You have it backwards.....Cirrhosis of the liver does NOT lead to Hepatitis C. Hepatitis C is caused by a virus and it's transmitted from blood contact....meaning if somehow, infected blood got into his blood. Risk factors include blood transfusions, IV drug use, tattoos, body piercings, etc.
Hepatitis C (as well as alcohol use) can cause cirrhosis. The fact that he stopped drinking probably helped his liver, but cirrhosis doesn't really go away by itself. Successful treatment for Hepatitis C sometimes reverses some of the damage.
Some people can clear the Hepatitis C virus on their own in the first six months after getting infected....but if your father had Hepatitis C for longer than 6 months, then he probably still has it.
Alcohol use doubles the rate of liver damage progression and it can make the Hepatitis C virus multiply. And if he already has cirrhosis, getting decompensated and needing a liver transplant in the future is a real possibility if he continues drinking.
Co writer is exactly right...HepC can lead to Cirrhosis. Cirrhosis does not cause HepC.
While it is possible to clear HepC on your own, that is not the norm. Most people don't even know they have HepC until they've had it for years. At that point the only way to rid yourself of HepC is to go on treatment that last many weeks. If your Dad has not done this...he still has HepC.
The 10 yr. hiatus of alcohol probably gave your Dad's liver a reprieve from the harsher symptoms of cirrhosis but it's doubtful that it eradicated it. Now that he is drinking again, he is pretty much throwing himself out of the frying pan and into the fire. His drinking will only cause more harm to his liver. His HepC will rev up and then he'll have that attacking his liver as well as the alcohol. A double whammy.
Does your Dad or did he see a Gastroenterologist or a Hepatologist? If not, he needs to see one soon. He needs to have his labs done, especially a liver panel to check his liver enzymes. He also needs to have the appropriate tests to check his HepC to see where he stands there in terms of viral load. I would also think he would need a liver biopsy, fairly simple procedure done on an out patient basis. The liver biopsy will tell him what the state of his liver is as far as Stage, which is the amount of damage to the liver and Grade which will indicate the level of necrosis (scarring) of the liver and the amount of inflammation.
Most of all he needs to have his doctor thoroughly educate him as to what alcohol is doing to his body and his chances of living a long life.
Thank you for updating my medical knowledge about the disease. Maybe I had the facts backwards, but I know my father no longer has Hepatitis C due to many months of giving himself shots, and was completely cleared by his doctor many years ago of the disease.
My question was in regards to any studies or statistics that prove starting to drink again will increase the likeliness of Hep C returning...that is our fear.
The question I am hoping someone out there can help me with is does his resumed drinking increase the changes that his cirrhosis or hepatitis will come back?
As suggested, your facts are incorrect.
(1) Cirrhosis does not cause Hepatitis C but hepatitis C can cause Cirrhosis.
(2) You cannot "recover" from Hepatitis C. Either your cured or you still have it.
(3) Drinking alcohol does not cause Hepatitis C.
(4) As to your question, his resumed drinking will not bring Hepatitis C back, although from your statements it's unclear if your father really has it and/or he really got rid of it. That said, his drinking could seriously harm him if he has cirrhosis.
I suggest your father see liver specialist (hepatologist) and find out what is really going on. Both with the Hep C and cirrhosis.
The specialist will probably run a viral load test to see if he has Hepatitis C or not. Equally important, he will evaulate your father's liver condition in terms of how much damage he has and come up with a plan moving forward.
Our posts crossed.
From what you say, it appears your father once had Hep C and was cured with treatment.
And while drinking won't bring back the Hep C, it can potentially can do even more damage depending on how much he drinks and what the condition of his liver is today.
Again, a good liver specialist (hepatologist) should be able to evaluate his condition and point both of you in the right direction.
I disagree with jmjm. After successful treatment for hepatitis C, small amounts of virus are left and it is believed that if your immune system at some points gets suppressed, the virus can become active again. And alcohol is an immune-suppressant.
Co: I disagree with jmjm.
You mean to say that you disagree with my doctors and our resident doctor here per his two posts. Had my docs told me "no alcohol" then I might just have had no alcohol.
As far as "small amounts of virus" being left -- without debating that point -- there areno cases I'm aware of where HCV has been "activated" post treatment by alcohol or any other means. The exception being 2-3 cases of postulated relapse due what I remember to be serious steroid therapy. to If you have any studies that suggest alcohol can reactivate Hep C, please post. But no quizzes :)
The issue that you discuss above, re-activation of the virus after achieving SVR, is a controversial subject that has not received sufficient long term study, other than statistical studies of SVR's, which show that about 98% of SVR's remain virus free over five to ten years. There are also a small number of those who 'relapse' after one or two years, after having been SVR, (the two percent above) and this is where the controversy becomes very cloudy.
