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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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96938 tn?1189799858
This is going to sound a little dumb.  I think that you were clear at the time of transplant and presumably the new liver was not hcv - positive.  If those two assumptions are correct, where did the virus come from?
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Just read Willing's post at end of closed thread so thought I'd pull it up here as he poses similar questions. As Willing, I also am a little confused as to why your virus didn't show up via senstive serum TMA if you relapsed because of your lowered anti-rejection dosage. Is it possible, it had nothing to do with the dosage reduction , but that you simply fell into a certain per cent of people who apparently have virus in liver cells but not in serum ? I wonder if this is something we all should be concerned about if our enzymes start to rise after SVR but starting to sound a little like DD now :)

Willing wrote at end of original "Mike Simon" thread" --

"welcome back to the recurrent nightmare (everybody on the bench get up and scoot over a bit). I'm sure there's deep disappointment, but from my ignorant perspective HCV resurgence looks like downright good news relative to rejection. Is the HCV titer you quoted (UND at 30iu) from serum? Your post makes it sound as if the in-house RT-PCR they ran on the biopsy tissue detected HVR RNA in cells through the serum test was und but I wasn't certain whether I read it correctly. I hope you are encouraged by his words about VX. Hopefully you'll be able to stay at the reduced dosage ifn/rbv if the goal is maintenance. Have you thought about whether alinia might be an alternative? I have to confess there's a lot about your post I don't understand. Elevated ALTs are definitely triggered by the immune response to HCV (stellate cells etc.) so that lowering the FK in the presence of virus explains that result, but what was/is keeping serum VL UND in the presence of FK-reduced immune response? Anyway, all the best. "
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Avatar universal
Fl Guy: I think that you were clear at the time of transplant and presumably the new liver was not hcv - positive. If those two assumptions are correct, where did the virus come from?
-------------------------------------------------------

I guess that is what I was trying to say in a more long-winded fashion :)

Let me throw out a couple of possiblities:

1) DD theory :) -- Virus was never fully eradicated, only eradicated in the serum but still lived on in the liver cells. The question here though is why didn't it jump back from the liver to the serum, especially since mike is taking I assume immunosuppresive drugs. Possibly a silver lining here for those of us who worry it might. And, of course, what is the clinical significance of being TMA negative in serum but positive in the liver cells?

2) Although unlikely, is it possible that Mike's transplanted liver could have belonged to someone who was tma negative but had hep c in the liver tissue? I believe -- could be wrong here -- that a very small per cent of the population may fall into that category. I also wonder if they actually run tma's on liver tissue prior to transplant or just in serum?

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I will also echo the previous questions.  How do they determine that virus is present in the liver, if the serum PCR says undetected.  Are they using another PCR for the biopsied tissue? (I assume the PCR ,30 IU result, you posted was the SERUM test?)

Or do they assume liver virus is active if you experience liver ALT activity, or inflammation?

Will your upcoming inf. tx provide a good likelihood of eradicating any existing liver HCV ?

Does your doctor have an opinion of the 'persistent HCV after SVR issue?  

I wish you the very best of luck in your new challenge.  You look to be in good shape liver-wise, and your attitude seems very good.  Go for it and finish up the job!!

Best Wishes!

DoubleDose
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Avatar universal
Just another quick question.  Do you find that the Liver surgeons and transplant specialists share the shame general conceptions about HCV as the general hepatologists and gastroenterologists?  Do the surgical docs. believe that the virus gets fully 'eradicated' with tx, and subsequent SVR.  Do they feel that the liver (and serum) are the only places that are truly 'infected' by the virus?  Do they worry about gastric tissues, bone marrow, brain tissue, salivary system, glands, etc. harboring the virus before or after tx???

Just curious as to how they perceive the issue of viral 'cure', viral persistence after SVR, occult virus (which apparently you are suffering from a version of currently), etc.

Thanks for your insights.

DoubleDose
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92903 tn?1309904711
Thanks for sharing and keeping us posted. What a very strange set of circumstances. Sorry you have to get back on the juice - even if it is better than some alternatives.
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Avatar universal
<a href="http://www.natap.org/2005/HCV/090505_20.htm">This</a> is the study I was looking for that shows HCV virus in the liver of some individuals with negative TMA.

