Mocroft A, Gill M J, Davidson W, Phillips A N
Royal Free Centre for HIV Medicine and Department of Primary Care and Population Sciences, Royal Free and University College London Medical School, UK.
AIDS. 1998 Nov 12;12(16):2161-7. doi: 10.1097/00002030-199816000-00011.
To investigate the factors related to viral load becoming undetectable among patients from Southern Alberta who started a protease inhibitor for the first time, and to determine the factors related to subsequent re-emergence of detectable viral load amongst those patients whose viral load initially became undetectable.
A total of 243 patients from the Southern Alberta Clinic had started a protease inhibitor for the first time and had been followed up for a median time of 32 weeks. Standard survival techniques including Kaplan-Meier techniques and Cox proportional hazards models were used to determine which factors were related to viral load becoming undetectable.
At 24 weeks after first exposure to a protease inhibitor, 52.8% of the patients [95% confidence interval (Cl), 45.2-56.6] had achieved an undetectable viral load. In a multivariate analysis, those with a higher initial viral load were less likely to become undetectable [relative hazard (RH), 0.50; 95% Cl, 0.35-0.70; P < 0.0001], whereas those starting more new drugs (RH per new drug, 1.54; 95% Cl, 1.01-2.11; P = 0.048) were significantly more likely to achieve an undetectable viral load. Amongst 111 patients whose viral load became undetectable, Kaplan-Meier analysis indicated that 15.5% of patients experienced re-emergence of detectable viral load at 24 weeks after the first undetectable viral load. A higher CD4 cell count was associated with a lower risk of viral load becoming detectable (RH, 0.73; 95% Cl, 0.53-1.00; P = 0.049), as was treatment with indinavir (versus any other protease inhibitor RH, 0.17; 95% Cl, 0.03-0.86; P = 0.033).
A significant proportion of patients in a routine clinic setting achieved an undetectable viral load measurement after first starting a protease inhibitor; viral load in patients with a higher CD4 cell count was more likely to become and stay undetectable. There was no evidence that patients who were drug-naive experienced significantly worse virological effects than drug-experienced patients, as long as the same number of new drugs was started at the date of first exposure to a protease inhibitor. Further follow-up of these patients is warranted to study the longer term effects of treatment with protease inhibitors.
调查首次开始使用蛋白酶抑制剂的南艾伯塔省患者中病毒载量变为不可检测的相关因素，并确定病毒载量最初变为不可检测的患者中随后病毒载量再次出现可检测的相关因素。
共有243名来自南艾伯塔诊所的患者首次开始使用蛋白酶抑制剂，并接受了中位时间为32周的随访。采用包括Kaplan-Meier技术和Cox比例风险模型在内的标准生存技术来确定哪些因素与病毒载量变为不可检测有关。
首次接触蛋白酶抑制剂24周后，52.8%的患者[95%置信区间（Cl），45.2 - 56.6]病毒载量变为不可检测。在多变量分析中，初始病毒载量较高的患者病毒载量变为不可检测的可能性较小[相对风险（RH），0.50；95% Cl，0.35 - 0.70；P < 0.0001]，而开始使用更多新药的患者（每增加一种新药的RH，1.54；95% Cl，1.01 - 2.11；P = 0.048）病毒载量变为不可检测的可能性显著更高。在111名病毒载量变为不可检测的患者中，Kaplan-Meier分析表明，15.5%的患者在首次病毒载量不可检测后24周病毒载量再次出现可检测。较高的CD4细胞计数与病毒载量变为可检测的风险较低相关（RH，0.73；95% Cl，0.53 - 1.00；P = 0.049），茚地那韦治疗（与任何其他蛋白酶抑制剂相比，RH，0.17；95% Cl，0.03 - 0.86；P = 0.033）也是如此。
在常规临床环境中，相当一部分患者首次开始使用蛋白酶抑制剂后病毒载量测量变为不可检测；CD4细胞计数较高的患者病毒载量更有可能变为并保持不可检测。没有证据表明初治患者的病毒学效果比经治患者显著更差，只要在首次接触蛋白酶抑制剂时开始使用的新药数量相同。对这些患者进行进一步随访以研究蛋白酶抑制剂治疗的长期效果是必要的。
