Aa
24 or 48 weeks Geno 1b, research please
Geno 1b
Starting VL 245,000
No liver damage
RVR UND Week 4 <15
Pegasus 2a 180 weekly/ Riba 1200 daily.
Currently waiting 12 week viral load results.
Please can I be directed to recent and relevant research that will enable me to make a decision about treatment - whether to continue for 48 weeks or to stop at 24.
Thanks Jankar
Starting VL 245,000
No liver damage
RVR UND Week 4 <15
Pegasus 2a 180 weekly/ Riba 1200 daily.
Currently waiting 12 week viral load results.
Please can I be directed to recent and relevant research that will enable me to make a decision about treatment - whether to continue for 48 weeks or to stop at 24.
Thanks Jankar
That's really tough starting a semester on tx. I pray his youth allows him the strength to cope. I hope he is taking a light load and maybe his easier classes during this semester.
Oh, my heart hurts with yours since I am also a mother. I so hope he will get cured, and I do believe he has a good shot at it. Did his biopsy show stage 3 then? I am not so good at gradings of biopsy, but if he has stage 3 I would say that is another reason to go 48 weeks. How strong of him to go through college during treatment. Treatment is quite an ordeal by itself.
I wish you both the best, and keep us posted how it goes for him.
Hugs,
Za
I wish you both the best, and keep us posted how it goes for him.
Hugs,
Za
I am so happy to hear that you no longer have HCV. Yay! It is good to hear you have no long term side effects also. 72 weeks is soooo long, 48 weeks seems way long enough.
My son is 21 and got Hep C, 1a - from blood transfusion as newborn baby. We found out when he was 4, it is so hard to watch and do nothing. I have never thought we would see "cure", and for many years resisted this treatment due to horror stories we read (Lloyd Wright). This summer he had not been feeling well and the liver biopsy showed early bridging fibrosis, he also had nodule ? near pancreas, possibly swollen lymph. Thankfully he has responded so well to treatment and liver enzymes seem much better. I worry most about his mental state, he seems "spacey" and frequently does not respond when talked to. He is on lexapro and Dr. increased dose about 2-3 weeks ago. He says his brain hurts?? and it is hard to describe. His headaches seem to be worse lately. He starts college again today, hope he can make it through this semester.
My son is 21 and got Hep C, 1a - from blood transfusion as newborn baby. We found out when he was 4, it is so hard to watch and do nothing. I have never thought we would see "cure", and for many years resisted this treatment due to horror stories we read (Lloyd Wright). This summer he had not been feeling well and the liver biopsy showed early bridging fibrosis, he also had nodule ? near pancreas, possibly swollen lymph. Thankfully he has responded so well to treatment and liver enzymes seem much better. I worry most about his mental state, he seems "spacey" and frequently does not respond when talked to. He is on lexapro and Dr. increased dose about 2-3 weeks ago. He says his brain hurts?? and it is hard to describe. His headaches seem to be worse lately. He starts college again today, hope he can make it through this semester.
Yes, 72 weeks worked and I no longer have HCV. I finished treatment last March, ie 9 months ago, and I have no long term side effects. So for me everything worked out fine. Hope it does for your son as well,
Za
PS I am positive your son will be UND at week 12. He probably was UND already at week 5 or 6. I think things are looking pretty good for him. Is he young? That is a positive factor for clearance.
Za
PS I am positive your son will be UND at week 12. He probably was UND already at week 5 or 6. I think things are looking pretty good for him. Is he young? That is a positive factor for clearance.
Thank you for your opinion. We will certainly be talking to our Dr. this month about this and I think he will also recommend treating 48 weeks. Guess we also have to wait for the 12 week test results, not until Jan. 21, hoping it will be undetected. I think unless the side effects are unbearable, 48 weeks seems like the right thing now.
It sounds like the 72 weeks worked for you?
I worry about the long term side effects.
Best wishes to you,
K
It sounds like the 72 weeks worked for you?
I worry about the long term side effects.
Best wishes to you,
K
Your son had a borderline result then. I had that at week 12, and because of that I decided to prolong my treatment to 72 weeks.
