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Understanding HCV Nonresponse and Identifying Candidates for Retreatment

Understanding HCV Nonresponse and Identifying Candidates for Retreatment

A new Clinical Care Options article.

See:  http://www.tiny.cc/ilRHl

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Mike
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Avatar_f_tn
This is a really good CME on who may benefit from re-treatment and who will not. Dr. Shiffman is a great hep doc.
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Avatar_f_tn
Thanks, Mike, for posting that.  Susan
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144210_tn?1273092382
Interesting. The article states that someone with a 2 log drop by week 12 can up the interferon.

quote"...it has been hypothesized that some patients with a partial treatment response can achieve undetectable HCV RNA if switched to a more intensive interferon regimen (Figure 6). The time at which to intensify the interferon regimen can be anywhere between 12 and 24 weeks.."unquote

I was under the impression that upping the peg initially (i.e.double dosing) is probably the best method to help achieve RVR or EVR.  Between weeks 12 and 24? did i read this right?
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Avatar_m_tn
Yes, you read it right but, that approach is just theoretical at this point - according to the article.
"Based on these observations, it has been hypothesized that some patients with a partial treatment response can achieve undetectable HCV RNA if switched to a more intensive interferon regimen (Figure 6). The time at which to intensify the interferon regimen can be anywhere between 12 and 24 weeks. However, the patient must be able to tolerate the higher dose of peginterferon alfa and be motivated to continue with treatment. The major limitation to this strategy is firstly the accessibility of higher dose of peginterferon alfa to many patients, as it is unlikely to be approved by many insurance companies without more concrete data supporting this approach and, secondly, the increase in the discontinuation rates because of tolerability issues. In patients treated with a more intensive interferon regimen, HCV RNA should continue to be monitored at monthly intervals. If the patient does not achieve undetectable HCV RNA within 12 weeks of dose intensification, treatment should be discontinued. By contrast, if the patient does achieve undetectable HCV RNA, this treatment should be continued for an additional 48 weeks. This is the typical duration of extended treatment in patients with slow virologic response."

As stated there need to be more "concrete data supporting this approach". I believe that extending treatment duration has more supporting data for achieving SVR but the dose increase seems to also include extending treatment 48 week post undetectable so maybe it's the best of both worlds - if you can tolerate it and either convince your insurance co to pay for it or pay for it out of pocket. The increased dose and duration will be hard to get approved in my opinion. Mike

Mike
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144210_tn?1273092382
If one did have access to the increased peg, then when the optimal time to take it seems to be pretty important. It always made the most sense to me to take it early to help achieve RVR.  I wonder where the 12 to 24 wk idea came from. I mean even a hypothesis has to have some sort of data to formulate a good hypothesis.
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179856_tn?1333550962
As stated there need to be more "concrete data supporting this approach". I believe that extending treatment duration has more supporting data for achieving SVR but the dose increase seems to also include extending treatment 48 week post undetectable so maybe it's the best of both worlds - if you can tolerate it and either convince your insurance co to pay for it or pay for it out of pocket.


Right..  However - the problem with interferon is you can't see the damage that it's doing to you on the outside.  With an increased dosage of that stuff also goes the better chance that you will ruin your thyroid for life. Since those sides match the tx sides almost exactly...nobody finds out until they finally get a TSH pretty well into treatment.  Is it better to take a bigger dose for a shorter duration or a smaller dose for a longer duration?  Who knows.  I am just pretty sure that in my mind...extending gives you such a better chance at getting 'them all' that to me - it was worth it.

Also Mike I agree with your assessment - what I think he says above is - at week 12 up the dose then continue on for 48 weeks. So that would seem to me that you ARE going to be doing the larger more damaging (potentially) dose for the extended period anyway.  I wouldn't want to think of what kind of shape I would be in today had I done both - I'm barely a viable human being at this point 8 months post with the thyroid and the anemia just as bad as when some people treat in the first place.
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144210_tn?1273092382
The SX are really whats driving my curiosity. I kind of thought "Hit it hard and hit Early", and then when the sides come on, taper down to a level that allows extended treatment. The above approach almost seems like an opposite effect. Start SOC, then at 12 to24 wks.. Hit it hard. Seems the sides would really be rearing there ugly heads by then. Doesn't make sense but sense may have nothing to do with it.
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164778_tn?1201445560
My reading of the 12-24 week theory stated above is this: it really is ideal to START treatment with a double dose at week 1-12; but for all the other reasons above - insurance non-payment, autoimmune problems, early discontinuance, unacceptable side effects - then perhaps the NEXT best thing for those who are partial responders at week 12 is to increase the dose for those people at that time. If we knew who would be early responders, who would be partial responders, who would be null responders, it would be SO much easier to plan treatment.

