EFFECTS OF COMBINED ANTIRETROVIRAL THERAPY ON COAGULATION FACTORS

包括硫酸吲地那韦在内的联合抗逆转录病毒疗法对患有血友病A或B的HIV-1血清阳性患者的凝血因子、对血小板聚集和对第VIII/IX因子的影响。该方案的目的是评估在被研究的特定人群中，硫酸吲地那韦的联合治疗是否会导致凝血系统中预期可识别的成分发生变化。先验的认识是，由于在联合NRTI治疗中不加入吲哚瓦硫酸盐的组是不可行的，所以不可能确定在没有吲哚瓦硫酸盐的情况下凝血系统会发生什么变化，如果有的话。然而，为了帮助评估输入因子VIII的药代动力学半衰期和恢复情况的变化，经历过HIV-1血清阳性血友病A的HIV-1血友病患者将作为实验室对照组。我们假设，在12周的治疗后，与实验室对照组观察到的变化相比，联合应用硫酸吲地那韦和NRTIs给未经治疗的HIV-1血清阳性血友病A患者输注的第VIII因子的药代动力学半衰期将减少。其次，在对酶抑制剂初治的HIV-1阳性血友病患者进行52周的联合应用硫酸吲地那韦和联合硝普钠治疗12周后：与实验室对照组观察到的变化相比，血友病A患者的输注因子的药代动力学恢复将降低；血友病B患者的输注因子IX的药代动力学半衰期将缩短，血友病B患者的输注因子IX的药代动力学恢复将降低。

Effects of Combination Antiretroviral Therapy including Indinavir Sulfate on Coagulation Factors, on Platelet Aggregation and on Factor VIII/IX in HIV-1 Seropositive patients with Hemophilia A or B. The objectives of this protocol are to assess whether, in the specific population being studied, a combined therapy of indinavir sulfate NRTIs induces changes in prospectively identified elements of the coagulation system. It is recognized apriori, that due to the nonfeasibility of having a group in which indinivar sulfate is not added to combination NRTI therapy, it will be impossible to determine what changes in the coagulation system, if any, would have been observed in the absence of indinivar sulfate. However, to help assess changes in the pharmacokinetic half-life and recovery of infused factor VIII, protease inhibitor-experienced HIV-1 seropositive hemophilia A patients will serve as a laboratory control group. We hypothesize that after 12 weeks of treatment, coadministration of indinavir sulfate and NRTIs to protease inhibitor-naive HIV-1 seropositive hemophilia A patients will decrease the pharmacokinetic half-life of infused factor VIII compared to pre-indinavir sulfate therapy baseline relative to changes observed in the laboratory control group. Secondarily, during a 52 week coadministration of indinavir sulfate and combination NTRI therapy to protease inhibitor-naive HIV-1 seropositive hemophilia patients after 12 weeks of treatment: the pharmacokinetic recovery of infused factor VIII in hemophilia A patients will be reduced, relative to changes observed in the laboratory control group; the pharmacokinetic half-life of infused factor IX in hemophilia B patients will be reduced and the pharmacokinetic recovery of infused factor IX in hemophilia B patients will be reduced.