A borderline result tells there IS virus, and we should not ignore this warning. I kept my eye on others with small viral loads at week 12 who only went 48 weeks, and everyone I noticed relapsed.
In my opinion your son should not shorten his treatment. He should go 48 weeks, and instead be happy that since he was almost undetectable at 4 weeks, he has a very good chance of becoming cured with 48 weeks. A better chance than most geno 1s.
Of course nobody knows the exact amount of weeks it takes to cure your son. There is only study data for 24 and 48 weeks. If it were me I would rather err on the safe side than gamble and pick a number in between.
Best wishes,
Za
A borderline result tells there IS virus, and we should not ignore this warning. I kept my eye on others with small viral loads at week 12 who only went 48 weeks, and everyone I noticed relapsed.
In my opinion your son should not shorten his treatment. He should go 48 weeks, and instead be happy that since he was almost undetectable at 4 weeks, he has a very good chance of becoming cured with 48 weeks. A better chance than most geno 1s.
Of course nobody knows the exact amount of weeks it takes to cure your son. There is only study data for 24 and 48 weeks. If it were me I would rather err on the safe side than gamble and pick a number in between.
Best wishes,
Za
I just want to clarify. The paper I mentioned is a study report. I think it is The Study which the EU approval is based on. You really ought to read it.
This is an excerpt I found interesting:
"The classification tree model demonstrated that a pretreatment HCV-RNA level of 250,000 IU/mL best discriminated between patients with or without a sustained virologic response after combination therapy with peginterferon alfa-2b and ribavirin for 24 weeks. Future prospective studies should investigate whether only one threshold differentiating between low and high pretreatment viremia is sufficient or whether several ranges of pretreatment HCV-RNA levels could be used to individualize treatment duration."
This is an excerpt I found interesting:
"The classification tree model demonstrated that a pretreatment HCV-RNA level of 250,000 IU/mL best discriminated between patients with or without a sustained virologic response after combination therapy with peginterferon alfa-2b and ribavirin for 24 weeks. Future prospective studies should investigate whether only one threshold differentiating between low and high pretreatment viremia is sufficient or whether several ranges of pretreatment HCV-RNA levels could be used to individualize treatment duration."
Personally, at this stage of treatment, I'd have to ask myself how much I have invested in my first 24 weeks, and how much of an outlay I would have to complete the entire 48 weeks...risk/reward etc.
...and secondly, do I have enough information to make such a mid treatment decision?
I believe a possible shortened treatment strategy should be decided prior to starting treatment for the best chance of success. For such a decision, I think an intense viral decline slope mapping would be required, and this could only be attained through, numerous PCR's in the first 12 weeks. For example, daily testing through the first phase of viral decline and multiples through the second phase, leading to the 4 week test..and of course, very few of us have this opportunity outside of a trial...
jmho, Pro
...and secondly, do I have enough information to make such a mid treatment decision?
I believe a possible shortened treatment strategy should be decided prior to starting treatment for the best chance of success. For such a decision, I think an intense viral decline slope mapping would be required, and this could only be attained through, numerous PCR's in the first 12 weeks. For example, daily testing through the first phase of viral decline and multiples through the second phase, leading to the 4 week test..and of course, very few of us have this opportunity outside of a trial...
jmho, Pro
Do you have a copy of your test results? I was wondering if it said undetected?
My son's 4 week viral test came back HCV RNA detected, but less than 10 iu/Ml, so it looks like that the virus was not completely eliminated from the blood and no tests have been done since. His upcoming 12 week viral check will hopefully show UND. I was hoping the treatment could also be shortened but I wonder if that would be the right thing to do also, since it was still detected, just very slightly at 4 weeks?
It seems that there would be more options than either 24 or 48 weeks, maybe something in-between? I guess no studies to show effectiveness of something else.
Thanks.
My son's 4 week viral test came back HCV RNA detected, but less than 10 iu/Ml, so it looks like that the virus was not completely eliminated from the blood and no tests have been done since. His upcoming 12 week viral check will hopefully show UND. I was hoping the treatment could also be shortened but I wonder if that would be the right thing to do also, since it was still detected, just very slightly at 4 weeks?
