摘要
目的比较聚乙二醇干扰素a-2a单药及联合阿德福韦酯或联合恩替卡韦治疗慢性乙型肝炎的疗效及安全性。方法采用开放、随机、对照研究方法,将141例HBeAg阳性入选病例分为聚乙二醇干扰素a-2a组(A组,46例),聚乙二醇干扰素a-2a联合阿德福韦酯组(B组,46例)和聚乙二醇干扰素a-2a联合恩替卡韦组(C组,49例)。分别在治疗4、12、24和48周及随访24周时进行疗效和安全性评估。结果联合治疗组HBV DNA阴转率及下降幅度、HBeAg阴转率、ALT复常率均优于聚乙二醇干扰素a-2a单药治疗,2种联合治疗方案都具有较强的病毒抑制作用,且安全性好;联合恩替卡韦组病毒的下降幅度和表面抗原降低程度均大于联合阿德福韦酯组。结论聚乙二醇干扰素a-2a单药联合联合阿德福韦酯或联合恩替卡韦治疗HBeAg阳性乙型肝炎安全性好,疗效均优于聚乙二醇干扰素a-2a单药治疗,且聚乙二醇干扰素a-2a联合恩替卡韦疗效优于聚乙二醇干扰素a-2a联合阿德福韦酯。
Objective To evaluate the efficacy and safety of peginterferon-a-2a（peg-IFN-a-2a）alone and in combination with nucleoside analogues for treatment of HBeAg-positive chronic hepatitis B（CHB）. Methods One hundred and forty-one patients with HBeAg-positive CHB were selected and randomly divided into three groups：group A（46cases）received peginterferon-a-2amonotherapy,group B（46cases）received peginterferon-a-2acombined with adefovir,and group C（49cases）received peginterferon-a-2acombined with entecavir.Efficacy and safety were analyzed at the end of week 4,week 12,week 24,and week 48 and at follow-up 24 weeks later.Results At the end of week 4,there were statistically significant differences in the rate at which patients tested negative for HBV DNA and the extent of the decrease in HBV DNA（χ2Rate at which patients tested negative for HBV DNA= 14.953,FExtent of the decrease in HBV DNA=8.351,P〈0.05 for all）.At the end of week12,there were statistically significant differences in the rate at which patients tested negative for HBV DNA and the extent of the decrease in HBV DNA（χ2Rate at which patients tested negative for HBV DNA=15.080,FExtent of the decrease in HBV DNA=5.432,P 0.05 for all）.At the end of week 24,there were statistically significant differences in the rate of ALT normalization,the rate at which patients tested negative for HBeAg,the rate at which patients tested negative for HBV DNA,and the extent of the decrease in HBV DNA（χ2Rate of ALT normalization= 14. 536,χ2Rate at which patients tested negative for HBeAg= 7. 167,χ2Rate at which patients tested negative for HBV DNA=21.468,FExtent of the decrease in HBV DNA=5.739,P〈0.05 for all）.At the end of week 48,there were statistically significant differences in the rate of ALT normalization,the rate at which patients tested negative for HBeAg,the rate at which patients tested negative for HBV DNA,the extent of the decrease in HBV DNA,and the extent of the decrease in HBsAg（χ2Rate of ALT normalization= 6.838,χ2Rate at which patients tested negative for HBeAg= 7.002,χ2Rate at which patients tested negative for HBV DNA=11.673,FExtent of the decrease in HBV DNA=5.338,FExtent of the decrease in HBsAg=3.963,P〈0.05 for all）.At the end of week 72,there were statistically significant differences in the rate of ALT normalization,the rate at which patients tested negative for HBeAg,the rate at which patients tested negative for HBV DNA,the extent of the decrease in HBV DNA,and the extent of the decrease in HBsAg（χ2Rate of ALT normalization=7.458,χ2Rate at which patients tested negative for HBeAg= 7.736,χ2Rate at which patients tested negative for HBV DNA= 11.341,FExtent of the decrease in HBV DNA=5.036,FExtent of the decrease in HBsAg=4.846,P〈0.05 for all）.Compared to peginterferon-a-2amonotherapy,combined treatment with peginterferon-a-2a（peg-IFN-1a-2a）and nucleoside analogues resulted in a better rate at which patients tested negative for HBV DNA,agreater extent of the decrease in HBV DNA,a better rate at which patients tested negative for HBeAg,and a better rate of ALT normalization.Combined treatment had greater viral inhibition and was safer.Compared to the group that received combined treatment with adefovir,the group that received combined treatment with entecavir had a better rate at which patients tested negative for HBV DNA and a greater extent of the decrease in HBsAg. Conclusion Combined treatment with peginterferon-a-2a（peg-IFN-a-2a）and nucleoside analogues has better efficacy and is safer than peginterferon-a-2amonotherapy.Peginterferon-a-2acombined with entecavir is better than peginterferon-a-2acombined with adefovir in treating HBeAg-positive CHB.
出处
《中国病原生物学杂志》
CSCD
北大核心
2015年第3期272-276,共5页
Journal of Pathogen Biology
