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Is it really necessary?
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Is it really necessary?

Been staying away, and yet having been looking in every now and then. Still impressed with the level of dialogue that goes on, and the wisdom of so many.
My question, Is it really necessary to push treatment 48 weeks?
If a VL comes down to 130 @ week 4, then is UND @ week 8 and remains UND, is it really necessary?
What is the logic and how is that value reached?
I have made up my mind...I am in it for the entire protocol! I have accepted the way I feel, and began doing things ie: cooking, housework, walking more and more. In fact have begun learning another software suite, Auto Cad 2014.
So by excepting my place in this, I have less time to feel miserable .
But my critical thinking still wants to know, " Is it really necessary, and do the benefits warrant the doubling of this protocol. Again I am it to win it!    
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1815939_tn?1377995399
And her is a link to an article the Journal of Viral Hepatitis (from 2009) which mentions several of the same observations. The section pertaining to Genotypes 2 and 3 is about 2/3 of the way down on the page (go to the link to see the Tables):  

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2759987/

Expert opinion on the treatment of patients with chronic hepatitis C

Genotypes 2 and 3

Interest has also focused on whether treatment duration could be individualized in some patients with genotype 2 and 3 infection; i.e. shortened due to the overall high rate of SVR (∼80%) achieved with the standard 24 weeks of treatment, or prolonged in slow responders.
Recommendations for optimizing treatment in patients with HCV genotypes 2 and 3

Shorter treatment for patients with a rapid virological response

A number of studies have investigated whether it might be possible to reduce treatment duration in some patients with chronic HCV genotypes 2 or 3 infection based on RVR. Several small studies have demonstrated comparable SVR rates after 16 weeks and 24 weeks treatment in patients with either genotype 2 (Table 2) or 3 (Table 3) infection who achieve an RVR [49–52]. However, in the large-scale randomized, multinational ACCELERATE study, in which a lower dose of RBV was used, overall SVR rates were lower following 16 weeks of peginterferon plus RBV compared with 24 weeks treatment in genotype 2 and 3 patients, although this difference only reached significance in genotype 2 patients [9]. Among the patients with an RVR, SVR rates were significantly higher in the 24-week group than in the 16-week group, both overall (85%vs 79%, P<0.001) and within each genotype group, although patients who achieved an RVR were more likely to achieve an SVR overall [9]. Overall, the significant difference seen in SVR rates was found to reflect a significantly higher relapse rate in the 16-week group (31%) compared with the 24-week group (18%; P<0.001); shorter treatment duration was associated with a significantly higher risk of relapse in both genotype 2 and 3 patients [9].

Overview of short-term treatment versus standard (24-week) treatment in patients (pts) with HCV genotype 3 infection

Overview of short-term treatment versus standard (24-week) treatment in patients (pts) with HCV genotype 2 infection

There is some evidence to suggest that genotype 2 and 3 may respond differently to treatment; overall SVR rates tend to be somewhat lower for genotype 3 patients who do not achieve an RVR compared with genotype 2 patients who do not achieve RVR, and also after shorter treatment duration in patients who do achieve RVR [9,50,51,53,54]. Whether genotype 3-infected individuals should not therefore be considered for shorter duration therapy requires further investigation.

Baseline HCV RNA levels also influence SVR rates and patients with low pre-treatment serum HCV RNA levels and RVR have been reported to respond equally well to both 16 and 24 weeks of therapy (SVR rates of 82–100% and 81–100%, respectively) [9,49,50,53]. It is possible, therefore, that these patients may be considered for shorter treatment duration.

Genotype 2 and 3 infected patients with severe fibrosis are less likely to achieve either RVR or SVR, and to relapse more frequently following 12–14 weeks of antiviral therapy [9,49,51,53]. Andriulli et al. found that patients with low pre-treatment ALT levels were also found to relapse more frequently following shorter treatment duration (14% after 12–14 weeks vs 2% after 24 weeks; P=0.04) [51]. These findings suggest that patients with severe fibrosis or normal pre-treatment ALT levels are most likely unsuitable candidates for short-term treatment, but prospective studies are needed to confirm these observations.