It seems that there would be more options than either 24 or 48 weeks, maybe something in-between? I guess no studies to show effectiveness of something else.
Thanks.
Tailored Treatment for Hepatitis C
Clin Liver Dis 12 (2008) 507–528
Thomas Berg, MD
Summary of the current concepts of tailoring treatment duration in patients who have hepatitis C virus type 1
Patients who have an RVR and low baseline viremia may be potential candidates for shortening treatment duration from 48 to 24 weeks.
Around 10% to 15% of all HCV type 1–infected patients reach these criteria. The optimal cutoff to define low viremia (400,000, 600,000, or 800,000 IU/mL) in this setting is still unclear.
As long as HCV RNA is undetectable by sensitive real-time PCR assays or TMA tests at week 4, however, levels of less than 600,000 IU/mL seem to be appropriate (more conservative physicians may even choose 400,000 IU/mL).
Because hepatitis C viremia may fluctuate in the natural course of the disease, however, it is desirable to have at least two measurements of HCV RNA before starting therapy to confirm low-level replication over time. To exclude to the best possible level the presence of minimal residual viremia at week 4, which clearly increases the likelihood of experiencing a relapse, the most sensitive HCV RNA assays should be used when shortening treatment duration is considered. Furthermore,
Principles of tailored treatment in hepatitis C virus type 1
Treatment response in patients who have chronic HCV infection is quite heterogeneous and depends on host factors (ie, age, gender, alanine aminotransferase [ALT] levels, stage of fibrosis, insulin resistance) and viral factors, such as serum concentration of HCV RNA at the time of initiation of antiviral therapy, including HCV genotypes [2–7].
Thus, virologic factors and host factors must be considered if one tries to get sound information on the individual likelihood of response. 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.
Viral kinetic studies have further expanded our knowledge of the mechanisms of IFNa action and have shown that the likelihood of achieving sustained virologic response (SVR) clearly depends on the speed of the response [8–10]. It is well established that the rate of SVR is inversely correlated with the time on treatment that is necessary to clear HCV RNA from serum.
Individual prognosis with respect to the long-term treatment outcome can therefore be best predicted by early viral kinetics, because all baseline factors finally alter the speed of response (Fig. 1). Indeed, if one includes viral kinetic parameters in multivariate models to predict SVR, most the baseline factors lose their predictive power.
The rational background any individualized therapy is based on the concept that rapid responders
need less therapy as compared with those patients who are slow responders.
Importance of the sensitivity of the hepatitis C virus RNA test Undetectable hepatitis C viremia on treatment, even when evaluated by standard qualitative HCV RNA tests (detection limit of 50 IU/mL) does not, per se, indicate that the virus was completely eliminated from the serum.
There is now emerging evidence that by applying more sensitive assays (eg, transcription-mediated amplification [TMA] or real-time polymerase chain reaction [PCR] assays with a detection limit!10 IU/mL), a significant proportion of patients who were shown to have undetectable HCV RNA levels by standard assay are still viremic (Figs. 3 and 4) [11,12].
This implies that many patients considered so far to have had a relapse might, in fact, have been nonresponders with a minimal replication level (minimal residual viremia) (see Fig. 2B).
Quite importantly, the detection of minimal residual HCV RNA levels at week 12 must be taken as a serious predictor for a possible later relapse event. Morishima and colleagues [12] provided evidence that all patients in whom a minimal residual viremia could be detected at week 12 and still confirmed at week 20 had a relapse.
The application of extremely sensitive HCV RNA tests to design individualized therapeutic strategies is therefore indispensable
Clin Liver Dis 12 (2008) 507–528
Thomas Berg, MD
Summary of the current concepts of tailoring treatment duration in patients who have hepatitis C virus type 1
Patients who have an RVR and low baseline viremia may be potential candidates for shortening treatment duration from 48 to 24 weeks.
Around 10% to 15% of all HCV type 1–infected patients reach these criteria. The optimal cutoff to define low viremia (400,000, 600,000, or 800,000 IU/mL) in this setting is still unclear.
As long as HCV RNA is undetectable by sensitive real-time PCR assays or TMA tests at week 4, however, levels of less than 600,000 IU/mL seem to be appropriate (more conservative physicians may even choose 400,000 IU/mL).
Because hepatitis C viremia may fluctuate in the natural course of the disease, however, it is desirable to have at least two measurements of HCV RNA before starting therapy to confirm low-level replication over time. To exclude to the best possible level the presence of minimal residual viremia at week 4, which clearly increases the likelihood of experiencing a relapse, the most sensitive HCV RNA assays should be used when shortening treatment duration is considered. Furthermore,
Principles of tailored treatment in hepatitis C virus type 1
Treatment response in patients who have chronic HCV infection is quite heterogeneous and depends on host factors (ie, age, gender, alanine aminotransferase [ALT] levels, stage of fibrosis, insulin resistance) and viral factors, such as serum concentration of HCV RNA at the time of initiation of antiviral therapy, including HCV genotypes [2–7].
Thus, virologic factors and host factors must be considered if one tries to get sound information on the individual likelihood of response. 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.
Viral kinetic studies have further expanded our knowledge of the mechanisms of IFNa action and have shown that the likelihood of achieving sustained virologic response (SVR) clearly depends on the speed of the response [8–10]. It is well established that the rate of SVR is inversely correlated with the time on treatment that is necessary to clear HCV RNA from serum.
Individual prognosis with respect to the long-term treatment outcome can therefore be best predicted by early viral kinetics, because all baseline factors finally alter the speed of response (Fig. 1). Indeed, if one includes viral kinetic parameters in multivariate models to predict SVR, most the baseline factors lose their predictive power.
The rational background any individualized therapy is based on the concept that rapid responders
need less therapy as compared with those patients who are slow responders.
Importance of the sensitivity of the hepatitis C virus RNA test Undetectable hepatitis C viremia on treatment, even when evaluated by standard qualitative HCV RNA tests (detection limit of 50 IU/mL) does not, per se, indicate that the virus was completely eliminated from the serum.
There is now emerging evidence that by applying more sensitive assays (eg, transcription-mediated amplification [TMA] or real-time polymerase chain reaction [PCR] assays with a detection limit!10 IU/mL), a significant proportion of patients who were shown to have undetectable HCV RNA levels by standard assay are still viremic (Figs. 3 and 4) [11,12].
This implies that many patients considered so far to have had a relapse might, in fact, have been nonresponders with a minimal replication level (minimal residual viremia) (see Fig. 2B).
Quite importantly, the detection of minimal residual HCV RNA levels at week 12 must be taken as a serious predictor for a possible later relapse event. Morishima and colleagues [12] provided evidence that all patients in whom a minimal residual viremia could be detected at week 12 and still confirmed at week 20 had a relapse.
The application of extremely sensitive HCV RNA tests to design individualized therapeutic strategies is therefore indispensable
Hey, I have some suff I will put together for you but it's too late tonite. Here is one article telling of the changes in Europe along with some other stuff posted here in the past concerning his matter. March 6th, 2007
PEGASYS(R) Gets European Approval for a Shorter Treatment Duration for Some Genotype 1 and 4 Hepatitis C Patients who Show a Rapid Response to Therapy
http://www.prnewswire.co.uk
- Shorter, Simplified Treatment Option May Encourage More Patients to Seek Treatment
Some hepatitis C patients with difficult-to-treat HCV genotype 1 who respond quickly to treatment with a combination of PEGASYS(R) (pegylated interferon alfa-2a (40KD)) plus COPEGUS(R) (ribavirin) can benefit from a shorter and simplified course of therapy, following Thursday's Commission decision. With the new approval, a subset of patients with genotypes 1 and 4 HCV who achieve rapid viral response can now receive a shortened, 24-week duration of treatment with Roche's PEGASYS plus COPEGUS. This is half the normal treatment duration.
Shorter, Simplified Treatment Shows Excellent Chance for a Cure
The EU approval is based on data from two pivotal clinical trials for PEGASYS plus COPEGUS.(1,2) Results from these trials show that among patients who achieved a rapid viral response (undetectable viral load at week 4) in the first month of treatment up to 93 per cent of patients with genotype 1 HCV with a low pre-treatment viral load and 83 per cent of patients with genotype 4 were cured following only 24 weeks of therapy - a similar cure rate to that seen following 48 weeks of therapy.(3)
"This is excellent news for patients with hepatitis C," said Dr Peter Ferenci, Professor of the Department of Internal Medicine IV, Gastroenterology and Hepatology, at the University of Vienna, Austria. "This means that patients can find out within one month of starting therapy if they have an excellent chance of being cured and can benefit from a shortened treatment duration. This is likely to encourage patients to seek treatment and motivate them to stay on therapy."
New Recommendations for Treatment
A shorter, 24-week course with PEGASYS plus COPEGUS is now an option for the following patients:(4)
Genotype 1 HCV with a low pre-treatment viral load (defined as <800,000 IU/mL) and an undetectable viral load at weeks 4 and 24;
Genotype 4 HCV regardless of pre-treatment viral load and an undetectable viral load at weeks 4 and 24.
"This licence change reflects Roche's commitment to finding better treatment solutions for patients with HCV by improving treatment with existing therapies and developing new medicines to treat hepatitis C," said Claire Steers, PEGASYS Lifecycle Leader at Roche in Basel, Switzerland. "Roche is committed to finding solutions for a broad range of hepatitis C patients by continuing to simplify treatment with PEGASYS."
Below is an excellent article from Clinics of Liver Disease on Tailored Treatment for G1s.
I have only copied the bits on Shortening Tx.
You may also want to check out this study.
Early Identification of HCV G1 Patients Responding to 24 Weeks Peginterferon a-2a (40 kd)/Ribavirin Therapy
(HEPATOLOGY 2006;43:954-960.) *
Tailored Treatment for Hepatitis C
Clin Liver Dis 12 (2008) 507–528
Thomas Berg, MD
Summary of the current concepts of tailoring treatment duration in patients who have hepatitis C virus type 1
Patients who have an RVR and low baseline viremia may be potential candidates for shortening treatment duration from 48 to 24 weeks.
Around 10% to 15% of all HCV type 1–infected patients reach these criteria. The optimal cutoff to define low viremia (400,000, 600,000, or 800,000 IU/mL) in this setting is still unclear.
As long as HCV RNA is undetectable by sensitive real-time PCR assays or TMA tests at week 4, however, levels of less than 600,000 IU/mL seem to be appropriate (more conservative physicians may even choose 400,000 IU/mL).
Because hepatitis C viremia may fluctuate in the natural course of the disease, however, it is desirable to have at least two measurements of HCV RNA before starting therapy to confirm low-level replication over time. To exclude to the best possible level the presence of minimal residual viremia at week 4, which clearly increases the likelihood of experiencing a relapse, the most sensitive HCV RNA assays should be used when shortening treatment duration is considered. Furthermore,
Principles of tailored treatment in hepatitis C virus type 1
Treatment response in patients who have chronic HCV infection is quite heterogeneous and depends on host factors (ie, age, gender, alanine aminotransferase [ALT] levels, stage of fibrosis, insulin resistance) and viral factors, such as serum concentration of HCV RNA at the time of initiation of antiviral therapy, including HCV genotypes [2–7].
Thus, virologic factors and host factors must be considered if one tries to get sound information on the individual likelihood of response. 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.
Viral kinetic studies have further expanded our knowledge of the mechanisms of IFNa action and have shown that the likelihood of achieving sustained virologic response (SVR) clearly depends on the speed of the response [8–10]. It is well established that the rate of SVR is inversely correlated with the time on treatment that is necessary to clear HCV RNA from serum.
Individual prognosis with respect to the long-term treatment outcome can therefore be best predicted by early viral kinetics, because all baseline factors finally alter the speed of response (Fig. 1). Indeed, if one includes viral kinetic parameters in multivariate models to predict SVR, most the baseline factors lose their predictive power.
The rational background any individualized therapy is based on the concept that rapid responders
need less therapy as compared with those patients who are slow responders.
Importance of the sensitivity of the hepatitis C virus RNA test Undetectable hepatitis C viremia on treatment, even when evaluated by standard qualitative HCV RNA tests (detection limit of 50 IU/mL) does not, per se, indicate that the virus was completely eliminated from the serum.
There is now emerging evidence that by applying more sensitive assays (eg, transcription-mediated amplification [TMA] or real-time polymerase chain reaction [PCR] assays with a detection limit!10 IU/mL), a significant proportion of patients who were shown to have undetectable HCV RNA levels by standard assay are still viremic (Figs. 3 and 4) [11,12].
This implies that many patients considered so far to have had a relapse might, in fact, have been nonresponders with a minimal replication level (minimal residual viremia) (see Fig. 2B).
Quite importantly, the detection of minimal residual HCV RNA levels at week 12 must be taken as a serious predictor for a possible later relapse event. Morishima and colleagues [12] provided evidence that all patients in whom a minimal residual viremia could be detected at week 12 and still confirmed at week 20 had a relapse.
The application of extremely sensitive HCV RNA tests to design individualized therapeutic strategies is therefore indispensable.
PEGASYS(R) Gets European Approval for a Shorter Treatment Duration for Some Genotype 1 and 4 Hepatitis C Patients who Show a Rapid Response to Therapy
http://www.prnewswire.co.uk
- Shorter, Simplified Treatment Option May Encourage More Patients to Seek Treatment
Some hepatitis C patients with difficult-to-treat HCV genotype 1 who respond quickly to treatment with a combination of PEGASYS(R) (pegylated interferon alfa-2a (40KD)) plus COPEGUS(R) (ribavirin) can benefit from a shorter and simplified course of therapy, following Thursday's Commission decision. With the new approval, a subset of patients with genotypes 1 and 4 HCV who achieve rapid viral response can now receive a shortened, 24-week duration of treatment with Roche's PEGASYS plus COPEGUS. This is half the normal treatment duration.
Shorter, Simplified Treatment Shows Excellent Chance for a Cure
The EU approval is based on data from two pivotal clinical trials for PEGASYS plus COPEGUS.(1,2) Results from these trials show that among patients who achieved a rapid viral response (undetectable viral load at week 4) in the first month of treatment up to 93 per cent of patients with genotype 1 HCV with a low pre-treatment viral load and 83 per cent of patients with genotype 4 were cured following only 24 weeks of therapy - a similar cure rate to that seen following 48 weeks of therapy.(3)
"This is excellent news for patients with hepatitis C," said Dr Peter Ferenci, Professor of the Department of Internal Medicine IV, Gastroenterology and Hepatology, at the University of Vienna, Austria. "This means that patients can find out within one month of starting therapy if they have an excellent chance of being cured and can benefit from a shortened treatment duration. This is likely to encourage patients to seek treatment and motivate them to stay on therapy."
New Recommendations for Treatment
A shorter, 24-week course with PEGASYS plus COPEGUS is now an option for the following patients:(4)
Genotype 1 HCV with a low pre-treatment viral load (defined as <800,000 IU/mL) and an undetectable viral load at weeks 4 and 24;
Genotype 4 HCV regardless of pre-treatment viral load and an undetectable viral load at weeks 4 and 24.
"This licence change reflects Roche's commitment to finding better treatment solutions for patients with HCV by improving treatment with existing therapies and developing new medicines to treat hepatitis C," said Claire Steers, PEGASYS Lifecycle Leader at Roche in Basel, Switzerland. "Roche is committed to finding solutions for a broad range of hepatitis C patients by continuing to simplify treatment with PEGASYS."
Below is an excellent article from Clinics of Liver Disease on Tailored Treatment for G1s.
I have only copied the bits on Shortening Tx.
You may also want to check out this study.
Early Identification of HCV G1 Patients Responding to 24 Weeks Peginterferon a-2a (40 kd)/Ribavirin Therapy
(HEPATOLOGY 2006;43:954-960.) *
Tailored Treatment for Hepatitis C
Clin Liver Dis 12 (2008) 507–528
Thomas Berg, MD
Summary of the current concepts of tailoring treatment duration in patients who have hepatitis C virus type 1
Patients who have an RVR and low baseline viremia may be potential candidates for shortening treatment duration from 48 to 24 weeks.
Around 10% to 15% of all HCV type 1–infected patients reach these criteria. The optimal cutoff to define low viremia (400,000, 600,000, or 800,000 IU/mL) in this setting is still unclear.
As long as HCV RNA is undetectable by sensitive real-time PCR assays or TMA tests at week 4, however, levels of less than 600,000 IU/mL seem to be appropriate (more conservative physicians may even choose 400,000 IU/mL).
Because hepatitis C viremia may fluctuate in the natural course of the disease, however, it is desirable to have at least two measurements of HCV RNA before starting therapy to confirm low-level replication over time. To exclude to the best possible level the presence of minimal residual viremia at week 4, which clearly increases the likelihood of experiencing a relapse, the most sensitive HCV RNA assays should be used when shortening treatment duration is considered. Furthermore,
Principles of tailored treatment in hepatitis C virus type 1
Treatment response in patients who have chronic HCV infection is quite heterogeneous and depends on host factors (ie, age, gender, alanine aminotransferase [ALT] levels, stage of fibrosis, insulin resistance) and viral factors, such as serum concentration of HCV RNA at the time of initiation of antiviral therapy, including HCV genotypes [2–7].
Thus, virologic factors and host factors must be considered if one tries to get sound information on the individual likelihood of response. 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.
Viral kinetic studies have further expanded our knowledge of the mechanisms of IFNa action and have shown that the likelihood of achieving sustained virologic response (SVR) clearly depends on the speed of the response [8–10]. It is well established that the rate of SVR is inversely correlated with the time on treatment that is necessary to clear HCV RNA from serum.
Individual prognosis with respect to the long-term treatment outcome can therefore be best predicted by early viral kinetics, because all baseline factors finally alter the speed of response (Fig. 1). Indeed, if one includes viral kinetic parameters in multivariate models to predict SVR, most the baseline factors lose their predictive power.
The rational background any individualized therapy is based on the concept that rapid responders
need less therapy as compared with those patients who are slow responders.
Importance of the sensitivity of the hepatitis C virus RNA test Undetectable hepatitis C viremia on treatment, even when evaluated by standard qualitative HCV RNA tests (detection limit of 50 IU/mL) does not, per se, indicate that the virus was completely eliminated from the serum.
There is now emerging evidence that by applying more sensitive assays (eg, transcription-mediated amplification [TMA] or real-time polymerase chain reaction [PCR] assays with a detection limit!10 IU/mL), a significant proportion of patients who were shown to have undetectable HCV RNA levels by standard assay are still viremic (Figs. 3 and 4) [11,12].
This implies that many patients considered so far to have had a relapse might, in fact, have been nonresponders with a minimal replication level (minimal residual viremia) (see Fig. 2B).
Quite importantly, the detection of minimal residual HCV RNA levels at week 12 must be taken as a serious predictor for a possible later relapse event. Morishima and colleagues [12] provided evidence that all patients in whom a minimal residual viremia could be detected at week 12 and still confirmed at week 20 had a relapse.
The application of extremely sensitive HCV RNA tests to design individualized therapeutic strategies is therefore indispensable.
I have an article from "Journal of Hepatology" here called "Efficacy of 24 weeks treatment with peginterferon alfa-2b plus ribavirin in patients with chronic hepatitis C infected with genotype 1 and low pretreatment viremia".
It is from "Journal of Hepatology" 44 (2006), page 97-103.
The authors are Zeuzem et al.
I only have a paper copy but it also says "Elsevier" on it, so I figure you can buy a copy from their site. It is an informative paper.
If you can not get hold of it anywhere, I could always make a copy and send it to you by regular mail.
It is from "Journal of Hepatology" 44 (2006), page 97-103.
The authors are Zeuzem et al.
I only have a paper copy but it also says "Elsevier" on it, so I figure you can buy a copy from their site. It is an informative paper.
If you can not get hold of it anywhere, I could always make a copy and send it to you by regular mail.
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