Many claim that the late relapsers were never really SVR at all, but just appeared to be clear of the virus (whatever that means), and others claim that they must have been re-infected with a brand new infection. The third camp believes that a this very tiny group of late relapsers have somehow 're-activated' their original viral infection, either by suppressing their immune system (through heavy drinking, opiate drugs, or immuno-suppressant drugs), and have actually 'relapsed. This would be dependent on the research theories that demonstrate an ongoing sub-detectable very low level viral infection long term AFTER SVR has been achieved.
On this board you will get lots of flak if you have an opinion that falls in line with this last group, or the 'viral persistence' camp. Even though a large number of independent HCV and viral researchers have demonstrated this 'persistent virus' to be a verifiable phenomenon after SVR, many either dismiss their findings out of hand, or assume that their findings must be flawed. To many out there, the fact that most Hepatologists call the treatment, and SVR a "CURE", then presumes that the virus must be completely eradicated and gone forever from all compartments in the body, and never can return.
This belief is still waiting for solid proof, one way of the other, and I think that only after more research, and also longer term studies following SVR's, and looking at any relapsers that develop, will we really get answers to these questions. Either the virus is in a sort of 'quasi-permanent' remission, or it is totally gone forever, CURED so to speak, and there is honestly no real final answer yet. Regardless of what either side claims on this forum, there is plenty of scientific ammunition to support either belief at this point, and nothing near a real consensus in the scientific community. Time will tell.
I didn't get the impression that "CO" was talking about viral persistence after SVR, an issue which I intentionally avoided per my first sentence second paragraph, last post.
Are you saying that you believe alcohol can "reactivate" Hepatitis C in an SVR? And I use reactivate in the sense of an SVR becoming HCV detectible using conventional PCR and TMA testing. My understanding is that is what "CO" is talking about, but I'm sure she will correct me if wrong.
I just read your post on the related alcohol thread and it leads me to believe that there are two different discussions going on here, since you appear to believe that light drinking SVR is OK. Again, I think what CO is talking about is alcohol turning an SVR into someone HCV positive via conventional testing. I'm assuming you agree this is not possible but certainly won't speak for you.
What I am saying is that CO's comments about remission, whether CO is aware of the 'persistence theory' or not, would necessarily be 'dependent' on this theory being valid, to take place. If there is actually a 'viral remission' that occurs after SVR, then the assumption would have to be that it COULD be reactivated potentially. Alcohol would be a likely cause for re-activation, if the 'remission' research and theory ends up being valid.
I am NO claiming that either belief is valid, since we do NOT have firm, final proof or consensus yet. We have statements, we have opinions, etc. But final, ultimate, agreed upon proof of either total eradication, or remission, is not here yet. Unless you know of some meeting between the various camps of viral researchers where the differences have been ironed out and agreed upon?
So, what I am saying, is that if CO's idea of remission is indeed an eventual reality, then their supposition that alcohol could possibly provoke a relapse, would not be an outlandish suggestion. Especially in light of the studies on HCV rates in alcoholics, etc. that we have discussed at length in the past.
We FIRST NEED a real consensus from the research and scientific community on the validity of either "total eradication, permanantly and forever', OR, "remission, based on some persistent viral mechanism, that is not well understood yet"
Note again, that I did not claim either opinion to be accurate or true. We don't have enough information yet.
OK, so you agree that's it's OK to drink lightly after SVR but you won't say that it realistically won't reactivate the virus? We're not talking about whether CO's comment is "outlandish" or not -- I never said that -- just that in the real world I haven't seen anything to suggest that one should modify one's drinking behavior (within the confines mentioned) because of HCV reactivation using the conventional definition which CO apparently does since she uses the phrase "become active again" which in common usage refers to what is commonly called "relapse" and nothing to do with the persistence theory. Not try to put you on the spot, just trying to clarify things for others in a discussion that is now starting to mix viral persistence theory with practical opinions re light alcohol use post tx.
What I'm saying -- and what I thought you said in another thread -- is that it's OK to drink alcohol post SVR within the limits mentioned. I believe that is the point that was being originally discussed and that many here may be interested in.
Yes I am saying it is probably OK to drink in very light, infrequent, moderate amounts, after SVR, and NO I don't think that this sort of drinking could ever 'reactivate' a virus. IF it were in remission. What I do think is this: if it turns out that HCV is actually 'in remission' after SVR, rather than absolutely eradicated and gone forever' , then I think that extremely heavy drinking, from everything that we know about the virus and alcohol abuse, would be a likely factor in potential viral 're-activation' , along with the other assumed culprits, like extreme immune system suppression. There are still about 2% of long term SVR's that have demonstrated late 'relapse' or viral infection, well after the one year point of SVR. Though a 'small' percentage, the cases are largely unexplained as to the EXACT and definite cause of relapse.