Mark
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144210_tn?1273092382
Got that right. All I know is that I was UND at 12 wks and EOT. But I relapsed. I will allow myself to believe I was an EVR (although it is possible I was an RVR) when formulating my next round of treatment. I know going in from past experience that I will be anemic and maybe worse. I know i can persevere through severe sides on pure will power for quite awhile; but over time they will wear me down.
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144210_tn?1273092382
..and besides, why would insurance cover extra meds any more readily at 12 wks than at start of treatment?
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144210_tn?1273092382
I believe it was FLGuy who double dosed on peg. Wonder if he did it at start or later; and if SX got worse than SOC.
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I did a couple of things.  Started full dose riba a week in advance and then doubled (Pegasys 180 x 2) for the first 4 weeks. Got to und. after week 2.  Starting vl was about 4 mil i/u..  The double peg was about 25% more sx than single peg.  Tolerable and do-able since I knew it was going to be brief.  Goal was to get to und as soon as possible and to be und for as long as possible for the duration.  Doc's benchmarks were und at 4 do 48, not und at 4 do 72.  G3 relapser.
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144210_tn?1273092382
Right. So at 4 wks you went to SOC. I too am around 4 mil and G3 relapser. Have you gone to 6 mos post yet?
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96938_tn?1189803458
I'm about 5 weeks post now.  Was und at 3 weeks post tx, but don't think that tells me a lot yet.  The 2nd tx was weight-based riba (1200), first time was only 800.
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Avatar_n_tn
it seems Shiffman updates his re-treatment survey on an annual basis but doesn't put that  much time into it. Some of the references in this edition are as recent as this year, but he doesn't seem to have tracked new results very closely. For example, if one looks on pubmed, there are lots of recent studies on induction dosing. Rather than falling back on "it has been hypothesized that " it would be more useful to dig in and make sense of what this new data is saying. In the case of dosage increases, the benefits don't  seem obvious.
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144210_tn?1273092382
it would be more useful to dig in and make sense of what this new data is saying. In the case of dosage increases, the benefits don't  seem obvious.
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Is this your opinion, or are is there evidence that dosage increases have no benefit?
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Avatar_m_tn
Admittedly, I haven't been number crunching laterly, but my doc told me that double-dosing might help my chances of SVR around 10%, and if memory serves me -- I think a similar figure was stated over at Clinical Care Options on perhaps the Dieterich/Jensen video. It's been awhile. Video I saw was "Doc Eye for the Hep Guy" and dealt with re-treatment issues.
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144210_tn?1273092382
Well, 10% is 10%. I'll take whatever I can get. thanks Jim.
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Avatar_n_tn
what I meant is not that dosage increases have no benefit, but that the data indicating where and how much they help is contradictory and thus confusing. I tend to give "my doc told me..." statements little credibility until I can see what data that opinion is based on. If you search pubmed with queries like '+induction +hcv' or ' "+dosage +hcv" it's easy to uncover quite a bit of recent work in this area. For example, carr'07 :
Efficacy of interferon alpha-2b induction therapy before retreatment for chronic hepatitis C.
Liver Int. 2007 Oct;27(8):1111-8.
PMID: 17845540

which, on fairly large patient groups (~200)  concluded

"Conclusion: For chronic HCV patients who have failed IFN, induction with retreatment does not improve SVR, but may be beneficial for patients with genotype non-1 HCV."

