Aa
Liver Disease with Undetectable HCV RNA
People infected with HCV (as indicated by antibodies in the blood) who have an undetectable viral load are usually considered to have inactive disease, and undetectable HCV RNA six months after completion of treatment is regarded as a cure. But a study in the December 2008 Hepatology suggests hidden HCV may still cause liver disease progression. M. Hoare and colleagues studied 172 HCV antibody positive but HCV RNA negative individuals who underwent liver biopsies between 1992 and 2000. After 102 were excluded for having other possible causes of liver damage, the remaining 70 participants were analyzed after a median seven years of follow-up.
Within this group, 5.7% became HCV RNA positive during follow-up, but the rest had continued undetectable viral load. Only five participants had normal liver biopsies; 82% had some fibrosis, with 24% having moderate to advanced fibrosis (Ishak stage 2-3). HCV RNA negative individuals had fewer CD4 T-cells and more CD8 T-cells than uninfected control subjects, but the same number as patients with detectable viral load. These findings suggest that HCV antibody positive people with undetectable HCV RNA have an ongoing immune response in the liver, supporting the view that the virus may persist in the liver in a majority of these cases.
Within this group, 5.7% became HCV RNA positive during follow-up, but the rest had continued undetectable viral load. Only five participants had normal liver biopsies; 82% had some fibrosis, with 24% having moderate to advanced fibrosis (Ishak stage 2-3). HCV RNA negative individuals had fewer CD4 T-cells and more CD8 T-cells than uninfected control subjects, but the same number as patients with detectable viral load. These findings suggest that HCV antibody positive people with undetectable HCV RNA have an ongoing immune response in the liver, supporting the view that the virus may persist in the liver in a majority of these cases.
Jeff, the quotes above are from the text of the article. Re your questions
>Had all of the patients cleared spontaneously with no INF/riba exposure?
yes - three groups were considered in the analysis (ab,rna-), (ab,rna+) and controls. none had treated
>If so, none of this might apply to those who have achieved SVR.
maybe, but then maybe not. Not much seems to be known about the 'natural history' of spontaneous clearance vs svr
>Why such a high number of participants with apparent relapse? Could this be to further exposure to the virus?
yes, as noted above the fraction of rna- patients who became viremic during the 7 year follow up seems higher than rates published for SVR durability studies - hence the glimmer of hope that SVR is better. There was no discussion of distinguishing new-infection vs progression though they do seem to have taken care to exclude all other possible risk factors for liver disease.
>Are there any biological indicators of the presence of the HCV virus outside >of evidence of inflammatory response? If not, it could be that there is a >persistent inflammatory response even though the virus is eradicated. >Would INF/riba-treated patients have the same persistent response?
They acknowledge that "inflammation in the liver is a sensitive indication of hepatic disorder , but indirect evidence of infection". Also they applied ultracentrifugation to the serum samples ala Castillo but still came up UND. They did not examine the bx tissue for HCV RNA. So maybe there is some mysterious factor that accounts for the inflammation other than virus - but Occam would argue against it.
>Does the study involve serial biopsies or was there just a single biopsy done?
>Without serial Bx's it's impossible to make conclusions about disease progression.
Serial bxs and progression assessment were not done - but they're not making any statement about progression. A single pathologist examined all slides.
>How long was the biopsy done after becoming HCV RNA negative? The >shorter the interval between becoming HCV RNA negative and the biopsy, >the more likely the inflammatory response was due to recent viral exposure.
good point - I couldn't find a clear answer. Re the sources of the bx data they state "... between July 1992 abd December 2000. During this period, all patients who were anti-HCV antibody positive were offered liver biopsy irrespective of RNA status".
So nothing is known about how much time lapsed between viral clearance and the bx. Still, fibrosis does not develop quickly and the average fibrisis scores for the rna- and rna+ groups were 1.92+-1.24 and 1.75+-0.75 respectively.
>Looks like the conclusion that "Nonviremic HCV antibody-positive patients >have a liver biopsy that is usually abnormal." is valid. The rest is conjecture.
agreed - but that conclusion, of itself, is pretty remarkable, particularly because the rna- and rna+ groups exhibited such similarity in CD8+ andCD4+ T cells. If the immune response of the hcv rna- group isn't fighting virus it sure is acting like it.
