Very little has been published about relapsers after SVR. There are several old articles about this, and provided the same Genotype is involved, it's assumed to be viral reactivation, rather than reinfection.
Only small studies have followed SVR patients for several years. A Spanish study showed persisting virus in blood monocytes, liver hepatocytes and fibrous tissue and in several other body tissues. These days, this is not a big deal. In the unlikely event that the virus may become uncontrollable again, the new DAA's will soon be available to deal with this.
Long-term Interferon has been trialled to minimise any risk of relapse. It has been discarded as it was obviously unpopular with patients, and any benefits were not conclusive.
The reality is that cirrhotics need long term exposure to DAA's. I hope cost will not affect this. Cheers.
TazKat said
Apr 19, 2014
my question too barnacle..
Barnacle said
Apr 19, 2014
Just a thought but if the higher rate of relapse among cirrhotics is due to virus hiding in the poorly perfused fibrous tissue I wonder why a post SVR treatment regimen wouldn't wouldn't be able to seek out those hiding little monsters. Or am I completely oversimplifying the issue?
patiently_waiting said
Apr 18, 2014
OldenSlow wrote:
PW - They need to put some hurry up in their research. I could use some regenerative help with more than just my liver.
Haha, you and me both partner. For me they should start right between my ears.
OldenSlow said
Apr 18, 2014
Malcolm - Thanks yet again for the clarity. I do think the subject will be of more than academic interest for some time to come, at least in this country. Until cost issues are resolved, the trend is towards later stage fibrosis as a qualifier for treatment. We can hope that the arrival of sof/ldv in the fall, along with its more complete study data, will help mitigate that. That's going to be one pricey miracle pill, though. Gilead may be able to offer steep discounts elsewhere, but it won't happen here. Our best bet, as usual, is competition in the marketplace. More sooner than later, I hope.
Gator - Appreciate and agree with your thoughts. The doc told me from the outset that even w/SVR, he will continue with twice yearly scans. I'm so accustomed to that schedule at this point, it's hard to even see it as inconvenience. I just show up down at the imaging center every 6 months, whether they like it or not.
PW - They need to put some hurry up in their research. I could use some regenerative help with more than just my liver.
patiently_waiting said
Apr 18, 2014
I'm also hopeful that regenerative medicine will advance to the point where it can help as well. There was a press release yesterday about a new cloning method for stem cells that adds new hope that soon we may be able to grow new tissue for transplantation, using the recipients own DNA so there's no rejection. While technically this has been done before, as I understand it, it was only successful when using infant cells and not adults. What they reported yesterday is taking cells from one middle aged and one senior and creating viable stem cells from them. Any practicable treatment from this is likely still a ways off but here's to hoping.
Thanks Malcolm for the concise summary and explanation that us fellow cirrhotics will be able to consider when we reach SVR. As I mentioned in a previous post, as recently as a year ago, I did not foresee that the new DAA's would be as effective as they appear to be. I am quite amazed that for the first time in thirty years, I have completely normal lab results which I assume is an indication that my liver is currently functioning well. The inconvenience of HCC monitoring in the future is a small price to pay if I can avoid the progression towards decompensation.
My physician did mention a cirrhotic patient who had achieved SVR a few years ago, but neglected to do any post-treatment follow-up imaging or exams. She recently returned to his care and was diagnosed with advanced HCC that has progressed too far for medical intervention. Very sad, but a good lesson learned for us advanced fibrotic/cirrhotics going forward.
Abstinence from alcohol and follow-up imaging should be obvious for us cirrhotics, although the former can be a challenge which I understand. I would add that it is easy to focus on our liver disease, but ignore the rest of the picture in the interim. I agree that one should not worry too much about numbers after SVR. Instead it seems like a good time to improve or implement some positive lifestyle changes, e.g. diet, exercise, et al., to go along with the extra miles gained with improved liver health. It would be pointless to finally beat Hepatitis C and then succumb to heart disease, diabetes or other chronic illnesses that can be influenced by lifestyle choices. I apologize if I sound too "preachy".
mallani said
Apr 17, 2014
Hi all,
There are many questions on the Forum about fibrosis regression after SVR. This is a complex subject.
Three genes have been identified, that hasten fibrosis progression in HepC. Hopefully, this is only of academic interest, as most patients will now be cleared of the virus before cirrhosis occurs.
The search goes on for biochemical markers that predict likelihood of fibrosis regression in HCV cirrhotics, and various antifibrotics have been mentioned. Studies show that in 1 year, post-SVR cirrhotics can achieve an improvement of at least one Fibrosis stage in ~50% of cases, 40% are unchanged, and 10% actually worsen. As more post-SVR cirrhotics become available for study, these figures may change.
Basically, a compensated cirrhotic has normal liver function. The important thing is to halt the progression of fibrosis. SVR does this in most cases. Whether the fibrous bands and bridging fibrosis are resorbed is not that important. The important thing is to reduce the portal venous pressure. The liver is keen to do this, as it requires oxygen from the portal vein. The fibrous tissue surrounding the portal sinusoids is attacked by macrophages, allowing the sinusoids to dilate. This increases the portal flow, and decreases the portal venous pressure. The back-pressure enlargement of the spleen eases, varices shrink (if present), and the liver gets a more normal blood flow from the gut via the superior mesenteric vein. This happens in virtually all cases, even through fibrous scars remain between lobes and lobules. The other post SVR change, is thinning of the limiting plate between the blood sinusoids and hepatocytes. This allows better perfusion of the hepatocyte with oxygen, drugs and nutrients. These last two vital changes are microscopic, and not necessarily associated with a decreased Fibroscan score.