Shiffman has been publishing that same re-treatment review for years now and it seems to serve as the basis for a lot of Continuing Medical Education (CME) presentations (the "echo chamber effect" - if you repeat something it becomes "true").  It would be useful if he took the time to actually make sense of what this new data shows...
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I haven't read the study you reference, but just wanted to comment on a few things peculiar to gauf's specific situation. First is that he's a geno 3, so the quote you reference above from the induction study conclusion may not be completely applicable to him. i.e. "...but may be beneficial for patients with genotype non-1 HCV."  Second are the particulars about gauf's treatment that in my view doesn't clearly label him as someone who has "failed IFN". If you examine gauf's specifics, he "failed" his first course simply because he got an infection and had to be discontinued at week 11 as a consequence of that. It wasn't because the IFN/riba weren't effectively eradicating his virus (as evidenced by his 12 week UND). Also, gauf has a high BMI and was only receiving 800mg of riba, and although apparently he did have some anemia issues, again it shows he was still nicely responsive even in the face of sub-weight based riba dasage. On gauf's second go around he was given 1000mg riba, still well below weight based riba levels for his size, and again managed to be UND by week 12 and throughout his remaining 24 week course. He did relapse after this, but it's clear he was responsive to IFN+riba even at sub-optimal riba levels (and perhaps even sub-optimal IFN dosage based on what some of these studies indicate). From where I'm sitting, it looks like gauf may have lain waste to his virus on his second go around with true weight  based riba (if he could tolerate it) and/or by simply extending his treatment to 48 weeks (or thereabouts). Considering gauf's confounding fatty liver, it's not really surprising that was enough to put the kibosh on his SVR with a mere 24 weeks and on low riba.
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Avatar_n_tn
I was commenting on the most recent edition of Shiffman's retreat survey, which Mike posted in the initial comment. With respect to gauf's specific case, given the details you describe, it sounds like correct dosing is more likely to be the issue than exploratory overdosing.

A recent large-scale study of weight-based riba dosing may be relevant to his case:

http://www.eurekalert.org/pub_releases/2007-10/jws-wdo100107.php

even  1g/day may not have been sufficient to meet their recommended dosage (which I think will fairly quickly replace the old binary 1/1.2 rule). Also note their observations on the benefits of the extra time for 2s/3s.
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Yes, I agree with your assessment, however I believe the NAFLD plays the largest role in my relapse. Weight based Riba may have been enough, but not certain by any means. (See my most recent post, DD for chubbs)  If I knew then what I know now, I would have lost the weight and potentially saved myself alot of suffering. I am afraid for G3's particularly because fatty liver is very prevalent with this Genotype. If they get a substandard doc (like I had), they are risking a relapse.
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I found the program informative. Perhaps I have not been reading the Clinical Care plans for over a year, so the Retreatment program was new to me.  

As I understand the benefit of these programs, it is to get the most recent information out to the medical profession who may not be hepatologists.  In this program he presents a lot of ideas on methods for retreatment that most average clinicians would not do.  Somehow we have to mainstream the information and this seems to be a viable option.  IThe information may not be the most recent , but  it is still way ahead of the curve for most gastro guys.

The one thing he said that I wonder the truth of is on breakthroughs.  He indicated that viral breakthroughs are almost always -- maybe he even said always - caused by dose reductions.  Either the physician dropped the dose because of side effects or the patient missed doses in error or on purpose.  I just wonder if that is true.

As to induction dosing, I too think it is imperative to knock it out fast.  I would be willing to do this.  However Shiffman also points out the difficulty gettng insurance companies to go along with anything other than SOC.  

The point I took away from the program is that you do need to make a change if you have a viral load at week 12.  Most of us knew this, but it was nice to read it.
frijole

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Avatar_n_tn
AMAZING!!!!  That they are finally figuring out what many of us, and some of the sharper HCV doctors have known for about ten years now (and let's not forget Dr. Ben Cecil)!  That you can increase the Interferon for slow responders, and see the viral load curve move down more rapidly.  This is exactly why I did the 'doubledose' of Peg-Intron, after my first long tx, which was a slow, slow, late response, and ultimate relapse.  Of course it makes sense that for a responder, using higher inf. horsepower leads to reduced time to undetected, and higher odds of SVR for the same length courses of tx.  But the catch is, that you have to maintain the dosage levels, and thus the viral decline curve!

Why more doctors are not already aggresively using flexible dosing approaches for marginal and late responders is really beyond me.  The approach might not work for the partial or non-responder, since the interferon obviously does not 'push the right buttons' to begin with for these individuals....but for those that do respond, even the very slow, drawn out responders...there is great logic, and also great demonstrated results...in using increased dosages.  I am talking about multiples here in dosing, not just pushing it up 10% or so...which is insignificant.  Doctors have used much higher dosages of interferon for other diseases, where necessary....so using a double dose of Peg is really not so earth shaking, nor frightening.  