>Had all of the patients cleared spontaneously with no INF/riba exposure?
yes - three groups were considered in the analysis (ab,rna-), (ab,rna+) and controls. none had treated
>If so, none of this might apply to those who have achieved SVR.
maybe, but then maybe not. Not much seems to be known about the 'natural history' of spontaneous clearance vs svr
>Why such a high number of participants with apparent relapse? Could this be to further exposure to the virus?
yes, as noted above the fraction of rna- patients who became viremic during the 7 year follow up seems higher than rates published for SVR durability studies - hence the glimmer of hope that SVR is better. There was no discussion of distinguishing new-infection vs progression though they do seem to have taken care to exclude all other possible risk factors for liver disease.
>Are there any biological indicators of the presence of the HCV virus outside >of evidence of inflammatory response? If not, it could be that there is a >persistent inflammatory response even though the virus is eradicated. >Would INF/riba-treated patients have the same persistent response?
They acknowledge that "inflammation in the liver is a sensitive indication of hepatic disorder , but indirect evidence of infection". Also they applied ultracentrifugation to the serum samples ala Castillo but still came up UND. They did not examine the bx tissue for HCV RNA. So maybe there is some mysterious factor that accounts for the inflammation other than virus - but Occam would argue against it.
>Does the study involve serial biopsies or was there just a single biopsy done?
>Without serial Bx's it's impossible to make conclusions about disease progression.
Serial bxs and progression assessment were not done - but they're not making any statement about progression. A single pathologist examined all slides.
>How long was the biopsy done after becoming HCV RNA negative? The >shorter the interval between becoming HCV RNA negative and the biopsy, >the more likely the inflammatory response was due to recent viral exposure.
good point - I couldn't find a clear answer. Re the sources of the bx data they state "... between July 1992 abd December 2000. During this period, all patients who were anti-HCV antibody positive were offered liver biopsy irrespective of RNA status".
So nothing is known about how much time lapsed between viral clearance and the bx. Still, fibrosis does not develop quickly and the average fibrisis scores for the rna- and rna+ groups were 1.92+-1.24 and 1.75+-0.75 respectively.
>Looks like the conclusion that "Nonviremic HCV antibody-positive patients >have a liver biopsy that is usually abnormal." is valid. The rest is conjecture.
agreed - but that conclusion, of itself, is pretty remarkable, particularly because the rna- and rna+ groups exhibited such similarity in CD8+ andCD4+ T cells. If the immune response of the hcv rna- group isn't fighting virus it sure is acting like it.
The fact that 82% had some fibrosis in the remaining group of 70 does not surprise me. Fibrosis does not reverse itself overnight. What would be very interesting is to see how their fibrosis evolved over the years after becoming SRV, by surveying their liver biopsies over time. I hope there will be more studies like this done with a larger sample of people. 70 is not that big.
To me SRV is still a great goal to achieve, some kind of milestone, but not the end of the "fight". Lifestyle, diet, good nutrition and exercise is the key to remain healtly all our lives regardless if we are HepC positive or not, becomes SRV or still carry some hidden virus. HepC has been a wake up call for me, it has changed my life dramatically. I have learned to take good care of myself since then. I have never been so healty in my life than now and probably better of now than many people who don't have Hepc but don't care at all about their health.
To me SRV is still a great goal to achieve, some kind of milestone, but not the end of the "fight". Lifestyle, diet, good nutrition and exercise is the key to remain healtly all our lives regardless if we are HepC positive or not, becomes SRV or still carry some hidden virus. HepC has been a wake up call for me, it has changed my life dramatically. I have learned to take good care of myself since then. I have never been so healty in my life than now and probably better of now than many people who don't have Hepc but don't care at all about their health.
Very good question. I know that elevated ALT is a marker for liver disease and higher mortality rates. It would make sense that low liver enzymes go along with decreased levels of inflammation since it is the enzymes leaking from the damaged liver cells that cause the higher levels in the blood.
