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Mike Simon Thread Continued

Mike,

The other thread was closed so I hope you didn't mind I grabbed an open slot so we can all follow your progress in one spot.

First, I guess a kind of congratulations in a weird way is in order! In fact, I think you mentioned earlier that you never thought you'd want the virus to return -- but it really appears to be the MUCH better of the two alternatives. Of really good note is that your liver is "soft" and only stage 2 out of 6. That's practically virginal!

I understand, based on some recent studies I've seen, that elevated enzymes can correlate with hepatitis C in the liver, even if non-detectible in the blood.

Assuming though that your're still hep c negative via senstive Heptimax TMA, then how will they monitor any future progress regarding viral eradication if that is their intent with the proposed peg and riba? Or, are they simply using peg and riba for mainteance until let's say Vertex proves itself -- and then they plan to try that.

Last question -- and if you're too worn out -- please don't bother to answer. When they found Hep C in your liver via biopsy, did they do any special tests to locate it -- or was it just a normal biopsy? I assume this was some special test they used since a number of people have post-tx biopsies but haven't heard any report back that they were hep c positive but VL negative.

Again, glad you're liver seems to be working out, and as for the pesky virus, I'm sure you'll have it beat. This also I guess accounts for why your wise transplant team has had your viral load tested every month after your SVR.

All the best.

-- Jim
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Avatar universal
Thanks Mike and I apologize for asking so many questions so don't feel you need to keep answering if you need some rest. In any event, last question for a while.

Did they actually do a PCR or TMA using your liver sample, or was the diagnosis made based on liver activity per the biopsy report.

Your report read in part ..."Chronic Hepatitis Viral Type C with mild activity and mild to.."

My biopsy report had similar language but I'm certain they didn't do a PCR or TMA on my liver tissue but probably just correlated the inflammation with HCV since that is what my serum tests showed. At least I guess that's how they came to that conclusion.

-- Jim
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The test used was an in-house quantitative real-time RT-PCR assy.
Mike
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Thanks for the clarification.
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I'll try to mail you the body of the <a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15996238&query_hl=42&itool=pubmed_docsum">Bizollon'05</a> study I linked below, along with an earlier paper from the same group since they may be relevant. The study followed 142 patients who received liver transplants between 90-01 and underwent tx (pre-peg). Their post SVR relapse stats were pretty low (2/34). One of these two relapsed after  a steroid "blast", as you described earlier:
<em>"Of the two relapsers, one developed virological relapse 3 months after steroid bolus therapy for severe rejection. In this case, rejection was largely favored by a significant decrease in immunosuppressive therapy justified by impaired renal function. This case does suggest maintaining a stable immunosuppressive therapy in patients with SVR."</em>

All of the patients were on immunosuppressants during tx, but they don't provide much information on the reduction schedule: <em>"Patients should be on cyclosporin or tacrolimus at the time of inclusion, but some patients did not receive the same immunosuppressive medication during the antiviral therapy. Immunosuppression was not adjusted in liver recipients with histologically documented recurrent chronic hepatitis C after OLT. "</em>.
What puzzles me is that the apparent late relapse happened not in the context of severe immune suppression, as you had been concerned, but in response to a strengthened immune system resulting the prograf reduction. Maybe these events were but unrelated, but from your description of Paulo's reaction, this is apparently not uncommon.

One possible clue, is that anti-HCV effect has been reported for cyclosporine, an alternative to prograf (<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=16611911&query_hl=12&itool=pubmed_docsum">Ishii'06</a>) and two abstracts from the recent DDW reference use of cyclosporine in tx (abstract ids 654 and T1538). Anyway, I hope there is some chance the virus returns to its previous, controlled status as you go back to last Feb's prograf dosage.

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I am so saddened to read your news.  Still better this way than the other possibility.
All the best to you and we will support you all the way.
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I'm very sorry to hear that the bugs are still floating around in you. I know how thrilled you were to finally have cleared the virus. Hopefully in the not-too-distant future you can truly say that SVR has been reached one-and-for-all.

It's good to know that they were able to quickly get the definitive answer and that your doc feels this is the "best-of-the-worst" of the various options that might have been causing the elevated LFT's. Also good to hear that they have a game-plan set for going forward.


One thing your episode shows is the huge limitations of current PCR/TMA testing methodologies. For example, a geno 1 patient who goes undetectable via serum at week #12, effectively "flys blind" for the next 36 weeks (and beyond if they don't relapse). It makes me wonder if the more sensitive testing of PBMC's will be able to give a much more fuller (and truer) picture, and have a greater correlation to viral levels that may exist in the liver and elsewhere in the body. Hopefully so. And hopefully they can have a PBMC (or equivalent) test available for the general population in the near-future.


Keep your chin firmly up, Mike. If you can bounce back from your bike accident like you already have (not to mention having had your liver swapped-out), dealing with your old nemesis HCV is eminently doable.


TnHepGuy
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