My attitude during both my first and second tx was to take enough interferon to eradicate the virus, and to stay on it until I was darn sure it would stay gone.  Both of my doctors were very enlightened, and supported my approach.  The only reason tx #1 did not work was my developing anemia that caused me to discontinue the high dose infergen after being undetected for only 5 months.  My next tx, for 72 weeks, using doubledose Peg-Intron hit the decline curve, and duration points necessary to get SVR.

Too many people out there don't want to acknowledge that pumping up the inf. can make a huge difference, and look for cases to support their stance, I believe, because they may want to justify not doing the necessary dosage, since it is very intimidating, and honestly can be scary.  But, I think time will show that it can really work.  Read some of Ben Cecil's case studies to see how he has approached the scientific quest for SVR.  I like how he calculates the decline curve, and eradication time estimates based on 'half life' theory.  It may not work exactly that way, but it sure is a close approximation.  He was not my treating doctor, by the way, but my doctors used somewhat similar approaches.  Getting the right decline curve, and maintaining it to the end, was their holy grail.

I hope you are all doing well, and having fun!!!

DoubleDose
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Avatar_n_tn
you're right, it is a good summary and I'm just being cranky. It's just that after

Shiffman ML.
Retreatment of patients with chronic hepatitis C.
Hepatology. 2002 Nov;36(5 Suppl 1):S128-34. Review.

Shiffman ML.
Retreatment of chronic hepatitis C virus infection in patients who failed to achieve sustained virologic response.
Minerva Gastroenterol Dietol. 2004 Mar;50(1):37-49. Review.


Shiffman ML.
Management of patients with chronic hepatitis C virus infection and previous nonresponse.
Rev Gastroenterol Disord. 2004;4 Suppl 1:S22-30. Review.

Sethi A, Shiffman ML.
Approach to the management of patients with chronic hepatitis C who failed to achieve sustained virologic response.
Clin Liver Dis. 2005 Aug;9(3):453-71, vii-viii. Review.

Sethi A, Shiffman ML.
Approach to the management of patients with chronic hepatitis C who failed to achieve sustained virologic response.
Infect Dis Clin North Am. 2006 Mar;20(1):115-35. Review.

among others, a look at the new data would be helpful. And speaking of new data, here's another induction study with rather complicated results

Wartelle-Bladou C, Arpurt JP, Renou C, Pariente A, Pillon D, Nalet B, Picon M, Glibert A, Chousterman M, Grasset D, Morin T, Bernard P, Fischer D, Ramdani M, Lagier E, Rotily M; Viral Hepatitis Group of the ANGH.

High dose daily interferon-alpha induction and secondary adjunction of ribavirin in treatment-naive patients with chronic hepatitis C. A multicentric, randomised, controlled trial.
Gastroenterol Clin Biol. 2006 Apr;30(4):525-32.

"CONCLUSION: A 4 week IFN-alpha induction significantly increases the EVR rate in patients with HCV genotype 1, 4 or 5. Late secondary adjunction of ribavirin to IFN-alpha for 6 months in HCV-RNA negative patients after 6 months of IFN-alpha significantly decreases the relapse rate in patients with HCV genotype 2 or 3, but not in patients with genotypes 1, 4 or 5."

Full text is free.
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Avatar_n_tn
>Getting the right decline curve, and maintaining it to the end, was their holy grail.

I  agree: the virus remains visible for such a comparably short time that unless you're seeing a consistently strong negative slope on the VL curve you're tx is quite likely headed into the weeds. However I disagree about   heavier dosage as the main tool for achieving that decline. Data like that reported in the7-day predictor thread above tends to confirm that part of not getting to SVR has to do with the inefectiveness of ifn in some individuals. As the arsenal of available tools widens, adding new drugs seems a better way to keep that curve. My current thinking for a  re-tx strategy is heading more along the lines of "test weekly; start with soc, when the week (n+1)-n drop is less than say 1.5 add X, then Y, then Z". where XYZ are vx950, R1626, NTZ in no particular order. That way you're challenging an ever-dwindling pool of virus to keep developing escape mutations.  Only trouble is, there's still years to go to get  the new meds.
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Avatar_m_tn
You seem to be going thru many of the same thought processes that i am going thru and for pretty much the same reasons.