You are also in the category of people who have (had) normal ALT levels while actively infected with HCV. There are studies that show that this group suffers less liver damage.
I'm sure that the authors of the study mentioned in this post checked the ALT levels of the patients that they followed. I wonder if the paper mentions these results.
Jeff
Facta non Verba
You are also in the category of people who have (had) normal ALT levels while actively infected with HCV. There are studies that show that this group suffers less liver damage.
I'm sure that the authors of the study mentioned in this post checked the ALT levels of the patients that they followed. I wonder if the paper mentions these results.
Jeff
Facta non Verba
My GI doc has never mentioned anything about a liver scan since I completed tx and have SVR. Should I insist that I have one? I just had my 2 year PCR(quant) on Tuesday and will have the results back mid week.
proud48
proud48
I am wondering, if you have liver enzymes within the healthy range for your BMI, can you still have a persistent inflammatory process ongoing in the liver? I am talking very low numbers here. Like in my case 9 for ALT and 18 for AST. I had normal liver enzymes before tx as well, but in the upper normal range, which in reality was unhealthy when consideration was taken to my BMI. Aren't low liver enzyme readings post tx a sign that the inflammatory process has stopped, or are they only a sign that the HCV is gone?
This study generates a lot of questions. I haven't read the entire journal article, so many of the answers may be in the article, but....
Had all of the patients cleared spontaneously with no INF/riba exposure? If so, none of this might apply to those who have achieved SVR.
Why such a high number of participants with apparent relapse? Could this be to further exposure to the virus?
Are there any biological indicators of the presence of the HCV virus outside of evidence of inflammatory response? If not, it could be that there is a persistent inflammatory response even though the virus is eradicated. Would INF/riba-treated patients have the same persistent response?
Does the study involve serial biopsies or was there just a single biopsy done? Without serial Bx's it's impossible to make conclusions about disease progression.
How long was the biopsy done after becoming HCV RNA negative? The shorter the interval between becoming HCV RNA negative and the biopsy, the more likely the inflammatory response was due to recent viral exposure.
Looks like the conclusion that "Nonviremic HCV antibody-positive patients have a liver biopsy that is usually abnormal." is valid. The rest is conjecture.
Anyone have the entire article?
Jeff
Facta non Verba
Had all of the patients cleared spontaneously with no INF/riba exposure? If so, none of this might apply to those who have achieved SVR.
Why such a high number of participants with apparent relapse? Could this be to further exposure to the virus?
Are there any biological indicators of the presence of the HCV virus outside of evidence of inflammatory response? If not, it could be that there is a persistent inflammatory response even though the virus is eradicated. Would INF/riba-treated patients have the same persistent response?
Does the study involve serial biopsies or was there just a single biopsy done? Without serial Bx's it's impossible to make conclusions about disease progression.
How long was the biopsy done after becoming HCV RNA negative? The shorter the interval between becoming HCV RNA negative and the biopsy, the more likely the inflammatory response was due to recent viral exposure.
Looks like the conclusion that "Nonviremic HCV antibody-positive patients have a liver biopsy that is usually abnormal." is valid. The rest is conjecture.
Anyone have the entire article?
Jeff
Facta non Verba
The word occult actually means 'hidden'...this is a very interesting thread...this virus is insidus...evil all the way....it even hides in 'steatlh mode' doining its dirty work..thats if the studies on this topic are real and accuate...a little depressing indeed...but the goods news is....if one does get SVR....odds are very high one will die from a gun shot living in a big city or killed by a moose in newfoundland
ive be having a beer the day i SVR...life is too dammn short
ive be having a beer the day i SVR...life is too dammn short
Very interesting topic indeed, replication below detectable limits and persistent damage over a longer period of time. One would have to wonder if after being hammered by the boosted interferon during treatment that the virus had adapted to replicate at just above the threshold of its extinction.
jasper
jasper
"There's some glimmer of hope that IFN-assisted HCV reduction is more effective than spontaneous"
This brings the whole question of 'how important is interferon in hepC tx' right back into focus.
