核苷(酸)单药与联合治疗失代偿期乙型肝炎肝硬化疗效的比较

目的 比较核苷(酸)单药与联合治疗对失代偿期乙型肝炎肝硬化患者的疗效.方法 回顾性分析130例核苷(酸)单药或联合治疗失代偿期乙型肝炎肝硬化患者的临床资料.单药组111例,其中恩替卡韦组(ETV)25例,阿德福韦酯组(ADV)45例,拉米夫定组(LAM)41例；联合组[替比夫定(LDT)+ADV]19例.于治疗后4、1...

Comparing the efficacy of monotherapy versus combination therapy of nucleos(t)ide analogues for decompensated HBV liver cirrhosis

Objective To compare the efficacy of monotherapy versus combination therapy with nucleos(t)ide analogues for decompensated HBV liver cirrhosis patients. Methods Antiviral therapy was retrospectively analyzed in 130 decompensated HBV liver cirrhosis patients, which included 111 patients treated with nucleos(t)ide monotherapy(25 patients with entecavir 0.5 mg/d,45 with adefovir 10 mg/d and 41 with lamivudine 100 mg/d) and 19 patients with combination therapy of telbivudine 600 mg/d and adefovir 10 mg/d. ALT level, CPS score and HBV DNA level at week 4, 12, 24, 48, and HBeAg loss rate, incidence of HCC, average times of hospitalization, drug resistance rate and so on at week 48 were analyzed. Results ALT levels decreased significantly at week 4. HBV DNA levels decreased significantly at week 12 in combination group and entecavir monotherapy group, at week 24 in lamivudine monotherapy group and at week 48 in adefovir monotherapy group (all P < 0.05). At week 4, more patients in combination group had HBV DNA<500 copies/ml than those in monotherapy group (P < 0.05). CPS scores decreased significantly from baseline to week 48 in each monotherapy group and to week 24 in combination group(P < 0.05). At week 48, the rate of HBeAg loss was higher in combination group (15.8%) than that in lamivudine group(4.9%) or adefovir group(4.4%), both P < 0.05. There was no significant difference in combination group and each monotherapy group. Cumulative rates of HBV resistance in lamivudine group and adefovir group were 24.4% and 6.7%, respectively, at week 48. No HBV resistance was detected in ETV or combination group. Conclusion Combination therapy of telbivudine and adefovir for decompensated HBV cirrhosis had rapid HBV DNA suppression, high rate of HBeAg loss, low rate of resistance, which is potential to be one of the optimal regimens for decompensated HBV cirrhosis.