Optimizing response by reducing relapse rates in patients with HCV genotypes 2 and 3

There is evidence that patients with HCV genotype 2 or 3 and higher baseline viral load have lower rates of SVR and higher relapse rates after 24 weeks of treatment than those with lower HCV RNA baseline levels [9,32,50,55], and that, in patients without RVR, the lowest rates of relapse are obtained with 48 weeks of treatment and a higher RBV dose [11]. Whether increasing treatment duration would help reduce relapse rates in patients with high baseline viral load requires further evaluation.

Although patients with genotypes 2 and 3 are generally considered to respond similarly to treatment, there is also some evidence to suggest that genotype 3 patients have lower SVR rates and subsequently higher relapse rates than genotype 2 patients [32]. An analysis of data from the WIN-R trial of peginterferon alfa-2b also demonstrated higher SVR rates and lower relapse rates in genotype 2 infected patients compared with genotype 3 (72%vs 63%, and 5%vs 10%, respectively) [56]. It is possible that genotype 3-infected patients would benefit from longer treatment duration and/or higher RBV dose compared with genotype 2-infected patients; however current data supporting this comes predominantly from retrospective analyses and requires evaluation in prospective clinical trials.

A recent study suggests that patients infected with genotype 3 who have cirrhosis are 10 times more likely to relapse following treatment with conventional or peginterferon plus RBV than those without cirrhosis [57], a finding consistent with the results from the trial by Hadziyannis et al. and described below [3]. If data from cirrhotic patients infected with HCV genotype 1 are extrapolated to those with other genotypes, it is likely that longer treatment duration may be beneficial in reducing relapse in genotype 2 and 3 patients with cirrhosis. However, this remains to be established in prospective clinical studies.

Proportion of HCV genotype 2 and 3-infected patients who could be considered for shortened or extended therapy duration

In general, patients infected with HCV genotypes 2 or 3 should not be routinely treated for less than the currently recommended 24 weeks to avoid an increased risk of virologic relapse. However, patients with a low pre-treatment viral load (≤400 000 IU/mL) and an RVR (as determined by a highly sensitive assay) have the highest probability of achieving an SVR with 16 weeks of therapy (Fig. 4). Such a regimen may be a reasonable option for these patients, especially if tolerability of longer treatment may be a concern. The cut-off for low-viral load in patients with genotypes 2 and 3 based on the ACCELERATE data is ≤400 000 IU/mL [9]. As with genotype 1, baseline viral load should be determined in two samples, taken at least 4 weeks apart.

Overview of the ACCELERATE data: 16 vs 24 weeks. SVR: sustained viral response.

Shortening of treatment duration should not be considered for patients with cirrhosis, persistently normal ALT values or co-infection with HBV or immunocompromised patients such as those with HIV infection or those who have undergone liver transplantation.

There may be patient subgroups with genotype 2 or 3 infection that might benefit from extended treatment duration to reduce relapse rates. Results from the trial by Hadziyannis et al. found evidence for reduced relapse rates in genotype 2 and 3 pts with advanced fibrosis/cirrhosis as well as high baseline viral load when treated for 48 weeks in comparison with 24 weeks [3].
15 Comments Post a Comment
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Avatar_m_tn
All that I can do is relate my experience and you can draw your own conclusion. I was und at week 4 of Incivek, und all through 48 weeks and relapsed at 1 month post end of treatment. For what it's worth...Mark
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766573_tn?1365170066
What with you being genotype 3A I am not sure what you mean.