I believe that the whole vaccine approach was predicated on some people being able to have spontaneous clearance. If this is in fact a myth then will vaccines ever be effective enough without interferon?
What about the ideal of being able to treat with a cocktail of drugs like for HIV, without using riba or inf.? It's all about whether it is possible to stop replication 100% and over time that's the end of it, or whether it will always be necessary to enlist the immune system (and inf.) for total clearance.
Well, lots of speculation and big implications for tx going forward, but no answers as yet. Very frustrating,
dointime
This brings the whole question of 'how important is interferon in hepC tx' right back into focus.
I believe that the whole vaccine approach was predicated on some people being able to have spontaneous clearance. If this is in fact a myth then will vaccines ever be effective enough without interferon?
What about the ideal of being able to treat with a cocktail of drugs like for HIV, without using riba or inf.? It's all about whether it is possible to stop replication 100% and over time that's the end of it, or whether it will always be necessary to enlist the immune system (and inf.) for total clearance.
Well, lots of speculation and big implications for tx going forward, but no answers as yet. Very frustrating,
dointime
thanks for posting - an interesting addition to the unfolding story. Unlike some of the recent technical lab-oriented,did/did-not mitogen stimulate PBMC skirmishes, it presents data with much broader implications. Basically, it sounds as if there's a *lot* of people out there who may think they cleared spontaneously but are heading down the same path as those with chronic infection (82% with biopsy-demonstrated fibrosis) albeit at a slower pace.
The methods section emphasizes they were careful to exclude all patients in which an alternate cause of liver diseases could be suspected (weight,alcohol,HBV, etc.).
From their conclusions:
"With the aid of liver biopsy in all of these patients and critically, careful subsequent exclusion of all patients with a possible alternative cause of chronic liver disease, we have been able to challenge the view that nonviremic HCV-exposed patients have resolved infection. First, viremia was detected eventually in 5.7% of this group, a proportion that may increase with time; second, just 7.5% of patients had normal histology; third, 92% of patients had inflammation within the liver, while 82% had fibrosis, which in about a quarter would have been sufficient to prompt consideration of antiviral therapy if the patients had been viremic; finally, when cases without viremia were compared with viremic patients matched for grade of inflammation and stage of fibrosis, the phenotype of the inflammatory infiltrate was similar and distinct from that in healthy controls."
None of these patients had been exposed to IFN. What bearing does this have for SVRs? There's some glimmer of hope that IFN-assisted HCV reduction is more effective than spontaneous : 5.7% is way higher than the SVR durability stats usually reported. They do cite one 2006 study in which 11.8% of SVRs relapsed but I think there's much more data going the other way.
Overall, I think this makes a pretty good case for an eventual post-SVR bx, not so much to check on fibrosis regression as to check presence/absence of inflammatory infiltrate
"Perhaps the most important question to address in this cohort is why such cases have lower levels of viral replication. The long-term histology in those treated successfully with pegylated interferon- and ribavirin will be of interest in this context, because loss of the inflammatory infiltrate would be consistent with eradication of HCV, while ongoing inflammation, as in this series, would be indicative of low-level HCV replication."
The methods section emphasizes they were careful to exclude all patients in which an alternate cause of liver diseases could be suspected (weight,alcohol,HBV, etc.).
From their conclusions:
"With the aid of liver biopsy in all of these patients and critically, careful subsequent exclusion of all patients with a possible alternative cause of chronic liver disease, we have been able to challenge the view that nonviremic HCV-exposed patients have resolved infection. First, viremia was detected eventually in 5.7% of this group, a proportion that may increase with time; second, just 7.5% of patients had normal histology; third, 92% of patients had inflammation within the liver, while 82% had fibrosis, which in about a quarter would have been sufficient to prompt consideration of antiviral therapy if the patients had been viremic; finally, when cases without viremia were compared with viremic patients matched for grade of inflammation and stage of fibrosis, the phenotype of the inflammatory infiltrate was similar and distinct from that in healthy controls."