I too believe that both of our non response was at least indirectly caused by steatosis.
Steatosis and HVL go together (not sure which one comes first). As does low cholesterol.
Low cholesterol with G3s seems to be a good indicator of slow response. An up side to this if that if Tx is working your cholesterol rises into the normal range and stays there. When Tx isnt working it drops and then returns to it previous low level. With relapse it rises and stays there all through Tx then drops back down to its pre Tx level after relapse has occured.

I intend to loose a few more Kilos (not that i have that much to loose) and quit smoking (smoking suppresses our immnue system) B4 I Tx again.

If you flick me an email I'll send some of the info I have if you like.
CS
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Avatar_m_tn
Like the way you think with add additional drugs to SOC.
CS
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Avatar_m_tn
As long as we're going through hypothetical out-of-the-box retreatment scenarios, let's consider pre-dosing ribavirn, as "FLGuy" did. He was UND at week TWO. with this approach. Haven't followed the induction discussion, but in the Dieterich/Jensen video -- Doc Eye for the Hey Guy -- the numbers looked good. I think a ten percent improvement.

Lastly, an idea I threw out around a year ago to very little enthusiasm -- and that is somehow timing the beginning of treatment with a low/lower viral count -- which studies suggest (low viral count) is a postive indicator of SVR. Viral load seems very cyclical in some of us (mine varied from 40 million to just over a hundred thousand over a three year period) so the idea might be to test viral load monthly and jump in when it hits a "trough". Of course for those who want/need to treat right away, would not work.

-- Jim
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Avatar_m_tn
Jim - somehow timing the beginning of treatment with a low/lower viral count
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Now thats something I hadnt thought of. Makes sense though.
CS
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223152_tn?1321976790
Nice summary - I get your point.  I will definitely check out the freebie!  Hopefully we will have an arsenal of drugs somewhere in the future.  But the fact is, right now, all we have is interferon and ribavirin.  I am not getting it that it takes so long to "get the word out" to insurance companies and doctors about options for slow viral responders.  I guess we need a lobby.
frijole
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Avatar_m_tn
Def don't want to open this can of worms, but did read that some on herbal preps reportdly  lowered some people's VL, although it could have been coincidental. Two most credible sources of herbs seem to be Dr. Misha Cohen in CA -- she wrote a book with Dr. Gish in CA. and Dr. Zhang of NYC. Of interest, is that I was supposed to treat a couple of years before I did when I had a high viral load -- over 20 million if I remember correctly. But due to enzyme elevations from some Chinese Herbs, my treatment was delayed. And then delayed further due to other stuff. By the time I was ready to treat, to my surprise my VL was a hundred thousand or so which rose to 1.5 million three months later, which was the day before. I sometimes wonder what my result would have been had I treated when I was supposed to. Besides the herbs, the only thing I did differently during that period was to go on a very low fat diet prior to treatment. But, of course, it could have been coincidental, and like I said, the herbs elevated my enzymes close to 1000. That said, I sometimes wonder if the apparent acute-like flare created by the herbs, somehow got my immune system jacked up to bring them back to earth. Could this have lowered my VL? All speculation.

-- Jim
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Avatar_m_tn
Your ALT flare is one of the reason why I dont like herbs. You just dont know whats in them, even when obtained from a reputable source. The flare could just as easily been liver toxicity rather than immune related so I'd bet on the low fat diet.

My ALTs were 84 at last blood test which is the lowest they have ever been. I kinda think thats diet related even though I still eat like cr@p. So I might try a low fat diet (Pritiken or something similar)
B4 my next VL test see what happens.

CS
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Avatar_m_tn
One other thing, I think we would both rather treat with a VL of 1,500,000 than with a VL of 20,000,000 even with RVR. You may have Double Dosed for longer at the very least.

CS
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Avatar_m_tn
I would think that herbs from the two sources mentioned would be more reliable from the "no-name" brand I used which were loose herbs (looked like weeds) made into a tea.

That said, my highly speculative point was that could it be possible that the seemingly toxic herbs triggered what basically amounted to an acute reaction and that the acute reaction then caused the immune system to go into overdrive resulting in less virons when all the dust settled?

