中华传染病杂志
中華傳染病雜誌
중화전염병잡지
CHINESE JOURNAL OF INFECTIOUS DISEASES
2011年
9期
553-557
,共5页
朱月永%董菁%陈攸涛%陈靖%江家骥
硃月永%董菁%陳攸濤%陳靖%江傢驥
주월영%동정%진유도%진정%강가기
肝炎,乙型,慢性%肝炎表面抗原,乙型%肝炎e抗原,乙型%DNA,病毒%干扰素α-2a%聚乙烯二醇类
肝炎,乙型,慢性%肝炎錶麵抗原,乙型%肝炎e抗原,乙型%DNA,病毒%榦擾素α-2a%聚乙烯二醇類
간염,을형,만성%간염표면항원,을형%간염e항원,을형%DNA,병독%간우소α-2a%취을희이순류
Hepatitis B,chronic%Hepatitis B surface antigens%Hepatitis B e antigens%DNA,viral%Interferon alfa-2a%Polyethylene glycols
目的 探讨聚乙二醇化干扰素（PEG-IFN α-2a）治疗HBeAg阳性慢性乙型肝炎(CHB)患者过程中预测HBsAg消失的相关因素。方法 对72例HBeAg阳性CHB患者，应用PEG-IFN α-2a 180 μg,每周1次，共48周。每3个月检测ALT、AST及HBV DNA、HBeAg和H BsAg定量，对48周治疗结束时HBsAg消失与基线、12周、24周的HBV DNA、HBeAg和HBsAg定量的相关关系进行分析。计数资料行Fisher精确检验及受试者工作特征(ROC)曲线分析。结果65例HBeAg阳性CHB患者完成本研究，其中7例HBsAg消失。48周时HBsAg的消失与治疗12周时H BeAg水平有关（Fisher确切概率法，P=0.023），与治疗24周时HBeAg水平高度相关 （Fisher确切概率法，P=0.004）,与12周或24周时HBsAg＜250 IU/mL相关(Fisher确切概率法，P=0.001,P=0.002)。与12周时HBV DNA阴转相关（Fisher确切概率法，P=0.039），而与24周时HBV DNA是否阴转无关（Fisher确切概率法，P= 0.130）。经ROC曲线分析显示，12周、24周HBsAg及24周HBeAg曲线下面积(AUC)分别为0.8584(P=0.0021)、0.9606(P=0.001)及0.8350(P=0.040)。结论 联合应用24周HBeAg和HBsAg定量水平可能是预测48周疗程结束时是否发生HBsAg消失的有效指标。
目的 探討聚乙二醇化榦擾素（PEG-IFN α-2a）治療HBeAg暘性慢性乙型肝炎(CHB)患者過程中預測HBsAg消失的相關因素。方法 對72例HBeAg暘性CHB患者，應用PEG-IFN α-2a 180 μg,每週1次，共48週。每3箇月檢測ALT、AST及HBV DNA、HBeAg和H BsAg定量，對48週治療結束時HBsAg消失與基線、12週、24週的HBV DNA、HBeAg和HBsAg定量的相關關繫進行分析。計數資料行Fisher精確檢驗及受試者工作特徵(ROC)麯線分析。結果65例HBeAg暘性CHB患者完成本研究，其中7例HBsAg消失。48週時HBsAg的消失與治療12週時H BeAg水平有關（Fisher確切概率法，P=0.023），與治療24週時HBeAg水平高度相關 （Fisher確切概率法，P=0.004）,與12週或24週時HBsAg＜250 IU/mL相關(Fisher確切概率法，P=0.001,P=0.002)。與12週時HBV DNA陰轉相關（Fisher確切概率法，P=0.039），而與24週時HBV DNA是否陰轉無關（Fisher確切概率法，P= 0.130）。經ROC麯線分析顯示，12週、24週HBsAg及24週HBeAg麯線下麵積(AUC)分彆為0.8584(P=0.0021)、0.9606(P=0.001)及0.8350(P=0.040)。結論 聯閤應用24週HBeAg和HBsAg定量水平可能是預測48週療程結束時是否髮生HBsAg消失的有效指標。
목적 탐토취을이순화간우소（PEG-IFN α-2a）치료HBeAg양성만성을형간염(CHB)환자과정중예측HBsAg소실적상관인소。방법 대72례HBeAg양성CHB환자，응용PEG-IFN α-2a 180 μg,매주1차，공48주。매3개월검측ALT、AST급HBV DNA、HBeAg화H BsAg정량，대48주치료결속시HBsAg소실여기선、12주、24주적HBV DNA、HBeAg화HBsAg정량적상관관계진행분석。계수자료행Fisher정학검험급수시자공작특정(ROC)곡선분석。결과65례HBeAg양성CHB환자완성본연구，기중7례HBsAg소실。48주시HBsAg적소실여치료12주시H BeAg수평유관（Fisher학절개솔법，P=0.023），여치료24주시HBeAg수평고도상관 （Fisher학절개솔법，P=0.004）,여12주혹24주시HBsAg＜250 IU/mL상관(Fisher학절개솔법，P=0.001,P=0.002)。여12주시HBV DNA음전상관（Fisher학절개솔법，P=0.039），이여24주시HBV DNA시부음전무관（Fisher학절개솔법，P= 0.130）。경ROC곡선분석현시，12주、24주HBsAg급24주HBeAg곡선하면적(AUC)분별위0.8584(P=0.0021)、0.9606(P=0.001)급0.8350(P=0.040)。결론 연합응용24주HBeAg화HBsAg정량수평가능시예측48주료정결속시시부발생HBsAg소실적유효지표。
Objective To identify the predictive factors associated with hepatitis B surface antigen (HBsAg) loss in hepatitis B e antigen (HBeAg)-positive chronic hepatitis B (CHB) patients treated with pegylated interferon (PEG-IFNα-2a). Methods Seventy-two HBeAg positive CHB patients were treated with PEG-IFNa-2a 180 μg weekly for 48 weeks. The serum levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST) and hepatitis B virus (HBV) DNA,HBeAg, and HBsAg were quantitatively detected every 3 months. The relationship between HBV DNA, HBeAg, and HBsAg levels at baseline, week 12, 24 of treatment and HBsAg loss was analyzed. The data were statistically assessed by Fisher's exact test, and receiver operating characteristic (ROC) curve. Results Totally 65 patients accomplished the therapy, and 7 (10.8％)patients achieved HBsAg loss. HBsAg loss at week 48 of treatment was associated with HBeAg level at week 12 of treatment (Fisher's exact test, P= 0. 023), HBeAg level at week 24 (Fisher's exact test, P=0. 004), and lower HBsAg levels (＜250 IU/mL) at week 12 and 24 of treatment (Fisher's exact test,P=0. 001 and 0.002, respectively). HBsAg loss was associated with HBV DNA negative ( ＜ 1000 copy/mL) at week 12 of treatment (Fisher's exact test, P = 0. 039), while not associated with HBV DNA negative at week 24 of treatment (Fisher's exact test, P=0. 130). ROC curve analysis revealed that the AUC was 0. 8584(P=0. 0021) of HBsAg level at week 12, 0. 9606(P=0. 001) of HBsAg level at week 24, and 0. 8350(P=0. 040) of HBeAg level at week 24. Conclusion Levels of HBsAg and HBeAg at week 24 of treatment might serve as effective factors to predict HBsAg loss in patients received PEG-IFN monotherapy.
