中华传染病杂志
中華傳染病雜誌
중화전염병잡지
CHINESE JOURNAL OF INFECTIOUS DISEASES
2009年
6期
338-342
,共5页
姚碧莲%张欣欣%杨劲%于德敏%张东华
姚碧蓮%張訢訢%楊勁%于德敏%張東華
요벽련%장흔흔%양경%우덕민%장동화
肝炎,乙型,慢性%抗病毒药%动力学%模型,理论%恩替卡韦%DNA,病毒
肝炎,乙型,慢性%抗病毒藥%動力學%模型,理論%恩替卡韋%DNA,病毒
간염,을형,만성%항병독약%동역학%모형,이론%은체잡위%DNA,병독
Hepatitis B,chronic%Antiviral agents%Kinetics%Models,theoretical%Entecavir%DNA,viral
目的 分析抗病毒治疗过程中病毒载量动态变化特点及其临床意义.方法 采用Neumann数学模型对门诊口服恩替卡韦治疗并早期规则随访(0、2、4、12、24周)的6例慢性乙型肝炎患者的血HBV载量及其相关参数进行分析.结果 恩替卡韦每天0.5 mg治疗HBeAg阳性C基因型慢性乙型肝炎患者,药物效力为99.970%(n=6),游离病毒半衰期为1.6 d(n=6),感染细胞半衰期为21.3 d(n=5).其中1例患者(例6)在随访至38周时发现有病毒学突破,与其他未发生病毒学突破的患者相比,其清除病毒的速度、药物效力、感染细胞消失的速度值较低,而游离病毒和感染细胞的半衰期较长.结论 抗病毒治疗过程中HBV DNA的二相下降模式可以由数学模型模拟,提示该模型对疗效具有一定的预测作用.
目的 分析抗病毒治療過程中病毒載量動態變化特點及其臨床意義.方法 採用Neumann數學模型對門診口服恩替卡韋治療併早期規則隨訪(0、2、4、12、24週)的6例慢性乙型肝炎患者的血HBV載量及其相關參數進行分析.結果 恩替卡韋每天0.5 mg治療HBeAg暘性C基因型慢性乙型肝炎患者,藥物效力為99.970%(n=6),遊離病毒半衰期為1.6 d(n=6),感染細胞半衰期為21.3 d(n=5).其中1例患者(例6)在隨訪至38週時髮現有病毒學突破,與其他未髮生病毒學突破的患者相比,其清除病毒的速度、藥物效力、感染細胞消失的速度值較低,而遊離病毒和感染細胞的半衰期較長.結論 抗病毒治療過程中HBV DNA的二相下降模式可以由數學模型模擬,提示該模型對療效具有一定的預測作用.
목적 분석항병독치료과정중병독재량동태변화특점급기림상의의.방법 채용Neumann수학모형대문진구복은체잡위치료병조기규칙수방(0、2、4、12、24주)적6례만성을형간염환자적혈HBV재량급기상관삼수진행분석.결과 은체잡위매천0.5 mg치료HBeAg양성C기인형만성을형간염환자,약물효력위99.970%(n=6),유리병독반쇠기위1.6 d(n=6),감염세포반쇠기위21.3 d(n=5).기중1례환자(례6)재수방지38주시발현유병독학돌파,여기타미발생병독학돌파적환자상비,기청제병독적속도、약물효력、감염세포소실적속도치교저,이유리병독화감염세포적반쇠기교장.결론 항병독치료과정중HBV DNA적이상하강모식가이유수학모형모의,제시해모형대료효구유일정적예측작용.
Objective To analyze the viral dynamics and clinical significance during the antiviral treatment by a mathematical model.Methods Six chronic hepatitis B patients were evaluated with a kinetic model(Neumann model)during dose of 0.5 mg/d oral entecavir.Blood samples were drawn for HBV DNA measurement at week 0,2,4,12,24.Non-linear modeling was used to fit individual patient data.Results The median effectiveness in blocking viral production was 99.970%(n=6).The median half-life of viral turn-over was 1.6 d(n=6).The median half-life of infected hepatocytes was 21.3 d(n=5).Compared with the other patients,the c(virions are cleared at a rate)、ε(effectiveness)、δ(infected cell are lost at a rate)value of one patient(eg.6)were all lower and the half-life of virus and infected cells were higher,and eg.6 developed viral break-through after 38 weeks of follow-up.Conclusions Viral load decay showed a biphasic pattern during entecavir therapy which can be described with a mathematical model.The model relates processes of viral infection and replication as well as drug efficacy to model parameters.It indicates the prediction of bio-mathematical model during antiviral treatment.