You may have realized that treatment for genotype 1 is an entirely different ballgame. As far as triple therapy for Genotypes 1a & 1b how long a person treats is  dictated by viral load measurement at certain stages of treatment

Here is the one for Victrelis (Boceprevir)
http://www.medhelp.org/user_photos/show/284656?personal_page_id=1282072

Here is the one for Incivek (Telaprevir)
http://www.medhelp.org/user_photos/show/288854?personal_page_id=1282072
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766573_tn?1365170066
Oh I see what you mean. You were not RVR and the SOC holds that treatment duration is extended from 24 weeks to 48 weeks.

http://onlinelibrary.wiley.com/doi/10.1111/j.1478-3231.2011.02715.x/full
http://www.medscape.com/viewarticle/739955_2

Hopefully the others with Genotype 3 will chime in. I am out of my element. I am not sure about the  relapse rates for those who truncate 48 weeks. Either way I know it can be frustrating finding out you have to do this longer than you may have been mentally prepared.
Best of luck & hang in there!!  :)
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1669790_tn?1333666195
"Is it really necessary to do the 48 weeks?"

Since we don't know the factors that went into making this decision to trt for 48 wks, its hard to weigh in with an opinion.  Your current health, state of fibrosis, genotype, previous relapser, etc. all have a factor in this decision.  And not being Und until 8 wks also could convince your doc to extend trt.  Also, are you doing just Inf/Riba, or one of the protease inhibitors in addition?
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1815939_tn?1377995399
Idyllic posted links to excellent articles. I just want to copy and paste the section about prolonging treatment for Genotype 3. This section is found on page 6 of the Medscape article:


"Which Patients Require an Extended Treatment"

"The final question is about who should not be absolutely treated for <24 weeks. The answer to this question is easily given. An RVR is usually obtained in nearly two-thirds of patients with genotype 2 and 3, although this rate may vary accordingly with the sensitivity of the assay used to assess whether HCV RNA is undetectable or not at week 4.[3] In the remaining one-third of patients with detectable HCV RNA at week 4, SVR is not higher than 50%.[2–7] In particular, in the studies randomizing patients at baseline independently of RVR, the rates of SVR range from 26 to 41%.[6,7] Whether there are chances of increasing rates of wk4-R in this subset of slow responders is not clear, but there are no doubts that these patients need 24 weeks of treatment.[27] One approach to increase SVR for patients with a slow on-treatment response has been the intensification of antiviral treatment. For patients infected with genotype 1 who did not attain wk4-R, prolonging treatment duration up to 72 weeks increased SVR rates by reducing the occurrence of relapse.[28] A retrospective analysis of a pooled database of non-RVR patients infected with genotype 2 and 3 by registration studies showed that, in patients treated for 24 or 48 weeks, prolonging the duration of treatment may be of some advantage.[29] In patients with genotype 3 only, the role of an extended treatment up to 36 weeks has been recently, prospectively, evaluated. Among patients with no wk4-R, rates of SVR were numerically but not significantly higher in the longer treatment duration arm as compared with the standard 24-week arm.[30] These results are only apparently in contrast with the evidences generated by Willems,[29] because as in that study genotype 2 and 3 were combined and analysed together, a direct comparison between the two studies is not feasible.

A second option to increase the rates of response in patients without wk-R has been the administration of higher doses of ribavirin. As shown by the results of Win-R study, rates of SVR were significantly lower in patients with genotype 2 and 3 receiving a flat 800 mg/day as compared with those attained with weight-based ribavirin dosages combined with PEG-α2b.[31] In this respect, we have also recently shown that only dosages equal to or higher than 15 mg/kg/day are associated with rates of RVR in patients with genotype 2 and 3.[32] Whether the genetic evaluation of patients with genotype 2 and 3 infection for IL28B gene variants will better address the issue of treatment of patients without wk4-R is under investigation by our group."

http://www.medscape.com/viewarticle/739955_6


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1815939_tn?1377995399
And her is a link to an article the Journal of Viral Hepatitis (from 2009) which mentions several of the same observations. The section pertaining to Genotypes 2 and 3 is about 2/3 of the way down on the page (go to the link to see the Tables):  

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2759987/

Expert opinion on the treatment of patients with chronic hepatitis C

Genotypes 2 and 3

Interest has also focused on whether treatment duration could be individualized in some patients with genotype 2 and 3 infection; i.e. shortened due to the overall high rate of SVR (∼80%) achieved with the standard 24 weeks of treatment, or prolonged in slow responders.
Recommendations for optimizing treatment in patients with HCV genotypes 2 and 3

