV RNA when used alone [28]. When combined with interferon, however, it more than doubles the virologic response rate
Ribavirin enhances virologic response by accelerating the decline in HCV RNA over that observed with interferon alone [30]. Although the combination of peginterferon and ribavirin does not increase the percentage of patients who achieve an RVR, it more than doubles (from 18% to 38%) the percentage of patients who become HCV RNA undetectable by treatment week 12
The starting dose of ribavirin may also play a role in enhancing virologic response. In several randomized controlled clinical studies a 3% to 9% higher virologic response rate was consistently observed when the starting ribavirin dosage was increased by 200 to 400 mg/d.
Cont.
Well you have had a 0.73 log drop. Which aint that good.
Unlike most of the others I don’t think it’s the Riba dose that produced such a poor 4 week result.
Although, It could well impact your ability to EVR.
Its your poor response to Interferon that’s the problem, OK the Riba dose isn’t helping. But your main problem is that IFN isn’t working that well.
“Santa - any1 can tell me what they think my chances of svr are”
Without Increasing the IFN and Riba dose and extending to 48 weeks if you respond to the higher doses - Not Good.
In saying that there is always a G3 that breaks the rules. Here hoping you are 1 of them.
G3s are supposed to be easy to treat.
Like me, You seam to be trying to prove that aint necessarily always the case.
If you are not careful you will be joining me in the G3 NR club.
No offence but for now I am going to reject your application.
So what can you do about it.
Here is what ML Shiffman Thomas Berg have to say.
Ask why you cant do it this way. Get your Dr to disagree with Shiffman and Berg rather than you.
Optimizing the Current Therapy for Chronic Hepatitis C Virus: Peginterferon and Ribavirin Dosing and the Utility of Growth Factors.
Clin Liver Dis 12 (2008) 487–505
Mitchell L. Shiffman, MD
This article focuses on how altering the doses of peginterferon and ribavirin can affect the three milestones leading to SVR, namely, virologic response, breakthrough, and relapse.
Patterns of virologic response
The term early virologic response refers to a 2-log decline in HCV RNA from the pretreatment baseline or being HCV RNA undetectable within 12 weeks after the initiation of treatment.
Approximately 80% of patients who have genotype 1 and virtually all patients who have genotypes 2 and 3 achieve an EVR. Patients without an EVR rarely if ever achieve an SVR
Patients who have genotypes 2 and 3 who do not become HCV RNA undetectable after week 4 have an SVR of only 49% [4], and a recent retrospective analysis has suggested that prolonging treatment in these patients could also reduce relapse
Effect of interferon dosing on virologic response
It has long been recognized that the ability of interferon to reduce HCV RNA in serum is a dose-dependent process.
Studies conducted at the author’s center longer than a decade ago demonstrated that increasing the dosage of standard interferon from 3 to 5 to 10 mU and then to 20 mU three times weekly every 3 months in those patients who remained HCV RNA positive led to a stepwise increase in the overall percentage of patients becoming HCV RNA undetectable.
Up to 80% of patients treated with this approach eventually became HCV RNA undetectable.
High daily dosages of consensus interferon (9–15 mg/d) and higher dosages of peginterferon, up to a peginterferon alfa-2a dose of 360 mg/wk and a peginterferon alfa-2b dose of 3.0 mg/kg/wk, respectively, have been shown to lead to a virologic response in approximately 15% to 20% of patients who previously failed to become HCV RNA undetectable after treatment with standard doses of interferon or peginterferon
The major limitation to using higher doses of interferon or peginterferon is the adverse events of these agents, which increase with increasing dose and cause patients to discontinue treatment.
The current recommended starting doses for the two peginterferons were derived by balancing response and discontinuation rates to achieve the highest overall rates of SVR. Because most patients respond to the current starting dosages of peginterferon (180 mg/wk for peginterferon alfa-2a and 1.5 mg/kg/wk for peginterferon alfa-2b), it is not appropriate to initiate treatment with higher doses of these medications.
In contrast, it is quite rationale to consider escalating the dose of peginterferon or switching to high doses of daily interferon in patients with a suboptimal response who could tolerate such a treatment strategy.
It is therefore reasonable to consider escalating the interferon dose in patients with a partial virologic response as soon as this response pattern is recognized.
This typically occurs between treatment weeks 12 and 24 (Fig. 4). If patients do not have a further decline in HCV RNA and become virus RNA undetectable with 3 additional months of high-dose interferon therapy, it is highly unlikely that a virologic response is going to occur and treatment thereafter should be discontinued.
If such patients do not achieve an EVR or become HCV RNA undetectable within 12 to 24 weeks of treatment, however, this approach should also be abandoned. In either situation, a higher dose of peginterferon or high doses of daily consensus interferon can be used.
Effect of ribavirin dosing on virologic response
Ribavirin is an essential ingredient in the treatment of chronic HCV and affects all three of the milestones required to achieve an SVR (see Table 1).
Ribavirin is a weak antiviral agent and does not cause a reduction in serum HCV RNA when used alone [28]. When combined with interferon, however, it more than doubles the virologic response rate
Ribavirin enhances virologic response by accelerating the decline in HCV RNA over that observed with interferon alone [30]. Although the combination of peginterferon and ribavirin does not increase the percentage of patients who achieve an RVR, it more than doubles (from 18% to 38%) the percentage of patients who become HCV RNA undetectable by treatment week 12
The starting dose of ribavirin may also play a role in enhancing virologic response. In several randomized controlled clinical studies a 3% to 9% higher virologic response rate was consistently observed when the starting ribavirin dosage was increased by 200 to 400 mg/d.
Cont.
I think you need to work with your doctors rather than working alone - you need professional back up if things become difficult. Another doctor, or take along the research and do not move until current dr gets some advice from another specialist.
I am 1 b, 75 kg and take 1200 riba per day. 6 weeks into treatment - unsure of my results to date but had a good EVR.
I am 1 b, 75 kg and take 1200 riba per day. 6 weeks into treatment - unsure of my results to date but had a good EVR.
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