And, NO, I disagree that remission has nothing to do with the 'viral persistence' research!!! Quite the contrary. I believe that the issue of 'remission' has EVERYTHING to do with persistent virus. I would think that this extreme, low level, persisting virus, hiding wherever it might be, would be the actual 'resting place' for the virus in remission. So maybe, the immune system somehow 'controls' the low level virus at some point, in SVR's, and holds it there permanently, in remission. Whether this 'remission' could lead to a re-activation is still very cloudy, and controversial. It would probably be extremely rare, but IF it can happen at all, ever, in just one case, then you have a situation of 'viral remission', and re-activation rather than total eradication. Just not enough long term study and validation on either front currently.
Again Jim, the final answers have NOT been resolved yet, or agreed upon by the top scientific researchers. You may believe that the answers are here now, firm and final. But that does not in fact mean that this is the case. I think that even HR leaves this door wide open in his past commentaries about viral persistence, and other forms of infection in cellular mediated tissues, etc.
I hope I am being clear, and that you do not misinterpret what I am claiming. Because, I am saying that we just don't really have these answers yet. I am not sure what you are claiming?
DD: Yes I am saying it is probably OK to drink in very light, infrequent, moderate amounts, after SVR, and NO I don't think that this sort of drinking could ever 'reactivate' a virus. IF it were in remission.
That was the only issue I was discussing and thought the only issue "CO" was discussing. So we agree at least on the above point. The rest has been covered -- both sides -- extensively in other threads.
Glad to see we are in agreement.
I don't think that CO is only referring to the sort of 'light drinking' that we discuss for SVR's though. It looks to me fro the psot that her husband is moving toward more problematic drinking, more frequently and with more alcohol heavy drinks (hard liquor, etc.) This could become a problem on several fronts. First, even without the possibility of remission/reactivation, a cirrhotic drinking hard liquor, on an increasing basis could easily increase the odds of HCC dramatically. This has happened MORE frequently in SVR's who were beyond stage 3. The second issue that I see, is that if there is really a possibility of 'reactivation' of the virus, heading toward problem drinking, and hard alcohole use is not the best direction to be heading. If the drinking spirals further into the 'heavy abuse' category, then 'reactivation' would be a 'concern' at least, if there is a true remission that takes place.
If the drinking remains very light, and 'safe' to some extent, then he should be relatively OK. We hope. Again, the cirrhotic issue is central.
Moderate to light amounts of alcohol consumption post SVR will not "reactivate" the virus (in the event the virus is even there at all). If it did, I never would have achieved and sustained my own SVR (along with a whol lotta other folks). Even heavy drinking will not "reactivate" the virus (again assuming it's even there). Also, the durability of SVR beyond 2 or 3 years is *extremely* reliable, and for all intensive and practical purposes constitutes an outright cure. The supposed "2%" of SVR's that DD refers to that "relapse" afterwards can very easily and reasonably be explained by (1) sampling/testing/experimental error, and (2) re-infection.
If I reach SVR and remain there and if I have small amounts of the virus left in my body what significance will that have if my liver health does not decline and as some state improves? Does it matter if there are trace amounts? It's certainly doesn't to me. I will not drink because my liver has been severely compromised and I will not insult it anymore than I already have. Personal choice.
Drinking post SVR cannot possibly cause relapse morever patients who have had transplant post SVR ( and there are such examples) do not relapse in the face of the harsh immuno-suppressant drugs given to prevent rejection.RNA traces found in SVR patients (often tested post mortem) are weak quasi-species and are not thought to invade cells liver or otherwise.
HCA: This is news to me. Weak quasi-species??? (Who has ever documented these?????) Not thought to invade liver cells??? RNA traces???? Where did you get this information. You are talking about something entirely different than the "persistent replicating virus" found in recent years by researchers in LIVE SVR's, years after finishing therapy. And the two suspected cases of relapse, by the way, were both in patients who had received heavy doses of immuno-suppresant drugs, after SVR. Both were suspected to be late relapses!
Mremeet you said: " The supposed "2%" of SVR's that DD refers to that "relapse" afterwards can very easily and reasonably be explained by (1) sampling/testing/experimental error, and (2) re-infection."
Well, yes you can explain it that way, if you assume that to be the case. These assumptions were never proven to be the case though. Just a possible explanation. Let's not confuse conjecture with proof. If you want to just 'blow off' the 2% fine. Don't call it science though!
