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Pre-treatment with Ribavirin Improves Response to Interferon-based Therapy for Hepatitis C

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http://www.hivandhepatitis.com/2010_conference/aasld/docs/1214_2010_a.html

HIV and Hepatitis.com Coverage of the

61st Annual Meeting of the American Association for the Study of Liver Diseases

(AASLD 2010)

October 29 - November 2, 2010, Boston, MA

Pre-treatment with Ribavirin Improves Response to Interferon-based Therapy for

Hepatitis C

SUMMARY: Ribavirin " priming " -- or starting ribavirin monotherapy before

adding pegylated interferon -- was associated with a small but significant

improvement in sustained virological response in patients with chronic hepatitis

C virus (HCV) infection, according to a German study presented at the recent

American Association for the Study of Liver Diseases " Liver Meeting " (AASLD

2010) in Boston.

By Liz Highleyman

B. Fueloep and colleagues retrospectively analyzed the effect of ribavirin

monotherapy followed by standard combination therapy (pegylated interferon plus

ribavirin) on initial decline in HCV viral load and overall treatment outcomes.

Addition of ribavirin reduces the risk of relapse after completing treatment,

and therefore increases the likelihood of sustained virological response (SVR)

to interferon-based therapy. Ribavirin is a weak inhibitor of the HCV NS5B RNA

polymerase in vitro, but its mechanism of action is not fully understood.

This analysis included 93 chronic hepatitis C patients from 5 centers in

Germany. Just over half were men and 78% had hard-to-treat HCV genotype 1.

Within this group, 43 were treatment-naive, 28 were prior relapsers, and 19 were

prior non-responders.

All participants were initially treated with ribavirin monotherapy, at an

average dose of 15.2 mg/kg, for an average duration of 39 days. They then added

pegylated interferon and continued for the usual standard duration of therapy.

Results

The average decline in HCV RNA during the ribavirin monotherapy period was 0.56

log.

Changes were variable, however, ranging from +1.07 to -1.76 log.

Viral load changes varied according to prior treatment status:

Prior relapsers: mean 0.67 log decline;

Treatment-naive: mean 0.48 log decline;

Prior non-responders: mean 0.28 log decline.

Patients with HCV genotype 3 showed the greatest viral load decline (0.95 log),

followed by those with genotype 4 (0.6 log).

Platelet counts increased by an average of 24 mcl (range 9-49 mcl) during

ribavirin priming.

ALT levels decreased by a mean 17 IU/mL (range 4-31 IU/mL) during the priming

period.

Hemoglobin decline during ribavirin monotherapy -- an indicator of anemia --

was not associated with initial viral kinetics.

6 prior non-responders experienced larger and faster viral load decline after

ribavirin priming compared with their previous treatment:

Week 4: 2.0 log after priming vs 1.2 log during first treatment;

Week 12: 3.6 vs 2.0 log, respectively;

Week 24: 6.0 vs 5.4 log, respectively.

At the time of abstract submission, 26 previously treated patients had

undergone 6 months of post-treatment follow-up.

Within this group, 12 prior relapsers (44%) and 2 prior non-responders (36%)

achieved sustained virological response.

" [R]ibavirin monotherapy induces a mild but significant decline in hepatitis C

viremia, " the investigators concluded. " The highest HCV RNA log10 decline after

ribavirin priming occurs in patients with prior relapse and genotype 3. "

Investigator affiliations: Gastroenterology and Hepatology, University Leipzig,

Leipzig, Germany; Gastroenterology and Hepatology, Charite, Berlin, Germany;

Gastroenterology and Hepatology, J.W. Goethe University, furt, Germany;

Hepatology, IFI Institute for Interdisciplinery Medicine, Hamburg, Germany;

Gastroenterology, Marienhospital Hamm, Hamm, Germany.

12/14/10

Reference

B Fueloep, P Rohde, P Buggisch, and others. The antiviral efficacy of ribavirin

priming. A follow up of 93 patients treated with ribavirin monotherapy followed

by standard combination treatment. 61st Annual Meeting of the American

Association for the Study of Liver Diseases (AASLD 2010). Boston, October

29-November 2, 2010. Abstract 980.

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