If the addition of amantadine to SOC can be proved to help even one person achieve SVR who would otherwise not have gotten there, I'm all for it. If we end up creating the viral equivalent of Methycillin Resistant Staph A. in the process, I feel it's too high a price to pay. Just an opinion.
Thank you for the link, I'll be watching with interest.
Hi desrt,
you asked for a repoert, here is one, a meta-analysis with 4831 patients, see below.
A double-blind PCS with 300 patients (TRELA) is ongoing. The study centres are within the best in Germany, and accepted as specialists wordwide, you will know some names: Zeuzem, Manns, Berg, Sarrazin and many others.
http://www.clinicaltrials.gov/ct/gui/show/NCT00299923?order=3
I will not judge pro or contra the use of amantadine as an add-on to treat HCV, before I know the results of this great study. HOW could we judge before we have seen the results? WHY should we? The data about amantadine and HCV remain controversial, sure, but I prefer to have all data available, before creating an opinion.
Discussions about treating influenca are not the point of discussion here. I think you will be absolutely right about amantadine and influenca, that is not my point, I have hep C.
EVALUATION OF AMANTADINE IN CHRONIC HEPATITIS C: A META-ANALYSIS
Pierre Deltenre, Jean Henrion, Hôpital de Jolimont, Haine-Saint-Paul, Belgium; Valérie Canva, Sébastien Dharancy, Frédéric Texier, Alexandre Louvet, Hôpital Claude Huriez, CHRU Lille, France; Stephane De Maeght, Hôpital de Jolimont, Haine-Saint-Paul, Belgium; Jean-Claude Paris, Philippe Mathurin, Hôpital Claude Huriez, CHRU Lille, France.
Abstract Body:
Identification of new drugs with antiviral activity against HCV replication constitutes a crucial challenge. However, the usefulness of combining amantadine with IFN alone (double therapy) or with IFN and ribavirin (triple therapy) has been suggested by some authors, but has not been confirmed by others, and remains controversial. Methods: We analyzed the effect of amantadine on the end-of-treatment virological response (ETR) and the sustained response (SR) using meta-analysis of randomized controlled trials. The intention to treat method was used. For each meta-analysis, the Peto and Der Simonian and Laird methods were used. In a first step, we performed an overall meta-analysis of RCTs regardless of the type of patients (naive, relapsers and non-responders) from the core group. In a second step we performed a subgroup analysis using a meta-analysis according to the type of patients: the first part involved naive patients, the second part relapsers and the third part non-responders. Results: Thirty-one studies involving 4831 patients were included. Overall analysis revealed a significant effect of amantadine and triple therapy was the best regimen for improving ETR (mean difference: 12 %, 95 % CI: 0.5 % to 23.5 %, p=0.04) and SR (mean difference: 8.4 %, 95 %, CI: 2.4 % to 13.8 %, p=0.002). In naive patients, amantadine did not have a significant effect on the ETR (mean difference: 3.6 %, 95 % CI: -2 % to 8 %, p=0.2) or on the SR (mean difference: 1.5 %, 95 % CI: -2.8 % to 5.7 %, p=0.5). In relapsers, amantadine did not have a significant effect on the ETR (mean difference: -3 %, 95 % CI: -27 % to 21.2 %, p=0.8) or on the SR (mean difference 6.4 %, 95 % CI: -9 % to 22 %, p=0.4) In non-responders, combination therapy with amantadine was associated with a significant effect on the SR (mean difference: 8.3 %, 95 % CI: 1.9 % to 14.6 %, p=0.01). In sensitivity analysis, double therapy did not improve virological responses. Conversely, triple therapy tended to improve the ETR (mean difference: 19.8 %, 95 % CI: -1.5 % to 41.1 %, p=0.07) and was associated with a significant effect upon the SR (mean difference: 12.7 %, 95 % CI: 3.8 % to 21.6 %, p=0.005), meaning that 8 patients would need to be treated with amantadine combination therapy in order to obtain one additional SR over the rate expected in the comparison group. Conclusions: Combination therapy with amantadine is of no effect upon naive patients or relapsers. In high-difficult to treat patients, triple therapy with amantadine improved the sustained response. In the future, large well-designed RCTs evaluating triple therapy with amantadine, ribavirin and pegylated IFN should be conducted in difficult-to-treat patients in order to confirm this meta-analysis.
www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1773921
January 2004
Randomized, double blind, placebo controlled trial of interferon, ribavirin, and amantadine versus interferon, ribavirin, and placebo in treatment naive patients with chronic hepatitis C
.........
"Conclusion: Response to triple therapy of interferon alfa, ribavirin, and amantadine was similar to standard therapy of interferon alfa and ribavirin. Our results suggest that amantadine has no role in the management of HCV."
I'd be happy to read any reports that contradict this or show that amantadine has regained any type of use in treating viral influenza.
Yes, I understand the difference between influenza and the common cold.
My comments in regard to H3N2 were an example of how over use of medications create viral drug-resistance - not about specifically about people with HCV and flu.
" - all without creating the resistant strains of virus that may result from using specific anti-viral drugs. We've created enough problems in the bacterial world by over-using antibiotics - we don't need to do the same thing with viruses."
desrt: That makes alot of sense. Keep on educating us.
Yvonne
were is the link for this statement?
"and was long ago discarded as adjunct to HCV therapy".
As far as I know, the studies are ongoing.
How many people do you know, who have Hep C, treat with SOC, and have influenca H3N2 at the same time? Influenca is not the same as cough and cold.
From the above referenced article:
Percentage of amantadine/rimantadine resistant H3N2 influenza A virus:
'04 flu season - 2%
'05 flu season - 11%
'06 flu season - 91%
Probable cause of H3N2 resistance : "...overuse of the drugs abroad, such as in countries that permit the drugs to purchased without a prescription."
http://www.msnbc.msn.com/id/10851668
1/14/06
"The government for the first time is urging doctors not to prescribe two antiviral drugs (rimantadine & amantadine) commonly used to fight influenza because of concerns about drug resistance..."
My point was that anti-inflamatories, marijuana, painkillers, etc. etc. can reduce side effects, enhance patient compliance, and ultimately result in a larger % of SVR - all without creating the resistant strains of virus that may result from using specific anti-viral drugs. We've created enough problems in the bacterial world by over-using antibiotics - we don't need to do the same thing with viruses.
>"Amantadine is no longer considered to even be very effective for flu in this country and was long ago discarded as adjunct to HCV therapy."
Could you please tell any citation for this statement? If you read the study carefully, you will notice, that A. is not suggested to increase SVR, but has shown beneficial efects of sides of therapy. This is a small, but important difference.
A meta analysis of 31 studies shows a better SVR rate in difficult to treat patients: http://tinyurl.com/33bd3j
Same results here: http://tinyurl.com/2pq2o5
More Clinical trials to compare SVR rates are still ongoing:
http://www.clinicaltrials.gov/ct/gui/show/NCT00299923?order=3
Be carefully with opinions, which are not a result of published facts.
Amantadine is no longer considered to even be very effective for flu in this country and was long ago discarded as adjunct to HCV therapy. Ribavirin is sold as an inhaler in Mexico to treat influenza and also has some pediatric uses in this country in aerosol form.
Not to discourage anyone, but I was on Ribavirin, Pegasys and Amantadine treatment (my 3rd). The conclusion of the Gastro was that it didn't make any difference...
Magnum
Always wondered why Ribavirin was never sold as a cure for the flu, nice to know amantadine is.
Whatever happened to conjugated Ribavirin, less anemia.
btw do you have any info on misletoe
CS