Shorter treatment for patients with a rapid virological response

A number of studies have investigated whether it might be possible to reduce treatment duration in some patients with chronic HCV genotypes 2 or 3 infection based on RVR. Several small studies have demonstrated comparable SVR rates after 16 weeks and 24 weeks treatment in patients with either genotype 2 (Table 2) or 3 (Table 3) infection who achieve an RVR [49–52]. However, in the large-scale randomized, multinational ACCELERATE study, in which a lower dose of RBV was used, overall SVR rates were lower following 16 weeks of peginterferon plus RBV compared with 24 weeks treatment in genotype 2 and 3 patients, although this difference only reached significance in genotype 2 patients [9]. Among the patients with an RVR, SVR rates were significantly higher in the 24-week group than in the 16-week group, both overall (85%vs 79%, P<0.001) and within each genotype group, although patients who achieved an RVR were more likely to achieve an SVR overall [9]. Overall, the significant difference seen in SVR rates was found to reflect a significantly higher relapse rate in the 16-week group (31%) compared with the 24-week group (18%; P<0.001); shorter treatment duration was associated with a significantly higher risk of relapse in both genotype 2 and 3 patients [9].

Overview of short-term treatment versus standard (24-week) treatment in patients (pts) with HCV genotype 3 infection

Overview of short-term treatment versus standard (24-week) treatment in patients (pts) with HCV genotype 2 infection

There is some evidence to suggest that genotype 2 and 3 may respond differently to treatment; overall SVR rates tend to be somewhat lower for genotype 3 patients who do not achieve an RVR compared with genotype 2 patients who do not achieve RVR, and also after shorter treatment duration in patients who do achieve RVR [9,50,51,53,54]. Whether genotype 3-infected individuals should not therefore be considered for shorter duration therapy requires further investigation.

Baseline HCV RNA levels also influence SVR rates and patients with low pre-treatment serum HCV RNA levels and RVR have been reported to respond equally well to both 16 and 24 weeks of therapy (SVR rates of 82–100% and 81–100%, respectively) [9,49,50,53]. It is possible, therefore, that these patients may be considered for shorter treatment duration.

Genotype 2 and 3 infected patients with severe fibrosis are less likely to achieve either RVR or SVR, and to relapse more frequently following 12–14 weeks of antiviral therapy [9,49,51,53]. Andriulli et al. found that patients with low pre-treatment ALT levels were also found to relapse more frequently following shorter treatment duration (14% after 12–14 weeks vs 2% after 24 weeks; P=0.04) [51]. These findings suggest that patients with severe fibrosis or normal pre-treatment ALT levels are most likely unsuitable candidates for short-term treatment, but prospective studies are needed to confirm these observations.

Optimizing response by reducing relapse rates in patients with HCV genotypes 2 and 3

There is evidence that patients with HCV genotype 2 or 3 and higher baseline viral load have lower rates of SVR and higher relapse rates after 24 weeks of treatment than those with lower HCV RNA baseline levels [9,32,50,55], and that, in patients without RVR, the lowest rates of relapse are obtained with 48 weeks of treatment and a higher RBV dose [11]. Whether increasing treatment duration would help reduce relapse rates in patients with high baseline viral load requires further evaluation.

Although patients with genotypes 2 and 3 are generally considered to respond similarly to treatment, there is also some evidence to suggest that genotype 3 patients have lower SVR rates and subsequently higher relapse rates than genotype 2 patients [32]. An analysis of data from the WIN-R trial of peginterferon alfa-2b also demonstrated higher SVR rates and lower relapse rates in genotype 2 infected patients compared with genotype 3 (72%vs 63%, and 5%vs 10%, respectively) [56]. It is possible that genotype 3-infected patients would benefit from longer treatment duration and/or higher RBV dose compared with genotype 2-infected patients; however current data supporting this comes predominantly from retrospective analyses and requires evaluation in prospective clinical trials.

