title: Effect of virological response to entecavir on the development of hepatocellular carcinoma in hepatitis B viral cirrhotic patients: comparison between compensated and decompensated cirrhosis.
abstract: OBJECTIVE
  This study aimed to evaluate the risk of development of hepatocellular carcinoma (HCC) according to underlying liver status and virological response (VR) to entecavir (ETV) in chronic hepatitis B patients with cirrhosis. Procollagen III N-terminal peptide (PIIINP) concentration during ETV treatment and its association with HCC development were also evaluated.
  
  
  METHODS
  A total of 306 patients with clinically diagnosed liver cirrhosis were treated with ETV for ≥12 months and were subsequently followed up for the occurrence of HCC (median follow-up duration: 37.0 months). Patients who developed HCC within 12 months were excluded. VR was defined as a hepatitis B virus DNA level <20 IU/ml at 12 months after ETV treatment.
  
  
  RESULTS
  A total of 209 patients (68.3%) had compensated cirrhosis, and the remaining patients (31.7%) had decompensated cirrhosis. The 5-year cumulative incidence of HCC was 26.8%. A multivariate Cox regression analysis identified the following independent risk factors for developing HCC in all the patients: age >50 years (hazard ratio (HR)=8.41; 95% confidence interval (CI)=3.86-18.28; P=0.000), male sex (HR=4.24; 95% CI=1.83-9.81; P=0.001), high serum PIIINP level at 12 months (HR=1.07; 95% CI=1.02-1.13; P=0.007), and no VR at 12 months (HR=2.10; 95% CI=1.02-4.33; P=0.043). The subgroup analyses showed that no VR at 12 months is a significant risk factor for developing HCC in the patients with decompensated cirrhosis (HR=7.74; 95% CI=1.34-44.78; P=0.022) but not in those with compensated cirrhosis (P=0.749).
  
  
  CONCLUSIONS
  The antiviral treatment with ETV did not completely eliminate the risk of developing HCC in our patients with cirrhosis. However, VR to ETV was associated with a low probability that the patients with decompensated cirrhosis would develop HCC.
authors.affiliation: Department of Gastroenterology, Ajou University School of Medicine, Suwon, South Korea.
authors.forename: Soon Sun
authors.initials: SS
authors.lastname: Kim
authors.affiliation: Department of Gastroenterology, Ajou University School of Medicine, Suwon, South Korea.
authors.forename: Jae Chul
authors.initials: JC
authors.lastname: Hwang
authors.affiliation: Department of Gastroenterology, Ajou University School of Medicine, Suwon, South Korea.
authors.forename: Sun Gyo
authors.initials: SG
authors.lastname: Lim
authors.affiliation: Department of Gastroenterology, Ajou University School of Medicine, Suwon, South Korea.
authors.forename: Seon Joo
authors.initials: SJ
authors.lastname: Ahn
authors.affiliation: Department of Gastroenterology, Ajou University School of Medicine, Suwon, South Korea.
authors.forename: Jae Youn
authors.initials: JY
authors.lastname: Cheong
authors.affiliation: Department of Gastroenterology, Ajou University School of Medicine, Suwon, South Korea.
authors.forename: Sung Won
authors.initials: SW
authors.lastname: Cho
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000998:Antiviral Agents / Q000627:therapeutic use*; D014408:Biomarkers, Tumor / Q000097:blood; D006528:Carcinoma, Hepatocellular / Q000453:epidemiology / Q000517:prevention & control / Q000821:virology*; D005260:Female; D006147:Guanine / Q000031:analogs & derivatives* / Q000627:therapeutic use; D019694:Hepatitis B, Chronic / Q000150:complications* / Q000188:drug therapy*; D006801:Humans; D015994:Incidence; D008103:Liver Cirrhosis / Q000188:drug therapy* / Q000821:virology*; D008113:Liver Neoplasms / Q000453:epidemiology / Q000517:prevention & control / Q000821:virology*; D008297:Male; D008875:Middle Aged; D056910:Republic of Korea / Q000453:epidemiology; D012189:Retrospective Studies; D012307:Risk Factors; D016896:Treatment Outcome
chemical_list: D000998:Antiviral Agents; D014408:Biomarkers, Tumor; C413685:entecavir; D006147:Guanine