None of these patients had been exposed to IFN. What bearing does this have for SVRs? There's some glimmer of hope that IFN-assisted HCV reduction is more effective than spontaneous : 5.7% is way higher than the SVR durability stats usually reported. They do cite one 2006 study in which 11.8% of SVRs relapsed but I think there's much more data going the other way.
Overall, I think this makes a pretty good case for an eventual post-SVR bx, not so much to check on fibrosis regression as to check presence/absence of inflammatory infiltrate
"Perhaps the most important question to address in this cohort is why such cases have lower levels of viral replication. The long-term histology in those treated successfully with pegylated interferon- and ribavirin will be of interest in this context, because loss of the inflammatory infiltrate would be consistent with eradication of HCV, while ongoing inflammation, as in this series, would be indicative of low-level HCV replication."
I was dismayed to read this study. I've been following the debate here on the board about whether the virus persists even after SVR and naturally I didn't want that to be true. However I had to admit that the jury is still out on it and more studies need to be done. So when I came across this study I felt it was important to add it to the pool of knowledge we have on the subject.
On a pragmatic level I agree with you Mike, it is surely better to be SVR than not. On a psychological level, the idea that I might never be rid of this virus, even if I SVR, is hard to take, but it could be the reality. This one study does not settle the question but I think any advancement is welcome.
dointime
On a pragmatic level I agree with you Mike, it is surely better to be SVR than not. On a psychological level, the idea that I might never be rid of this virus, even if I SVR, is hard to take, but it could be the reality. This one study does not settle the question but I think any advancement is welcome.
dointime
As some of you may remember I finished TX 10 months ago and SVR'd about 4 months ago. I was a genotype 3a, had been infected aproximately 30 years and was a stage 3 fibrosis at my biopsy 7 years ago. So I was probably a late stage 3 or early stage 4 when treating as my blood tests were normal except for elevated ALT and AST.
What I am getting at is I drank occasionally on treatment. I am not reccomending this but I would drink about 6 beers on a friday night every month or 6 weeks depending on how I felt. This did not stop me from attaining SVR. So who really knows.
What I am getting at is I drank occasionally on treatment. I am not reccomending this but I would drink about 6 beers on a friday night every month or 6 weeks depending on how I felt. This did not stop me from attaining SVR. So who really knows.
Trinity: I will not leave the health of my liver to chance.
----------
That's how I feel about my cardiac health when I weigh any potential risks of alcohol to my liver against what both my cardiologist and hepatologist advise, plus of course, my not so great family cardiac history. Certainly respect your opinon, however, and the pro's and con's of alcohol -- not just for us HCV folks -- will probably continue forever :)
-- Jim
----------
That's how I feel about my cardiac health when I weigh any potential risks of alcohol to my liver against what both my cardiologist and hepatologist advise, plus of course, my not so great family cardiac history. Certainly respect your opinon, however, and the pro's and con's of alcohol -- not just for us HCV folks -- will probably continue forever :)
-- Jim
Yes, there is general agreement that people should not drink alcohol during treatment, although not sure if ever studied in terms of moderate use during treatment. I certainly did not drink any alcohol during treatment and would never suggest anyone else should.
Before, during or after Port, I will not risk it. Period. Some studies may indicate moderate alcohol consumptions does not damage the liver even after SVR but that's not good enough for me. Not going to take the chance, ever.
Some studies indicate age and degree of fibrosis do not impact on SVR rates. I don't believe that either. Too many variables, too many things we don't really know despite all these studies. I will not leave the health of my liver to chance.
Trin
Some studies indicate age and degree of fibrosis do not impact on SVR rates. I don't believe that either. Too many variables, too many things we don't really know despite all these studies. I will not leave the health of my liver to chance.
Trin
Oh my, and I was so hoping for a line up.
Here is the abstract:
Hoare M, Gelson WT, Rushbrook SM, Curran MD, Woodall T, Coleman N, Davies SE, Alexander GJ.
Department of Medicine, School of Clinical Medicine, University of Cambridge, Cambridge, UK.
