𝔖 Bobbio Scriptorium
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Chronic hepatitis C genotype 2 or 3 short treatment

✍ Scribed by Ricardo Moreno-Otero; María Trapero; José A. Moreno-Monteagudo


Book ID
102239407
Publisher
John Wiley and Sons
Year
2008
Tongue
English
Weight
45 KB
Volume
47
Category
Article
ISSN
0270-9139

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✦ Synopsis


Dalgard et al. 1 reported interesting data on 14 versus 24 weeks of combination therapy in patients with hepatitis C virus (HCV) genotype 2 or 3, and they concluded that it is rational to treat those patients with rapid virological response (RVR) for only 14 weeks. Adequate treatment duration is generally considered decisive in order to improve adherence and reduce side effects. At present, the strategy involves adapting therapy to each individualized case instead of adapting the patient to an established regimen. 2,3 Young, white, nonobese patients with low viremia, infected by genotype 2 or 3 HCV, with low fibrosis and RVR could receive shorter treatment. 2,3 However, the point regarding duration may be elusive and, in spite of some studies, 4,5 definite conclusions are still lacking.

The current experience of our group is in agreement with the results by Dalgard et al. 1 The well-documented case of a patient adds further support to the value of the short regimen in patients with genotype 2 or 3 and RVR. A 34-year-old Spanish woman, with a body mass index of 21 kg/m 2 , moderate alanine aminotransferase (ALT) serum levels (64 IU/L), HCV-3a genotype infection, HCV RNA 5.7 ϫ 10 5 IU/mL, and mild chronic hepatitis on biopsy (grade 2, stage 1-2), was initiated treatment with peginterferon ␣-2a (180 g/weekly) plus ribavirin (800 mg/daily) on August 29, 2001. At week 4, the patient attained an RVR with normal ALT levels (13 IU/L). The tolerance was excellent but after receiving combination therapy during 10 weeks, she presented with fever and productive cough; chest radiography led to a diagnosis of pulmonary tuberculosis, documented by bacilli culture and sputum smears. Premature withdrawal (November 6, 2001) from antiviral treatment was required. Then, tuberculostatic therapy was started and maintained for 36 weeks with good tolerance. During this time, serum ALT levels were persistently normal and HCV RNA remained negative in three determinations carried out at weeks 12, 24, and 48. A second liver biopsy obtained at year 4 after antiviral withdrawal demonstrated no inflammation (A0) or fibrosis (F0).

It can be concluded that: (1) Fewer side effects and their more limited duration are in favor of the short treatment regimen in patients with genotype 2 or 3 and RVR; (2) Short therapy is able to eradicate HCV and cure chronic hepatitis C in these patients; (3) Optimal treatment duration needs to be defined for each individualized patient; and (4) Further studies including customized management and therapeutic regimens based on virological characteristics (genotype and viremia), demographic aspects, liver disease severity, and individual genomic-marker analysis are warranted. Whether all points of this strategy have similar relevance with imminent new therapies remains to be investigated.


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In hepatitis C virus (HCV) genotypes 2 and 3 patients, the high rate of relapse after 12 to 16 weeks of antiviral therapy is the main concern for shortening treatment duration. This study was undertaken to delineate predictors of relapse after short treatment in patients with undetectable HCV RNA at