A recent study suggests that patients infected with genotype 3 who have cirrhosis are 10 times more likely to relapse following treatment with conventional or peginterferon plus RBV than those without cirrhosis [57], a finding consistent with the results from the trial by Hadziyannis et al. and described below [3]. If data from cirrhotic patients infected with HCV genotype 1 are extrapolated to those with other genotypes, it is likely that longer treatment duration may be beneficial in reducing relapse in genotype 2 and 3 patients with cirrhosis. However, this remains to be established in prospective clinical studies.

Proportion of HCV genotype 2 and 3-infected patients who could be considered for shortened or extended therapy duration

In general, patients infected with HCV genotypes 2 or 3 should not be routinely treated for less than the currently recommended 24 weeks to avoid an increased risk of virologic relapse. However, patients with a low pre-treatment viral load (≤400 000 IU/mL) and an RVR (as determined by a highly sensitive assay) have the highest probability of achieving an SVR with 16 weeks of therapy (Fig. 4). Such a regimen may be a reasonable option for these patients, especially if tolerability of longer treatment may be a concern. The cut-off for low-viral load in patients with genotypes 2 and 3 based on the ACCELERATE data is ≤400 000 IU/mL [9]. As with genotype 1, baseline viral load should be determined in two samples, taken at least 4 weeks apart.

Overview of the ACCELERATE data: 16 vs 24 weeks. SVR: sustained viral response.

Shortening of treatment duration should not be considered for patients with cirrhosis, persistently normal ALT values or co-infection with HBV or immunocompromised patients such as those with HIV infection or those who have undergone liver transplantation.

There may be patient subgroups with genotype 2 or 3 infection that might benefit from extended treatment duration to reduce relapse rates. Results from the trial by Hadziyannis et al. found evidence for reduced relapse rates in genotype 2 and 3 pts with advanced fibrosis/cirrhosis as well as high baseline viral load when treated for 48 weeks in comparison with 24 weeks [3].
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4705307_tn?1412366616
Again thank you for your input!
1st to maybe: In your circumstance I find a lot of my frustration. When I brought this subject up with my Doc. He assured me there are no guarantees. No matter how long I treat, 24, 36 or 48 weeks. But that there are "Better drugs in the pipeline", basically no more interferon. So if this tx fails... I could consider another protocol.
2nd to idyllic: thank you for the the web sites. I will review them to be sure, I have become very aware of the differences in being a 1 or 3. Although I still don't understand how we as a people with a disease can delineate one from another. Then too this is an issue that carries over my experiences in twelve step programs. No addiction is greater than another, it is still addiction and all who are there are seeking help to understand their addiction process.
3rd to flcyclist: Basically I have gt 3a, was first diagnosed  in in 2003, VL was 176,000. I had not seen a doctor again until last May, where through my  blood work, ( elevated enzyme levels). My primary care, knowing I have hep c referred me to specialist. Where through more testing found my VL to be log 5.71 (514,000). AST: 230, ALT 400. All other values within the ref. ranges. The only other test was an ultrasound, through which it was found, in short.. I have a "fatty liver". No other tests were preformed. Fibrosis ? I have no idea.
This is my first attempt to rid my body of this virus, hopefully it will be successful and I will attain an SVR by or after next October 25th, whose counting right...
I am going to open my trackers, I closed them in a moment of discomfort with myself. So beyond that I shall keep my hope in the Doctors and my faith in a higher power I choose to call God.
Thank you again!        
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1815939_tn?1377995399
The articles give you the data behind the reasons for extending treatment. But I also want to address your questions:


"My question, Is it really necessary to push treatment 48 weeks? If a VL comes down to 130 @ week 4, then is UND @ week 8 and remains UND, is it really necessary?"
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You did not attain an RVR. You were still DET at week 4. This is a predictor of response. Those who do not attain an RVR have a higher relapse rate and a lower SVR rate. By prolonging treatment one has a better chance of completely eradicating the virus by giving the drugs a longer period of time to complete their "job."

