Monforte d'Arminio A
Department of Primary Care and Population Sciences, Royal Free and University College Medical School, London, United Kingdom.
HIV Clin Trials. 2006 Nov-Dec;7(6):271-84. doi: 10.1310/hct0706-271.
Few published studies have considered both the short- and long-term virologic or immunologic response to combination antiretroviral therapy (cART) and the impact of different cART strategies.
To compare time to initial virologic (<500 copies/mL) or immunologic (>200/mm3 cell increase) response in antiretroviral-naïve patients starting either a single protease inhibitor (PI; n = 183), a ritonavir-boosted PI regimen (n = 197), or a nonnucleoside reverse transcriptase inhibitor (NNRTI)-based cART regimen (n = 447) after January 1, 2000, and the odds of lack of virologic or immunologic response at 3 years after starting cART.
Cox proportional hazards models and logistic regression.
After adjustment, compared to patients taking an NNRTI-regimen, patients taking a single-PI regimen were significantly less likely to achieve a viral load (VL) <500 copies/mL (relative hazard [RH] 0.74, 95% CI 0.54-0.84, p = .0005); there was no difference between the boosted-PI regimen and the NNRTI regimen (p = .72). There were no differences between regimens in the risk of >200/mm3 CD4 cell increase after starting cART (p > .3). At 3 years after starting cART, patients taking a single-PI-based regimen were more likely to not have virologic suppression (<500 copies/mL; odds ratio [OR] 1.60, 95% CI 1.06-2.40, p = .024), while there were no differences in the odds of having an immunologic response (>200/mm3 increase; p > .15). This model was adjusted for CD4 and VL at starting cART, age, prior AIDS diagnosis, year of starting cART, and region of Europe.
Compared to patients starting an NNRTI-based regimen, patients starting a single-PI regimen were less likely to be virologically suppressed at 3 years after starting cART. These results should be interpreted with caution, because of the potential biases associated with observational studies. