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

OBJECTIVES: 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.