From the articles:

"There is evidence that patients with HCV genotype 2 or 3 and higher baseline viral load have lower rates of SVR and higher relapse rates after 24 weeks of treatment than those with lower HCV RNA baseline levels [9,32,50,55], and that, in patients without RVR, the lowest rates of relapse are obtained with 48 weeks of treatment and a higher RBV dose [11]."

"Results from the trial by Hadziyannis et al. found evidence for reduced relapse rates in genotype 2 and 3 pts with advanced fibrosis/cirrhosis as well as high baseline viral load when treated for 48 weeks in comparison with 24 weeks [3]. "

(The cut-off for low-viral load in patients with genotypes 2 and 3 based on the ACCELERATE data is ≤400 000 IU/mL [9].)


"What is the logic and how is that value reached?"
----------------------------
The value is reached by doing studies which tell the researchers which treatments work the best.

Dr. Kenneth Sherman gave an excellent presentation at the liver conference in which he had graphs which displayed the mechanism of viral eradication and the amount of time it takes to totally eradicate the virus based on the response rate. That presentation is no longer available to view for free, but I watched it about 10 times, LOL. Basically, the virus decreases at a mathematical rate. What he explained is that seemingly minute differences in the amount of time it takes to get to a certain level (lets just say VL at week 4) translates into large differences how fast the VL decreases because it decreases at a mathematical rate. So, if person A reaches a certain benchmark in 2 weeks and person B reaches that same benchmark in 4 weeks, it is going to take person B much longer to totally eradicate the virus. He was talking in terms of days, but it was many days difference (as an example, 100 days versus 200 days or 100 days versus 300 days). Those were not his numbers. I am just trying to explain what he was talking about.

I don't know if that helps explain it or not, but the point it, successful treatment results in a mathematical rate of decrease in virus population and so treatment  success depends on treating long enough to totally eradicate the virus (as well as having a high enough blood level of the treatment drug in the body). Let's say the mathematical rate of virus decrease would get a person to total eradication in 26 weeks. Well, 24 weeks is not going to cut it for that person. Same thing, if the mathematical rate of decrease would get a person to total eradication in 30 weeks. Again, 24 weeks is not going to cut it for that person either. Some people may need 47 weeks to completely eradicate the virus. And, unfortunately, some people still have not been able to eradicate the virus at 48 weeks. So they relapse.

Here is another presentation, an excellent presentation with slides, and you will notice towards the middle and end of the presentation that the presenter states, more than once, that treatment success depends on treating with a high enough dose for a long enough period of time. He also talks about methods to overcome or counteract some negative prognostic aspects (mainly increase dosages and lengthen treatment).

http://74.43.177.57/courses/2010/pg/pawlotsky/player.html

He is talking about Genotype 1, but a lot of what he says applies to Genotype 3 also. You can skip the part on DAAs if you like (slides 17 through 31) but I think it would be important to watch slide 32 and the rest of them all the way through slide 68 because he explains a lot about treatment failure, which is primarily due to insufficient response to Interferon and Ribavirin. You just have to extrapolate what applies to Genotype 3.


"But my critical thinking still wants to know, " Is it really necessary, and do the benefits warrant the doubling of this protocol. "
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Well, the studies seem to indicate that the relapse rate is lower and the SVR rate is higher with the longer treatment. A person could take his chances and do only 24 weeks instead of 48 weeks. Maybe the person would attain SVR and maybe the person would not attain SVR. The question is, knowing that the rate of SVR is higher if one does 48 weeks (in your circumstances), is it worth the gamble NOT to do the 48 weeks. It is sort of like Russian Roulette because
one is, in fact, gambling with one's life and one's health when one starts second guessing the studies and the study results. And this does not even take into account the misery of months of treatment, only to relapse because treatment was cut short.

I was detectable at week 4 and I did 48 weeks of treatment. So did several others on the forum. We are attaining SVR. Would we have attained SVR on 24 weeks. Well, maybe, maybe not, but we were not going to risk that so we continued on with the recommended length of treatment and we are now reaping the rewards.