Isn't this parlty what happens in those acutes who clear spontaneously. In other words, is it possible that the herbs somehow helped in an unexpected way, a la Nietzhe's "if it doesn't kill you it makes you stronger". Just speculating as part of a discussion, so please no one take the above as what I believe or advocate.

-- Jim
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My guess is that the herbs you took which caused the ALT spike were probably just plain toxic and that's why the enzymes soared. Unless you had a bad allergic recation to them, but then you probably would have noticed that. As far as I know a toxic substance (like herbs or alcohol or CCl4 etc) wouldn't cause an immunological response similar to what would happen if a viral or bacterial invader was detected. So I'm not sure that would have been responsible for your subsequent rather dramatic viral decline afterwards. I know you weren't seriously suggesting that's what happened, just freely associating on the matter. Plus who knows, maybe a non-pathogenic toxin could cause an immunological response similar to the acute syndrome you mentioned above? I just haven't heard anything along those lines myself is all.
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Avatar_m_tn
Probably. Even most probably.

But as long as I'm speculating freely, it's possible the hebologist got it "sort of" right but with just too high a dose for my particular system. The other thing I should probably add is that I had a Hep B booster shot that same week.

After graphing out the dates of the herbal treatment and the booster shot, at first glance the booster shot looked like a candidate. In discussing with my hepatologist at the time, he didn't discount the possiblity that the booster shot caused the elevation, although he did put his money on the herbs.

He also threw out the possiblity that it may have been a combination of events (herbs plus booster)  which goes back to the idea of possibly that the herbal mixture was an immune booster but just too toxic for my inidividual system to handle at the time. I actually saved one "potion" of the herbs for future analysis, but they accidently got thrown away and with that goes the identity of what I actually consumed.

The other problem is that there was a couple of year gap between my 40,000,000 viral load (pre herbs) and my hundred thousand something viral load closer to treatment. Had I done a viral load at the time of the flare and maybe monthly thereafter, could have come up with some interesting data.

-- Jim
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Avatar_m_tn
Third variable is that I had a long and hard cardio workout the day after the booster shot and while doing the herbs. Sometimes overdoing it physically can lower the immune system, as "HR" has pointed out. In fact, during my twenties, I had 2-3 relapses (dark urine, sky high enzymes, fatigue, etc) that were in each case caused by very strenuous physical activity. I happened to be one of those rare birds with a very obvious acute stage (the first one) and therefore I can pinpoint how long I've had Hep C, with good accuracy which would be about 38 years. No doubt, having an acute stage may have worked to my favor in that I appeared to only have progressed to stage 2 or 3 in 38 years. Studies do suggest that those with an acute stage have slower progression.
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Avatar_m_tn
Should be those with a "symptomatic" acute stage have slower progression. Everyone has an acute stage just not everyone knows it.
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151263_tn?1243377877
Yeah sounds like the hep B vaccination would be a likely culprit, certainly other vaccinations are known to provoke immune responses that go beyond the scope of of the limited immune response they're intended to provoke. I've heard from many people getting a flu shot and then coming down with either the flu, or flu like symptoms immediately thereafter. As far as the herbs possibly being immune boosters, I've always been pretty dubious of those claims. I tried a lot of different stuff over the years, and never really observed any correlation with my VL going down in concordance with any of them (or experiencing any apparent/observable immunostimulative effects). But obviously that's really tough to nail down with such a purely anecdotal experience like that. I do believe that some herbs probably have at least some direct anti-viral efficacy against some viruses. For example, I'm pretty sure there is documented evidence that licorice does have antiviral properties against certain viruses (don't recall which offhand). But to my knowledge the antiviral effects are fairly mild and inconsistent, and I've never seen convincing evidence it would work in any meaningful way against HCV. Not to say that some witches brew might someday be put together with other herbs/supplements that might actually influence hep C viral load though. But getting back to its long term influence on VL, even if whatever herbs you took did have direct antiviral efficacy, your VL would have probably quickly rebounded after stopping them (similar to what usually happens when IFN/riba are stopped).

Also you mentioned: "In fact, during my twenties, I had 2-3 relapses (dark urine, sky high enzymes, fatigue, etc) that were in each case caused by very strenuous physical activity."

