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Differential Effect of HCV Eradication and Fibrosis Grade on Hepatocellular Carcinoma and All-cause Mortality

  • Yun Bin Lee
  • , Joon Yeul Nam
  • , Jeong Hoon Lee
  • , Young Chang
  • , Hyeki Cho
  • , Young Youn Cho
  • , Eun Ju Cho
  • , Su Jong Yu
  • , Hwi Young Kim
  • , Dong Ho Lee
  • , Jeong Min Lee
  • , Seong Gyu Hwang
  • , Yoon Jun Kim
  • , Jung Hwan Yoon

Research output: Contribution to journalArticlepeer-review

12 Scopus citations

Abstract

Whether a sustained virological response (SVR) improves long-term outcomes in chronic hepatitis C patients with earlier-stage fibrosis has not been established. We investigated the differential effect of SVR on the risk of outcomes according to hepatic fibrosis grade. Fibrosis grade was categorised using FIB-4: <1.45, low-probability of significant fibrosis; 1.45–3.25, intermediate-probability; and ≥3.25, high-probability. Primary and secondary endpoints were hepatocellular carcinoma (HCC) occurrence and death, respectively. Among 1,373 included chronic hepatitis C patients, 744 patients were treated with interferon-based or –free regimens and 622 (83.6%) achieved SVR. SVR was independently associated with lower risk of HCC (vs. untreated: adjusted hazard ratio [aHR], 0.165; 95% confidence interval [CI], 0.077–0.350; P < 0.001) and overall death (vs. untreated; aHR, 0.146; 95% CI, 0.050–0.424; P < 0.001) during the median observation of 3.5 (interquartile range, 1.9–6.6) years. The SVR group had significantly lower risk of HCC than the untreated group among patients with intermediate-probability (n = 492: aHR, 0.171; 95% CI, 0.051–0.578; P = 0.004) and high-probability (n = 446: aHR, 0.243; 95% CI, 0.107–0.551; P < 0.001) of significant fibrosis. HRs were maintained after balancing with inverse probability weighting. SVR was associated with reduced risk of HCC development and all-cause mortality in patients with chronic hepatitis C.

Original languageEnglish
Article number13651
JournalScientific Reports
Volume8
Issue number1
DOIs
StatePublished - 1 Dec 2018

Bibliographical note

Publisher Copyright:
© 2018, The Author(s).

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