Treatment of Chronic Hepatitis C With Amantadine

Hubert, I.; Lunel, F.; Cadranel, Jean–François; Oberti, Frédéric; Calès, Paul

doi:10.1111/j.1572-0241.1999.2316b.x

Cited by 6 publications

(2 citation statements)

References 3 publications

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“…Six patients had normal alanine aminotransferase (ALT) and negative hepatitis C virus (HCV)-RNA at the end of therapy, and four had a sustained response (SR) [4]. The effectiveness of these tricyclic amines as antiviral agents against HCV was challenged by subsequent trials of AMA [5][6][7][8][9][10][11] and of RIMA [12], both in non-responders to IFN and in naïve patients. These studies have shown almost uniformly some reduction of ALT, ranging from 0 to 58% of patients while on therapy, but no consistent effects on HCV-RNA.…”

mentioning

confidence: 99%

Amantadine for chronic hepatitis C: a magic bullet or yet another dead duck?

Craxı̀

Iacono

2001

Journal of Hepatology

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confidence: 99%

Amantadine for chronic hepatitis C: a magic bullet or yet another dead duck?

Craxı̀

Iacono

2001

Journal of Hepatology

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“…Besides its beneficial effects in Parkinson's disease, amantadine has broad virostatic activity against toga-, myxo-, arena-, corona-, and flaviviruses and is being clinically used in influenza A virus infections [9,10]. Several trials of amantadine monotherapy resulted in biochemical responses but not in virological response [11][12][13][14][15][16]. Randomized studies of interferon plus amantadine versus interferon monotherapy yielded controversial results in treatmentnaive patients [17][18][19][20][21] and failed to demonstrate an antiviral effect of amantadine in nonresponders to interferon monotherapy [22,23].…”

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confidence: 99%

Retreatment of patients with chronic hepatitis C not responding to interferon/ribavirin combination therapy with daily interferon plus ribavirin plus amantadine

Stauber

Hofer

Hackl

et al. 2004

Wien Klin Wochenschr

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There is currently no accepted therapeutic regimen for patients with chronic hepatitis C who failed to respond to standard combination treatment with interferon-alpha plus ribavirin. We investigated triple combination treatment with induction dosing of interferon-alpha plus ribavirin plus amantadine in these difficult-to-treat patients. Nonresponders (n = 67), breakthroughs (n = 16) and relapsers (n = 19) to previous interferon/ribavirin combination treatment of at least 6 months were included. For the first 16 weeks, patients received interferon-alpha2a 6 MU daily, ribavirin 800-1200 mg/d, and amantadine 200 mg/d. In cases of undetectable HCV RNA at week 12, treatment was continued with interferon-alpha2a 6 MU every other day and the same doses of ribavirin and amantadine until week 48. In cases of HCV RNA positivity at week 12, treatment was stopped. A total of 102 patients were enrolled (80%: genotype 1, 19%: cirrhosis). HCV RNA was negative in 35/102 patients (34%) at week 12 and in 27/ 102 patients (26%) at the end of treatment. Virological response was sustained in 15/102 patients (15%). On-treatment virological response was higher in previous relapsers/breakthroughs than in previous nonresponders (week 12: 49% vs. 27%, p < 0.05; week 48: 46% vs. 16%, p < 0.01) but no such difference was found for sustained virological response (20% vs. 12%, NS). In conclusion, triple combination treatment with daily interferon-alpha plus ribavirin plus amantadine for 3 months can induce virological response in a considerable number of nonresponders/relapsers to previous dual combination treatment, but the sustained virological response rate remains low.

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