| Literature DB >> 30381417 |
Norio Akuta1,2, Fumitaka Suzuki3,2, Hitomi Sezaki3,2, Masahiro Kobayashi3,2, Shunichiro Fujiyama3,2, Yusuke Kawamura3,2, Tetsuya Hosaka3,2, Mariko Kobayashi4, Satoshi Saitoh3,2, Yoshiyuki Suzuki3,2, Yasuji Arase3,2, Kenji Ikeda3,2, Hiromitsu Kumada3,2.
Abstract
Little is known about the effects of virus- and host-related factors on hepatocarcinogenesis in patients who show viral clearance after HCV RNA eradication by direct-acting antivirals (DAAs). The subjects of this retrospective study were 1,922 patients with HCV genotype 1 (HCV-1)- or HCV-2-related chronic liver disease who showed a sustained virological response (SVR; defined as negative results for HCV RNA at 12 weeks after the cessation of all-oral DAAs). All patients were confirmed to be hepatocellular carcinoma (HCC) free before and during DAAs. HCC was diagnosed in 43 patients during the follow-up, with an incidence rate per 1,000 person years of 9.44. The cumulative HCC rates were 1.2, 2.0, and 3.1% at the end of 1, 2, and 3 years, respectively. The annual rate of HCC during the first 3 years was 1.0%. The incidence rate was significantly higher in patients infected with the HCV-1b core amino acid (aa) 70 mutant than in those infected with HCV-2a/2b, and the rate in patients infected with the HCV-1b core aa 70 wild type tended to be higher than that in patients infected with HCV-2a/2b. The rate in patients infected with the HCV-1b NS5A aa 93 mutant was significantly higher than that in patients infected with HCV-2a/2b. However, the rate was not different between patients infected with the IL28B rs8099917 TT genotype and patients infected with the non-TT genotype. Multivariate analysis identified a Wisteria floribunda agglutinin-positive Mac-2 binding protein (WFA+M2BP) cutoff index (COI) of ≥2.5 and infection with the HCV-1b core aa 70 mutant subgroup to be pretreatment predictors of posttreatment HCC. The same analysis identified an alpha-fetoprotein concentration of ≥5 μg/liter and an WFA+M2BP COI of ≥1.0 to be predictors of HCC at 24 weeks after the end of antiviral therapy. We conclude that both virus- and host-related factors seem to influence the development of HCC after HCV RNA eradication.Entities:
Keywords: HCV; IL-28B; NS5A; WFA+M2BP; core; direct-acting antivirals; hepatocellular carcinoma; mutant; sustained virological response; wild
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Year: 2019 PMID： 30381417 PMCID： PMC6322466 DOI： 10.1128/JCM.01463-18
Source DB: PubMed Journal: J Clin Microbiol ISSN： 0095-1137 Impact factor: 5.948