I do want to to add that there are some who do everything they are supposed to do and still do not attain SVR. So there is never a 100 % chance. But, if one relapses despite having done everything possible/right to attain SVR and do treatment as recommended, at least one knows that one did everything one could possibly do and one is not kicking oneself around the block for taking shortcuts.

Best of luck. You can do it.
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766573_tn?1365170066


Wow hrsepwrguy was right there really are lots of factors that go into the consideration of treatment duration with Genotype 3. Especially with fatty liver

http://tinyurl.com/co63jl2
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766573_tn?1365170066
Hey sorry if I quoted the wrong person on here,.
Here is that link.

http://www.hcvadvocate.org/hepatitis/Basics/steatosis.pdf

It is from HCV Advocate and is about Steatosis. I have seen elsewhere on the forum that fatty liver is associated with Genotype 3 so sorry if this is redundant as I bet the OP already knows.

I hope this all works out and you become more confident in your treatment duration :)
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317787_tn?1373214989
Hi I wanted to wish you the best during your tx.  Everyone will be more than happy to help in any way they can with the side effects that you may have along the way.
I am sorry you have to do 48 weeks, it is a long time.  I did it, was UND at 4 and 8 weeks, was stopped at 43 weeks and relapsed.  You only want to have to do this tx once.
Dee
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4113881_tn?1415853876
Hey Timothy...glad to see you still pushing forward. Im not going to add anything to the above as it seemed everybody thoroughly covered the topic. You know my situation and Im a 3a who extended treatment to 28 weeks instead of 24 since I technically didn't clear at 4 weeks. If my insurance would have went for it, Id have done 36 weeks because I didnt RVR. Since you didnt clear at 4 weeks either...being a G3...Id roll with the 48 if you can tolerate it. Especially since you say your Ultrasound showed a Fatty Liver.
Anyways...glad to see you back posting my friend.

ABN
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4705307_tn?1412366616
Thank you, I really had a rough month! I don't know if the shuffle in dosing between my ninth and twelfth injections were the cause...but honestly I feel better, not to be confused with good by no means! LOL But I am now in my eighteenth week and have regained some cognitive abilities.
I know thinking that others thought I had purposefully sabotaged my program hurt. I take this stuff so serious I m definitely anal about it.
As far as the fatty liver issue, its true but like so many things.. I pushed off to the side thinking it meant little if anything at all.            
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4113881_tn?1415853876
I got diagnosed with a Fatty Liver 3 years after I caught Hep C. I didnt think nothing of it either until I started reading about it. It seems that it is definitely a negative factor. Anyways...18 weeks is good...I think once you get into the 20's you will feel a....second wind so to speak....I did at least. Although I felt awful...mentally I felt a ton better once I hit the 20's. I banged out #28 on Easter...so thats it for the interferon for me. One more week of Riba and its the waiting game.
Im glad your doing better cognitively my friend....thats definitely a plus.
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4705307_tn?1412366616
Just got back to the site...I agree with you. After reading just a little info on Fatty Liver, freaked me out. The first article calls it a precursor to cancer. After the initial sock and I to read more, the most important thing to remember, this to is reversible!!! The most important thing we can do is continue doing that which we are doing, get healthy!!!
Again I haven't read much as of yet, not sure I want to until I talk to my doctor on the 12th.
Yes I feel better, but I have begun pushing the envelope, probably to much but I compare it when I first started pushing weight, I need to cause my body to work, regardless of how much "the committee" says no.
I really am at a loss as to why you and others are being cut off at 28...
Have you tried contacting Genetech (pegasys)? They have a patient assistance program, if it were not for them I would never have been able to do this tx in the first place.
pooh5811 truly pointed out some very enlightening studies to me. I have no doubt about the protocol.
You seem very intelligent, please contact pegasys they are involved in more than just the dual tx I am on, not sure if you are too.
Again thank you too for your input.  
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