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day of NA administration and the survival time was confirmed through the end of 2018.
Results:
Patients with decompensated cirrhosis had significantly lower baseline serum HBV DNA levels
than compensated cirrhotic patients (4.98±1.91 vs. 5.67±1.26 log10 IU/ml, P=0.031). The mean
follow-up duration was 84 and 42 months in compensated cirrhotic and decompensated cirrhotic
patients (P<0.0001), respectively. For 59 decompensated cirrhotic patients, 27.1% (16/59) of patients
achieved CTP class A and 23.7% (14/59) showed improvement in the CTP score of ≧ 2 points after
2 years of NA treatment. The 1, 2 and 3-year cumulative survival rates were significantly higher in
compensated cirrhotic patients than those with decompensated cirrhosis (100%, 98.5%, 98.5% vs.
81.2%, 75.6%, 69.5%; P<0.0001). Multivariate analysis for risk factors of mortality in cirrhotic
patients showed that older age (hazard ratio: 3.28, 95% CI: 1.25-8.62, P=0.016) and decompensated
cirrhosis (hazard ratio: 8.30, 95% CI: 2.45-28.06, P=0.0007) were independently associated with
liver-related mortality. A total of 31 patients, 37.3% of compensated cirrhotic and 10.2% of
decompensated cirrhotic patients, developed HCC during the follow-up. The 1, 2 and 3-year
cumulative survival rates were not different between compensated cirrhotic patients with and without
HCC development (96%, 96%, 96% vs. 100%, 100%, 100%; P=0.577) (Figure 2). Similarly, the 1, 2
and 3-year cumulated survival rates were comparable between decompensated cirrhotic patients with
and without HCC development (83.3%, 83.3%, 66.7% vs. 81%, 74.7%, 69.8%; P=0.528). Among
patients with HCC, 70.9% were at the earlier stages of BCLC system, and 83.8% received potentially
curative treatment.
Conclusions:
Antiviral therapy improves liver function of HBV-related cirrhotic patients and provides a better
chance of curative treatment in those with HCC development. Decompensated cirrhosis is a risk
factor for liver-related mortality in this special clinical setting. (Word count:438)