I believe that I concur with Dr. Shiffman on this one:
For immediate release:
VCU Communications and Public Relations
Current treatment for Hepatitis C can be considered a cure, VCU researcher announces
Disease is leading cause of cirrhosis, liver cancer and the need for transplants
Video Clip 1: "THIS LONG-TERM STUDY SHOWS THAT 99 PERCENT OF PATIENTS WERE CURED OF THE HEPATITIS C VIRUS."
The use of peginterferon alone, or in combination with ribavirin, points to a cure for hepatitis C, the leading cause of cirrhosis, liver cancer and the need for liver transplant, a Virginia Commonwealth University researcher said today.
Mitchell Shiffman, M.D., professor in the VCU School of Medicine, and chief of hepatology and medical director of the Liver Transplant Program at the Virginia Commonwealth University Medical Center, is one of the lead investigators in the study, which was presented at the 38th annual Digestive Disease Week conference in Washington, D.C. VCU was among about 40 sites worldwide studying pegylated interferon alfa-2a, manufactured by Roche Inc.
Nearly all — 99 percent – of patients with hepatitis C who were treated successfully with peginterferon alone, or in combination with ribavirin, had no detectable virus up to seven years later. Researchers say this data validates the use of the word "cure" when describing hepatitis C treatment as successful treatment is defined as having undetectable hepatitis C virus in the blood six months following treatment.
"We at VCU are encouraged by this data because it is rare in the treatment of life-threatening viral diseases that we can tell patients they may be cured," Shiffman said. "In hepatitis C today, we are able to help some patients achieve an outcome that effectively enables them to put their disease behind them."
There are still about 2% of long term SVR's that have demonstrated late 'relapse' or viral infection, well after the one year point of SVR. Though a 'small' percentage, the cases are largely unexplained as to the EXACT and definite cause of relapse.
"Again Jim, the final answers have NOT been resolved yet, or agreed upon by the top scientific researchers."
The world population purportedly has a 3% hep c rate (I heard this on the radio the other day, don't know where they got the stats). If that's true, I don't know why its so outlandish to believe that 2% of the folks who were SVR got reinfected. And you know what else I think? I think addiction is a very difficult thing and I think that there are some addicts who have hep c who use IV drugs off and on for years. They may stay sober for years at a time, but then they fall of the wagon from time to time and start using drugs again. There are TONS of fifty and sixty year old IV drug addicts in the county where I live, and many of them are treating hep c. A LOT of them are treating at UAB. It is certainly not beyond the scope of imagination that some of them have been in these studies during periods of sobriety and have then been reinfected. And it would also seem to me to stand to reason that there would be more people of the same genotype in these population areas where a lot of IV users cluster.
So if some of these folks were in a study and then went back to their old ways, with their same friends, it wouldn't be a huge mystery that they came up with the same genotype again.
Also, if 3% is really the number of people with hep c in the world, then it's not that weird if one or two percent of the people who are SVR are somehow, on purpose, by accident, or by misadventure, infected again a few years later, particularly since many of the people on this board have no risk factors and don't know how they were infected.
I think that re-infection makes more logical sense to me than this virus lurking in some strange place in my body that nobody can even really adequately explain to me. If we had issues with people re-infecting themselves, HIV patients who were formerly SVR would be dropping like flies. They have the worst immune systems around.
Who is it, and I'm asking because I honestly don't know, who hasn't resolved this question, which scientists? And do they still feel that way in light of Virginia's research last year?
Says.............So if some of these folks were in a study and then went backBack pain - low
Back strain treatment to their old ways, with their same friends, it wouldn't be a huge mystery that they came up with the same genotype again.
And..............I think that re-infection makes more logical sense to me than this virus lurking in some strange place in my body that nobody can even really adequately explain to me
You get my vote for the best answer....... Best to you girl
the type of therapy you describe with your father taking a lot of shots - but I didn't hear you say anything about pills with the shots - sounded to me like he might have been on interferon monotherapy.
You said he cleared, but I was wondering if he went back and had his re-check at 1 year. That 1 year re-check is pretty essential in making sure that you're really SVR. After we finish treatment successfully, we kind of hold our breath a little until we get our 1 year clearance, and then we know we're good to go. I'd make sure he goes back and asks for a viral load test, particularly if he didn't get that 1 year check.
IF he is clear, I wouldn't worry about the drinking reactivating his hep c virus. The problem with your father is that he already has a lot of damage to his liver - from what you're telling us. He definitely needs his enzymes checked and possibly some other testing per his doctor to see how much additional damage he has. Additional alcohol can only hurt his liver more. I'd take things one at a time though, and get the medical testing done (hopefully he'll agree to that) and then go from there.
Sorry, alagirls comment should have read..................So if some of these folks were in a study and then went back to their old ways, with their same friends, it wouldn't be a huge mystery that they came up with the same genotype again.