- VernacularTitle:恩替卡韦治疗104例乙型肝炎肝硬化患者96周的疗效观察
- Author:
Yan XU
1
;
Jiang-bin WANG
;
Jie XU
;
Jian JIAO
;
Yong-gui ZHANG
;
Shang-wei JI
;
Ping ZHAO
;
Hong-hua GUO
;
Yan LI
;
Chang-yu ZHOU
Author Information
- Publication Type:Clinical Trial
- MeSH: Adult; Alanine Transaminase; blood; Antiviral Agents; therapeutic use; DNA, Viral; blood; Female; Genotype; Guanine; analogs & derivatives; therapeutic use; Hepatitis B e Antigens; blood; Hepatitis B virus; drug effects; genetics; isolation & purification; Hepatitis B, Chronic; complications; drug therapy; virology; Humans; Liver Cirrhosis; drug therapy; etiology; virology; Male; Middle Aged; Time Factors; Treatment Outcome; Virus Replication; drug effects
- From: Chinese Journal of Hepatology 2010;18(2):109-112
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo analyze antiviral effects of entecavir in patients with hepatitis B virus-related cirrhosis.
METHODS104 patients of hepatitis B virus-related cirrhosis with no previous history of antiviral therapy were treated with entecavir 0.5 mg once daily. 37 patients were taken hepatic histologic examination before and after the treatment.
RESULTSMean reductions of serum HBV DNA was 5.1 log10 96 weeks after the treatment, HBV DNA became undetectable in 98.1% patients, and ALT became normal in 80.7% patients; HBeAg seroconversion occurred in 13.9% of the 72 HBeAg positive patients; 61.5% of these patients were infected with genotype C HBV, and 26.9% were infected with genotype B HBV. The genotype of HBV was not associated with the therapeutical effect. Child-pugh score was associated with the progression of the disease: the proportion of patients with disease progression was highest in Child-Pugh C grade patients and lowest in Child-Pugh A grade patients. The level of the HBV DNA load was positively correlated with Knodell HAI score at the baseline and 96 weeks after the treatment.
CONCLUSIONEntecavir treatment results in suppression of HBV replication and delayed progression of fibrosis in patients with hepatitis B virus-related cirrhosis.