So, fellow cirrhotics, don't get too concerned about numbers after SVR. Any fibrosis resolution may take years, but your liver will be working well. Remodelling will continue, so the risk of HCC is still there ( but much reduced). Don't drink alcohol and get your followup imaging. Cheers.
Hi David,
Very little has been published about relapsers after SVR. There are several old articles about this, and provided the same Genotype is involved, it's assumed to be viral reactivation, rather than reinfection.
Only small studies have followed SVR patients for several years. A Spanish study showed persisting virus in blood monocytes, liver hepatocytes and fibrous tissue and in several other body tissues. These days, this is not a big deal. In the unlikely event that the virus may become uncontrollable again, the new DAA's will soon be available to deal with this.
Long-term Interferon has been trialled to minimise any risk of relapse. It has been discarded as it was obviously unpopular with patients, and any benefits were not conclusive.
The reality is that cirrhotics need long term exposure to DAA's. I hope cost will not affect this. Cheers.
my question too barnacle..
Haha, you and me both partner. For me they should start right between my ears.
Malcolm - Thanks yet again for the clarity. I do think the subject will be of more than academic interest for some time to come, at least in this country. Until cost issues are resolved, the trend is towards later stage fibrosis as a qualifier for treatment. We can hope that the arrival of sof/ldv in the fall, along with its more complete study data, will help mitigate that. That's going to be one pricey miracle pill, though. Gilead may be able to offer steep discounts elsewhere, but it won't happen here. Our best bet, as usual, is competition in the marketplace. More sooner than later, I hope.
Gator - Appreciate and agree with your thoughts. The doc told me from the outset that even w/SVR, he will continue with twice yearly scans. I'm so accustomed to that schedule at this point, it's hard to even see it as inconvenience. I just show up down at the imaging center every 6 months, whether they like it or not.
PW - They need to put some hurry up in their research. I could use some regenerative help with more than just my liver.
www.cell.com/cell-stem-cell/abstract/S1934-5909(14)00137-4
Thanks Malcolm for the concise summary and explanation that us fellow cirrhotics will be able to consider when we reach SVR. As I mentioned in a previous post, as recently as a year ago, I did not foresee that the new DAA's would be as effective as they appear to be. I am quite amazed that for the first time in thirty years, I have completely normal lab results which I assume is an indication that my liver is currently functioning well. The inconvenience of HCC monitoring in the future is a small price to pay if I can avoid the progression towards decompensation.
My physician did mention a cirrhotic patient who had achieved SVR a few years ago, but neglected to do any post-treatment follow-up imaging or exams. She recently returned to his care and was diagnosed with advanced HCC that has progressed too far for medical intervention. Very sad, but a good lesson learned for us advanced fibrotic/cirrhotics going forward.
Abstinence from alcohol and follow-up imaging should be obvious for us cirrhotics, although the former can be a challenge which I understand. I would add that it is easy to focus on our liver disease, but ignore the rest of the picture in the interim. I agree that one should not worry too much about numbers after SVR. Instead it seems like a good time to improve or implement some positive lifestyle changes, e.g. diet, exercise, et al., to go along with the extra miles gained with improved liver health. It would be pointless to finally beat Hepatitis C and then succumb to heart disease, diabetes or other chronic illnesses that can be influenced by lifestyle choices. I apologize if I sound too "preachy".
Hi all,
There are many questions on the Forum about fibrosis regression after SVR. This is a complex subject.
Three genes have been identified, that hasten fibrosis progression in HepC. Hopefully, this is only of academic interest, as most patients will now be cleared of the virus before cirrhosis occurs.
The search goes on for biochemical markers that predict likelihood of fibrosis regression in HCV cirrhotics, and various antifibrotics have been mentioned. Studies show that in 1 year, post-SVR cirrhotics can achieve an improvement of at least one Fibrosis stage in ~50% of cases, 40% are unchanged, and 10% actually worsen. As more post-SVR cirrhotics become available for study, these figures may change.
Basically, a compensated cirrhotic has normal liver function. The important thing is to halt the progression of fibrosis. SVR does this in most cases. Whether the fibrous bands and bridging fibrosis are resorbed is not that important. The important thing is to reduce the portal venous pressure. The liver is keen to do this, as it requires oxygen from the portal vein. The fibrous tissue surrounding the portal sinusoids is attacked by macrophages, allowing the sinusoids to dilate. This increases the portal flow, and decreases the portal venous pressure. The back-pressure enlargement of the spleen eases, varices shrink (if present), and the liver gets a more normal blood flow from the gut via the superior mesenteric vein. This happens in virtually all cases, even through fibrous scars remain between lobes and lobules. The other post SVR change, is thinning of the limiting plate between the blood sinusoids and hepatocytes. This allows better perfusion of the hepatocyte with oxygen, drugs and nutrients. These last two vital changes are microscopic, and not necessarily associated with a decreased Fibroscan score.
So, fellow cirrhotics, don't get too concerned about numbers after SVR. Any fibrosis resolution may take years, but your liver will be working well. Remodelling will continue, so the risk of HCC is still there ( but much reduced). Don't drink alcohol and get your followup imaging. Cheers.