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Association of liver stiffness and steatosis with hepatocellular carcinoma development in patients with hepatitis C virus infection who received direct‐acting antiviral therapy and achieved sustained virological response
Author(s) -
Tada Toshifumi,
Nishimura Takashi,
Matono Tomomitsu,
Yoshida Masahiro,
Yuri Minako,
Fujiwara Aoi,
Yuri Yukihisa,
Takashima Tomoyuki,
Aizawa Nobuhiro,
Ikeda Naoto,
Enomoto Hirayuki,
Kumada Takashi,
Iijima Hiroko
Publication year - 2021
Publication title -
hepatology research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.123
H-Index - 75
eISSN - 1872-034X
pISSN - 1386-6346
DOI - 10.1111/hepr.13677
Subject(s) - hepatocellular carcinoma , medicine , steatosis , gastroenterology , cumulative incidence , transient elastography , proportional hazards model , univariate analysis , incidence (geometry) , hepatitis b virus , fibrosis , virus , multivariate analysis , immunology , liver fibrosis , cohort , physics , optics
Aim The pathogenic process underlying the development of hepatocellular carcinoma (HCC) is not yet clear in patients with chronic hepatitis C virus who receive direct‐acting antiviral therapy and achieve sustained virological response. This study investigated two risk factors for HCC in these patients; specifically, hepatic fibrosis and steatosis. Methods A total of 355 patients in whom hepatitis C virus was eradicated by direct‐acting antiviral were evaluated. Fibrosis and steatosis were assessed using transient elastography (TE) and the controlled attenuation parameter (CAP). Inverse probability weighting was applied to patient age, sex, albumin–bilirubin, α ‐fetoprotein, history of HCC, TE, or CAP. Results The 12‐, 24‐, and 36‐month cumulative incidence rates of HCC were 0.9%, 2.4%, and 4.1%, respectively. Univariate analysis with the Cox proportional hazards model showed that whereas a high TE value (≥10 kPa) was significantly associated with HCC development (HR 7.861, 95% CI 2.126–29.070; p = 0.002), CAP was not. Additionally, univariate analysis with the Cox proportional hazards model adjusted by inverse probability weighting showed that a high TE value was significantly associated with HCC development (HR 3.980, 95% CI, 1.036–15.290; p = 0.044), whereas CAP was not. The cumulative inverse probability weighting‐adjusted incidence of HCC rates at 12, 24, and 36 months were 0.0%, 0.5%, and 1.7%, respectively, in patients with a low TE value, and 2.5%, 5.1%, and 7.6%, respectively, in those with a high TE value. Conclusion A high TE value was a risk factor for HCC in hepatitis C virus patients who received direct‐acting antiviral therapy and achieved sustained virological response.