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Re-treatment of Patients with HCV
Excerpted from NIH HCV Consensus Development Conference Draft Report (June
2002)
Reported by Jules Levin
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Patients who may benefit from re-treatment include those whose HCV infection
failed to
achieve SVR. Decisions regarding re-treatment should be based upon: (1)
previous type of
response, (2) the previous therapy and the difference in potency of the new
therapy, (3) the
severity of the underlying liver disease, (4) viral genotype and other
predictive factors for
response, and (5) tolerance of previous therapy and adherence.
Relapsers achieve an initial end of treatment response (ETR) for their HCV
disease, but it
is not sustained over time (i.e., no SVR). Nonresponders never achieve an
EVR, ETR, or SVR.
Among the nonresponders, there is a subset of persons who have a substantial
reduction of HCV
RNA (1 to 2 log units or more) during therapy, and who can be categorized as
partial responders.
Even in the absence of SVR, treatment may be associated with improved
histology.
Preliminary results suggest that overall only 15 to 20 percent of
nonresponders treated
with standard interferon/ribavirin combinations achieved an SVR on
re-treatment using PEG-
interferon with ribavirin. Patients with genotypes 2 or 3 have better
response rates to re-treatment than genotype 1.
The ability to achieve SVR following re-treatment with
PEG-interferon/ribavirin in
patients who relapsed following interferon monotherapy or standard
interferon/ribavirin therapy is currently being evaluated. However, in cases
where the same regimen has been used for re-treatment, virtually all patients
relapse again after treatment is stopped. Extending the duration of
re-treatment without changing the dose or regimen may reduce the relapse
rate, but this has not yet been proven prospectively.
Patients whose HCV infection does not respond to the current optimal therapy
with PEG-
interferon and ribavirin present a significant problem, particularly in the
presence of advanced
fibrosis or cirrhosis. The possible role of maintenance therapy with PEG-in
terferon alone in
preventing further progression of cirrhosis, clinical decompensation, or
development of
hepatocellular carcinoma is currently the focus of a large-scale, multicenter
United States trial,
HALT-C. Until the results of HALT-C or similar studies are available, the
role of long-term,
continuous therapy with PEG-interferon (or ribavirin or both) for
nonresponders must be
considered experimental.
Knowledge of the severity of the underlying liver disease is important in
recommending
re-treatment. Patients with advanced fibrosis or cirrhosis are at increased
risk for developing
hepatic decompensation and should be considered for re-treatment, especially
if they were
originally treated with interferon monotherapy. For the re-treatment of
patients with intermediate degrees of fibrosis and disease activity,
clinicians should consider the factors enumerated above.
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