Abstract
The data are limited on the long-term clincial outcome of monotherapy versus combinations of nucleos(t)ide analog (NUCs) for hepatitis B related decompensated cirrhotic patients. This study was to evaluate the efficacy in treatment-naive patients using NUCs monotherapy or combinations. Three hundred and six patients with decompensated hepatitis B cirrhosis were selected from cirrhosis cohort and divided into treatment-naive (n = 260) and control groups (n = 46). Antiviral therapies included monotherapy of lamivudine (LAM, n = 39), adefovir (ADV, n = 73), telbivudine (LDT, n = 36), entecavir (ETV, n = 48), and combinations of LAM+ADV (n = 39) or LDT+ADV (n = 25). Of these patients, 193 in antiviral therapy and 39 in control group were included for analysis over two years. The cumulative drug-resistance rate at two year was higher in the LAM (37.9%), ADV (21.2%), LDT (23.3%) than in the ETV monotherapy (2.6%), and with combinations of LAM+ADV (8.7%) or LDT+ADV (6.3%), respectively, P < 0.001. Serum hepatitis B virus (HBV) DNA undetectability in the ETV and the LDT+ADV group was higher than in the LAM, ADV and LAM+ADV group at over two years (P < 0.05). The child-pugh score (CPs) in the antiviral therapy group was decreased at two years (P < 0.05). In the control group and drug-resistant patients, however, CPs was increased. The two years cumulative incidence of liver failure in the antiviral therapy group was significantly less than the control group (OR 24.9, 95%; CI 6.5 to 94.7, P = 0.001). The total cumulative survival rate in the antiviral therapy group was higher than in control group (OR 4.2, 95%; CI 1.4 to 12.9, P = 0.017). The combinations of NUCs therapy and ETV momotherapy are optimum management for hepatitis B related decompensated cirrhotic patients. Key words: Hepatitis B, decompensated cirrhosis, nucleos(t)ide analogs, hepatocellular carcinoma, drug resistance.
Highlights
Chronic hepatitis B virus (HBV) infections, the main etiology of liver cirrhosis and hepatocellular carcinoma (HCC) remain a major public health problem worldwide, especially in China (Lok and McMahon, 2009; Liaw et al, 2008; Tanaka et al, 2011)
These included (1) chronic hepatitis B history and/or signs; (2) abnormal liver function accompanied by portal hypertension, such as hepatic encephalopathy, ascites or variceal bleeding with child-pugh scores (CPs) score ≥ 7; (3) B-ultrasound scanning (LOGIQ9, GE Company, USA) and CT (GE HISPEED DXI, GE company, USA) consistent with the signs of liver cirrhosis without images of liver cancer; and (4) no nucleos(t)ide analogs (NUCs) medicine taken prior to study entry
Age, family history of hepatitis B, alcohol abuse, CPs or HBeAg positive and HBV DNA level was seen between groups at baseline (P > 0.05; Table1)
Summary
Chronic hepatitis B virus (HBV) infections, the main etiology of liver cirrhosis and hepatocellular carcinoma (HCC) remain a major public health problem worldwide, especially in China (Lok and McMahon, 2009; Liaw et al, 2008; Tanaka et al, 2011). After infection with HBV, the cumulative 5-year incidence of liver cirrhosis is 8 to 20%; among these cases, the annual incidence of HCC is 2 to 5% (Tanaka et al, 2011; Tan, 2011; Asia-Pacific Working Party on Prevention of Hepatocellular Carcinoma, 2010). The most effective methods to preventing HCC is to control HBV infection through vaccination (Asia-Pacific Working Party on Prevention of Hepatocellular Carcinoma, 2010; Lim et al, 2009). Antiviral drug resistance is important in determining the success of long-term therapy for chronic hepatitis B patients (Yeh et al, 2011; Papatheodoridis et al, 2010)
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