When you say "relapses" do you just mean symptomatic flare ups? If so I recall a few times in my 20's (before finding out my HCV+ status) coming down with these strange persistent flu like symptoms (when I usually never got sick), usually after smooching with a new girlfriend. I never knew what it was (no it wasn't STD's before anyone chimes in!), but I suspect the challenge confronted to my immune system by a new person's "germs" was somehow enough to cause my immune response to HCV to flare up. So considering my minimal damage after 24 years maybe there's something to the acute-symptomatic-minimal fibrosis thing.
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Avatar_m_tn
we'll test that theory, I had both A & B vacs(prior to beginning treatment), A took B didn't...Redoing B, first shot was a few months back, second one is in Feb....Got my flu shot today...Here is a question (which I knew would drive me nuts when the meds were handed to me!!) Have been doing the redipen 120 @ .5 setting...Now I have a months supply of 150 redipens(samples) and was told to do .4 setting...Think there would be any benefit to doing the full 150 @ the . 5 setting for the 4 weeks? I'm sure my next batch will be 120 again...my negative thought would be on the reduction back down to 120. I believe the 150 @ .4 is higher dose than 120 @ .5, so regardless I'm already increasing some....thought for fodder...pro
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Avatar_m_tn
I was told it is more common than one would expect, one vac taking and the other not. Didn't matter A or B
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Avatar_m_tn
Re Relapses...

My initial reaction to the HCV virus was a classical full-blown acute infection  -- Jaundice skin, yellow eyes, dark urine, light stools, extreme fatigue and sky high enzynmes -- forgot how high but ALT way over 1000. I was around 20 at the time.

Being young and "invicincible"  (and totally uneducated in a condition caused by a virus that hadn't been discovered yet) I didn't particularly treat the situation with any more seriousness than one might treat a common cold. Maybe because of that I had a "relapse" around three months later.

When I say "relapse" I mean that the aforementioned symptons went away after a period of time -- three months the first time -- they then came back in full-force, the jaundice, dark urine, high enzymes, all of it. After my first relapse, I started to take things more seriously, saw my first hepatologist, had my first biopsy, and was told to have total bed rest for six to eight weeks.

This pattern played itself out several times in my twenties, and the trigger always seemed to be intense physical activity. You might say around half of my twenties were lost to HCV in one way or another. Of course the other half was quite active, physical and typical of men in their twenties. It seemed I was either in fourth gear or reverse during that time. Should add no drug use or heavy alcohol consumption during that period.

Then, around age 32 --the pattern thankfully stopped.  No more relapses in spite of heavy physical activity until my mini-relapse at age 57 during a week when I took Chinese Herbs, had a Hep B booster and did some heavy workouts. I cal it a "mini relapse", because unlike the others the only symptons were fatigue and elevated enzymes -- I think just under 1000. No jaundice, dark urine, white stools, etc.

I was seriouslly thinking of treating around the time of the let's call it "Chinese Herb Relapse" but my hepatologist at the time decided maybe I should wait until the enzymes normalized which he predicted they would in 4-6 months, and he was correct. A couple of years later I finally treated.


-- Jim





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151263_tn?1243377877
Sorry I'm not familiar with the redipens, I used the pegasys one shot deal. So I wouldn't know what setting would be advisable or what would be the appropriate dosage for someone of your weight (without looking it up). But in general, the more I learn the more I have the stance that if I had to do treatment again, I'd go with with a bolder dosage strategy. I'd probably go with a higher than normally prescribed dose of IFN and/or riba during the first phase of treatment (lasting anywhere from the first 4-12 weeks). But since you're already knee deep into an extended treatment, not sure if a slightly higher dose of IFN would be advisable or make much of diff at this point. But if you think you can tolerate it and the risk of it causing a discontinuance (due to low ANC's etc) seems minimal, then that's probably what I would do. Good luck whatever you decide.
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151263_tn?1243377877
Interesting story. Not to be nosy, and obviously no need to reply if you don't want, but do you know how you came into contact with the disease? 1969 was a good year to be 20, can't help but wonder.
;-)
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Avatar_m_tn
thanks for the input..after a bit more sleep replenishment and a clearer mind, I've decided just to do what was advised and go with the flow till the end. High dose riba already has me tettering on the edge, as you say, this far along, probably best not to risk going over the edge playing with the peg.
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