Please note this editorial note:

"..immediately below is a brief commentary. In a following email is a longer EDITORIAL from JID discussing and questioning the study methods and findings. Two important points are raised: was the study methodology reliable in detecting HCV RNA in PBMCs & the liver; if reliable, what are the clinical importance of such findings. One potentially important point of clinical significance is that HIV+ individuals who test HCV RNA negative in blood may have HCV-infection, but not realize it."
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I my surgeon Paulo feels that the virus was never fully eradicated but a low enough VL that my serum tested undetectable per Heptimax. As Paulo explained it, when the immunesuppressive drugs are reduced to a certain level (different for each patient) the enzymes can become elevated due to the immune system tying to eradicate the virus in the liver cells. This did not surprise him at all. In fact, when he came into the room he was looking at my labs (serum) and he said that it looks like HCV to him. I asked what the biopsy said and he asked did I get it already. He had been in South America and just got back late Sunday. I said I had the biopsy Friday and he found the report and confirmed the HCV. The full report had not been transcribed yet but I have the abbreviated report. He is scheduled to go over it in depth with the liver pathologist but he doesn't think anything will change with a closer inspection. He characterized it as a tricky balancing act with the anti rejection drugs and the HCV.
Paulo didn't mention any suspicions that the virus is elsewhere aside from my liver. It just didn't come up. As far as how his views coincide with the hepatologists the only clue I got was that he told me he didn't want me fooling with the hepatologists at the center - that they can screw things up easily.
In case it's not clear I had HCV prior to transplantation so that accounts for my having it post TP.
Kalio: Believe me when I say that I am not trying to goad you in any way but when Paulo palpated my liver and found it soft and normal I told him that I could feel it like I could when I had active HCV - before clearing with TX. I asked him about the "restructuring" and he laughed and said " It's crazy what some people say - it's swelling that you feel". I just wanted you to know what he said. I know that he's not God and he could be wrong but this guy does a lot of transplants - sometimes 2 in a day - and he knows this stuff better than anyone I have every talked with.
Mike
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I asked Paulo what happens to HCV patients with undetectable serum who get a "blast" (steroid intravenous) and he said the HCV can bloom quickly and he's seen it a number of times. Jim or willing - whoever speculated that was why I got so many Heptimax tests -you're likely right on that one.
Mike
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Avatar universal
Thanks for the explanation. What I'm still confused about is how did he make the determination that you still have HCV virus in your body, albeit at levels below Heptimax? The only way I would imagine this to be possible is if he did some sort of PCR or TMA on your actual liver tissue.

Maybe this sentence in your prev post gives a clue:

"As far as how his views coincide with the hepatologists the only clue I got was that he told me he didn't want me fooling with the hepatologists at the center - that they can screw things up easily."

LOL about how different specialists view each other. Still, I wonder in lieu of actual tissue testing for HCV, what conclusions a hepatologist would come to regarding to whether or not the virus has indeed return. Not to say who might be right or wrong. Still a bit beyond my head.

All the best.

-- Jim
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They tested the tissue sample. Mike
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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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Avatar universal
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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Avatar universal
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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the transplant drs in the above paper seemed to have reached the same conclusion:
<em>"In our previous study, we reported that the late virological relapser was the only patient positive for HCV RNA in the graft at inclusion. A separate manuscript detailing our center's experience about using tissue HCV RNA RT-PCR as a more accurate predictor of SVR is currently in preparation. In fact, many questions, such as the optimal duration of therapy have still not been resolved in the treatment of recurrent HCV infection and it is interesting to speculate that the direct detection of HCV RNA may suggest longer durations, resulting in improved SVR (16,17), especially in patients with genotype 1."</em>

sounds like RNA quant of biopsy tissue might become more routine, at least for transplants.
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I Just want to weigh in with my good thoughts and hopes for you. You were one of the first people who responded to me when I was confused about my 12 week log drop. Your steady,kind comments to all for the year I've been on this board have been appreciated by more of us then you will probably ever know--even us only occasionally posting lurkers! Good luck to you--you certainly have Karma on your side!

Tracy
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I don't even know what to say.  I have learned so much from you and what has been said of your experience with HCV.  My gosh, if someone is testing your strength they can quit anytime as you have won.
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I wish you had gotten good news instead of the bad news, but it is better than the worse news.  Rest up, we are saving you room on the "GROUP W" bench!
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Mike
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I think I should clarify Paulo's comment that he wanted me to stay away from the hepatologists at the center. I think what he was saying is that I didn't need to be on big doses of interferon and ribavirin and that the hepatologists might treat me like any HCV patient and vigorously attack the virus with standard doses. I may be reading a little into this but that is my belief and I certainly don't want to disparage or make it seem as though Paulo was disparaging that group of doctors because that certainly wasn't his intent, nor is it mine. It was meant more in a humorous manner when I wrote that. Sort of a little comic relief, if that term can apply to this serious thread. Again I can not express how overwhelmed I am at your wonderful reponse to my situation. I feel a little awkward and undeserving but I am trying hard to get over it. You people are just so great and you've really helped me get through this "little bump in the road". You really have and I am so touched by all of your comments. Every one of you has touched my heart. Thank you so much. Mike
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