I remember reading a study here at MH about statins and HCV. I hope someone can find it. I'd like to give a copy to my heart doc.
let me clarify my post, i did not mean will taking heptapro & probiotic help my lipids, what i meant is will it help someone stage 1 to keep damage to a minimum while waiting for better drugs to be approved? thanks
My doctor (one of the "big" names in NYC hep circles) strongly insisted I take a statin during treatment. Part of the reason was that I have a fatty liver, or steatohepatitis, and he believes that the statins are beneficial. In addition there is a study that came out in 2006 during the AASLD about statins having an anti-hepc virus effect. Quoting here...
"... they evaluated the anti-HCV activities of five statins: atorvastatin, fluvastatin, lovastatin, pravastatin and simvastatin. When the statins were tested alone, all except pravastatin inhibited HCV replication. Fluvastatin had the strongest effect. Atorvastatin and simvastatin had moderate effects while lovastatin had a weak effect. ..."
thanks mark, i have had a few hepatologist including the one in boston tell me a statin would be ok for me to take. yes, i'm aware of the study done with statins, they seemed to have backed off for the time being on statins for HCV. i wish more research would be done on it and other drugs. there has to be more drugs that are already FDA approved like aliana that could help with HCV cure. i do not have fatty liver but my lipids are bad, all of them! i most likely will give the statin a try, only thing that bothers me is i have read that once you start them you are on them for life? your liver becomes dependent on them............
I posted again to bring this back to top of forum, I hope you will comment on this subject. i'm sure many would like to hear your thoughts. have a happy thanksgiving
From: Viewpoint: What Is the Risk of Developing Hepatotoxicity From Statin Therapy in Hyperlipidemic Patients With Hepatitis C?
David A. Johnson, MD, FACG, FACP
Drug-related hepatotoxicity cannot be viewed as a single disease. Many different mechanisms lead to hepatotoxicity, which may be predictable or unpredictable. In the case of statin-related injury, it seems to be an idiosyncratic reaction that is not predictable. Additionally, the evidence would support that no relation exists between the type of statin used and the occurrence of liver abnormalities. On the basis of these study findings, it also appears that in patients with hepatitis C and well-compensated liver disease, these agents can be used in a manner that is comparable to that in patients without chronic liver disease.
These findings are very much supported by a recent liver expert panel recommendation to the National Lipid Association. This panel that (1) asymptomatic increases in aminotransferases represent a class effect associated with statin use and do not necessarily indicate liver dysfunction; (2) fulminant liver disease associated with statins is very rare; (3) routine monitoring of liver biochemistries is not warranted for patients receiving statin therapy; (4) well-compensated chronic liver disease and Child's A cirrhosis are not contraindications to statin use; and (5) statins can be used in patients with nonalcoholic fatty liver disease and steatohepatitis.
Appropriate use of statins in an expanded population of eligible patients should hopefully lead to improvement in the cardiovascular health of appropriately selected at-risk patients. Additionally, these agents may improve the hepatic disease — especially in those patients with hyperlipidemic-related nonalcoholic steatohepatitis.
Statins May Hold Promise for Chronic Hepatitis C Infection
NEW YORK (Reuters Health) Jul 10 - Findings from a new study indicate that statins, particularly fluvastatin, can inhibit the replication of hepatitis C virus (HCV). As such, these drugs may serve as a useful adjunct to interferon therapy, the authors conclude.
Dr. Nobuyuki Kato, from Okayama University Graduate School of Medicine in Japan, and colleagues note that while interferon plus ribavirin is the current treatment of choice for HCV infection, it is only effective in about 55% of patients. Thus, there is a need for new therapies.
Recent reports have described an anti-HCV effect of lovastatin. In the present study, reported in the July issue of Hepatology, the researchers used an HCV replication assay they had created, called OR6, to evaluate the effects of several statins alone or in combination with pegylated interferon.
As noted, fluvastatin showed the strongest anti-HCV activity. Atorvastatin and simvastatin had the next strongest effects followed by lovastatin. Pravastatin, by contrast, displayed no anti-HCV activity. Adding mevalonate or geranylgeraniol reversed the anti-HCV effects.
"The results of the present study suggest that statins other than pravastatin are good reagents for combination therapy with interferon-gamma in patients with chronic hepatitis C," the researchers conclude.
I also came accross a poster at the AASLD, in the antifibrosis section, that showed statins to have an antifibrotic effect. By time constraints,I was unable to engage into a finer analysis ( patient/control numbers, variables/methods used to assess fibrosis, timeframes, intensity/significance of results, side effects like LFT elevations etc.
Statins have also been reported to have antiinflammatory effects independent of their effects on lipid metabolism.
Furthermore, the reported effects on HCV replication merit close attention.
On the other hand remarks from the Lipid panel liike Mike cites it above, make you think:
"This panel concluded that (1) asymptomatic increases in aminotransferases represent a class effect associated with statin use and do not necessarily indicate liver dysfunction;"
Meaning that the fact that they all -"class effect" -, cause increased liver cell necrosis/apoptosis -"asymptomatic increases in aminotransferases"- should not be considered a sign of relevant liver toxicity?
And before we were told that they liver toxicity was more of an "idiosyncratic" event - for individuals with a rare genetic propensity -this somewhat contradicts the class effect.
All in all, it might well be possible that the sum of the beneficial effects, in particular the lowering of the cardiovascular risk, that exists independent of the liver disease outweighs the potential for liver toxicity, in particular when LFTs are monitored tightly. You copy, could for instance simply measure VL before and after a month of statin therapy, see if the above envisioned VL effects pertain to you personally, then you will know/use this knowledge when your future combotherapy will start.
One must be aware that the funding of research re statings is powerful -not always for the right reasons - and a very careful , detalled analysis is necessary before meaningful judgments can be made.
Here we have a similar situation as with ACE/ARB inhibitors, as already discussed.
And then again, all those those are now available and have other benefits.
Not to change subjects, but I'm curious, since you did attend aasld. Did you hear much about ribavirin? I had an appointment today with my NP, and as usual we got yacking, and she made the comment to me, that after aasld, it appeared there were opinions floating around about riba having more direct antiviral effects than previously thought..Any comments or info? TIA
The direct antiviral effect of riba was specifically addressed in a large auditorium presentation at this AASLD and was said to be about 0.5 logs on average on its own.
The growing opinion seems, that despite its low direct antiviral power it assumes a crirtical synergistic function with IFN in the combo.
My dr. put me on zetia, because it isn't metabolized by the liver (or something like that).
I was taking Zetia because the Side Effects from the Statins were brutal. Statins are a wonder drug for cholesterol but not everyone can take them. Zetia works in your digestion. I quit taking it because, bowel movements would hit frequently, unexpected, at any time, and didn't allow much time to respond.
Which statin and what kind of side effects did you have? Thanks.
thanks everyone. really good info. happy thanksgiving to all of you.
I first was on Zocar and complained about the Side Effects to my Cardiologist. He switched me over to Lipitor. I don’t know why because they are basically the same thing. One of the side effects was muscle and joint pain. I was at work, unloading steel from an 18-wheeler, operating a Lull (Forklift). This took about 2 hours. When I climbed off of the Forklift, I went straight to the asphalt because me legs could not hold me up. It was all I could do to get through work every day. When I got home I would go straight to the couch and would not get up until it was time to go to work again. Yes, it lowered my Cholesterol but I would rather shave a year or two off my life than not enjoy life at all.
Rglass: and didn't allow much time to respond
Hey, like FEMA in New Orleans, you could always respond after the fact..."Whoa, what a stinking muddy mess...."