Pangenotypic direct-acting antiviral agents for mixed genotype hepatitis C infection: a real-world effectiveness analysis

Ding, Y.-J.; Lu, C.-K.; Chen, W.-M.; Tung, S.-Y.; Wei, K.-L.; Shen, C.-H.; Hsieh, Y.-Y.; Yen, C.-W.; Chang, K.-C.; Chiu, W.-N.; Hung, C.-H.; Lu, S.-N.; Chang, T.-S.

Journal of Gastroenterology and Hepatology 36(10): 2911-2916


ISSN/ISBN: 1440-1746
PMID: 33978973
DOI: 10.1111/jgh.15546
Accession: 080351429

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Pangenotypic direct-acting antiviral agents (DAAs) glecaprevir/pibrentasvir (GLE/PIB) and sofosbuvir/velpatasvir (SOF/VEL) are effective against all hepatitis C virus (HCV) genotype infections. However, data on pangenotypic DAA treatment for mixed genotype HCV infection are sparse. This is a retrospective, single site cohort study analyzing all patients with mixed HCV genotype infections treated with GLE/PIB or SOF/VEL from August 2018 to August 2020 in Chiayi Chang Gung Memorial Hospital, Taiwan. The primary study endpoint was sustained virologic response (SVR) 12 weeks after treatment cessation. We also reported adverse events (AEs). A total of 108 patients with mixed infections of any two or three genotypes of 1a, 1b, 2, 3, and 6 received pangenotypic DAAs during the study period. A total of 67 patients received GLE/PIB and 41 received SOF/VEL. The evaluable population analysis revealed SVR rates of 94% (63/67) and 95.1% (39/41) for GLE/PIB and SOF/VEL therapy, respectively, and the per-protocol analysis revealed an SVR of 100% for both regimens. Four patients in the GLE/PIB group and two patients in the SOF/VEL were lost to follow-up. The most common AEs for GLE/PIB versus SOF/VEL therapy included pruritus (14.9% vs 2.4%), fatigue (6.0% vs 7.3%), abdominal discomfort (4.5% vs 7.3%), and acid reflux (3.0% vs 4.9%). DAA-related significant laboratory abnormalities occurred in three patients with > 1.5 × elevated bilirubin level in the GLE/PIB group. None of the above AEs resulted in DAA discontinuation. Pangenotypic DAAs are well tolerated by and yield high SVR rates in patients with mixed genotype HCV infection.