It is unclear whether hepatitis C virus (HCV) has been eradicated or persists at a low level in HCV antibody-positive HCV RNA-negative individuals. The natural history and liver histology are not well characterized. One hundred seventy-two HCV antibody-positive, serum HCV RNA-negative patients underwent diagnostic liver biopsy between 1992 and 2000 and were followed a median 7 years (range, 5-12). Patients with any possible cause of liver injury other than HCV were excluded. A single histopathologist scored sections using Ishak criteria. Characterization of the inflammatory infiltrate in selected cases used a novel semiquantitative technique and compared with HCV RNA-positive patients and healthy controls. One hundred two patients were excluded because of a risk factor for liver injury other than HCV. Seventy patients met the study criteria; four (5.7%) became HCV RNA-positive during follow-up. Sixty-six cases remained HCV RNA-negative; five (7.5%) had a normal liver biopsy; 54 (82%) had fibrosis (stage 2 or 3 in 16 (24%)). Nonviremic cases revealed expanded portal tracts (P < 0.05), with fewer CD4+ (P < 0.05) and more CD8+ cells (P < 0.05) than healthy controls, but were indistinguishable from HCV RNA-positive cases for these parameters. Lobular CD4 staining, absent in healthy controls, was noted in both HCV RNA-negative and -positive cases and was more marked in the latter (P < 0.05) with a sinusoidal lining cell distribution. Conclusion: Nonviremic HCV antibody-positive patients have a liver biopsy that is usually abnormal. Fibrosis was present in most with similar inflammatory infiltrate to viremic cases. The presence of a CD8+ rich inflammatory infiltrate suggests an ongoing immune response in the liver, supporting the view that HCV may persist in the liver in the majority of HCV RNA-negative cases.
Here is the abstract:
Hoare M, Gelson WT, Rushbrook SM, Curran MD, Woodall T, Coleman N, Davies SE, Alexander GJ.
Department of Medicine, School of Clinical Medicine, University of Cambridge, Cambridge, UK.
It is unclear whether hepatitis C virus (HCV) has been eradicated or persists at a low level in HCV antibody-positive HCV RNA-negative individuals. The natural history and liver histology are not well characterized. One hundred seventy-two HCV antibody-positive, serum HCV RNA-negative patients underwent diagnostic liver biopsy between 1992 and 2000 and were followed a median 7 years (range, 5-12). Patients with any possible cause of liver injury other than HCV were excluded. A single histopathologist scored sections using Ishak criteria. Characterization of the inflammatory infiltrate in selected cases used a novel semiquantitative technique and compared with HCV RNA-positive patients and healthy controls. One hundred two patients were excluded because of a risk factor for liver injury other than HCV. Seventy patients met the study criteria; four (5.7%) became HCV RNA-positive during follow-up. Sixty-six cases remained HCV RNA-negative; five (7.5%) had a normal liver biopsy; 54 (82%) had fibrosis (stage 2 or 3 in 16 (24%)). Nonviremic cases revealed expanded portal tracts (P < 0.05), with fewer CD4+ (P < 0.05) and more CD8+ cells (P < 0.05) than healthy controls, but were indistinguishable from HCV RNA-positive cases for these parameters. Lobular CD4 staining, absent in healthy controls, was noted in both HCV RNA-negative and -positive cases and was more marked in the latter (P < 0.05) with a sinusoidal lining cell distribution. Conclusion: Nonviremic HCV antibody-positive patients have a liver biopsy that is usually abnormal. Fibrosis was present in most with similar inflammatory infiltrate to viremic cases. The presence of a CD8+ rich inflammatory infiltrate suggests an ongoing immune response in the liver, supporting the view that HCV may persist in the liver in the majority of HCV RNA-negative cases.
Port: We all agree alcohol is harmful when HCV-RNA positive. What do we do if we SVR,
---------------
Respectfully, we don't. Not here, and not in the medical literature. *Moderate* alcohol consumption is not associated with either the progression of fibrosis or with SVR rates.
http://www.clevelandclinicmeded.com/online/monograph/hepc/biopsy.htm#cofact
http://www.natap.org/2004/HCV/040104_02.htm
http://www.medscape.com/viewarticle/488940_3 (free Medscape Registration Required)
---------------
Respectfully, we don't. Not here, and not in the medical literature. *Moderate* alcohol consumption is not associated with either the progression of fibrosis or with SVR rates.
http://www.clevelandclinicmeded.com/online/monograph/hepc/biopsy.htm#cofact
http://www.natap.org/2004/HCV/040104_02.htm
http://www.medscape.com/viewarticle/488940_3 (free Medscape Registration Required)
This is a single study based on fewer than seventy participants whose author merely says the findings are 'suggestive'. I won't line up on the basis of such slim pickings. Some of the participants relapsed from SVR, anyway.
Who knows why C-4 cells were lower in the study? There could have been other reasons. Single small studies are single small studies and when they conclude as merely suggestive, it's a bit rich to view this as an absolute validation for or against drinking in moderation, after SVR.
On the other hand, more than 50% of Americans will die of heart disease (that means 50% of us). Cardiologists can draw on a lot more than one study of fewer than 70 when they endorse one or two glasses of red wine a day for your heart health and longevity.
We all agree alcohol is harmful when HCV-RNA positive. What do we do if we SVR, though? In the end, we don't really know what will take us out. I'll gamble on heart disease for me. If I SVR, I'll drink my glass of resveratrol, despite Hoare's one small study.
He did get his article published, but that doesn't mean much, as we know from the fallout about Cell.
Who knows why C-4 cells were lower in the study? There could have been other reasons. Single small studies are single small studies and when they conclude as merely suggestive, it's a bit rich to view this as an absolute validation for or against drinking in moderation, after SVR.
On the other hand, more than 50% of Americans will die of heart disease (that means 50% of us). Cardiologists can draw on a lot more than one study of fewer than 70 when they endorse one or two glasses of red wine a day for your heart health and longevity.
We all agree alcohol is harmful when HCV-RNA positive. What do we do if we SVR, though? In the end, we don't really know what will take us out. I'll gamble on heart disease for me. If I SVR, I'll drink my glass of resveratrol, despite Hoare's one small study.
He did get his article published, but that doesn't mean much, as we know from the fallout about Cell.
My doctor (and even the study nurse) were surprised that I'd stopped drinking completely on my dx considering I only had the occasional half beer. Maybe it depends on the condition of the liver, I dunno.
Certainly on tx it makes no sense what-so-ever to drink. I don't even think I could. I just managed my first cup of morning-tea for this week. (Oh it was wonderful!)
Certainly on tx it makes no sense what-so-ever to drink. I don't even think I could. I just managed my first cup of morning-tea for this week. (Oh it was wonderful!)
Is it "occult/persistent" HCV or simply that the study is picking up damage already done which could be exacerbated by any number of reasons including weight, lifestyle choices, etc. Also, hard to comment fully based of the synopsis but at face value the statement " Within this group, 5.7% became HCV RNA positive during follow-up" makes no sense if it's referring to individuals who were SVR. If not, what is the reference? As to alcohol -- and I can't believe (OK, I CAN believe LOL) this has once again been interjected -- I'll just add a balancing point of view that both myself (and many others who have posted in the past ) have been told it's OK to drink in moderation after SVR. In fact, my liver specialist encouraged me to drink a nightly glass of wine to help with my cardiac profile. Last post on this topic due to both common sense, but most some tendonitis in my arm today.
-- Jim
-- Jim
Me too charm. Told to not drink even with SVR. Doc summed it up like this. You could enjoy 1 glass of wine on a special occasion such as the birth of a grandchild. To me that means very very few glasses of wine.
Trin
Trin
I imagine thats why the hepatologist advised me even if SVR you MUST have liver scan (with iodine) done every year without fail.
My gastro told me the same.
No alchohol no matter what!
My gastro told me the same.
No alchohol no matter what!
Might be why all my docs told me I could never drink again, even after I had reached SVR and even if I did have fibrotic reversal. Occasionally yes but moderately or regularly no.
Might be a good reason we continue to have hep panels even after we have SVR. Might also give us reason to have another biopsy every few years (as much fun as that sounds).
Might be a good reason we continue to have hep panels even after we have SVR. Might also give us reason to have another biopsy every few years (as much fun as that sounds).
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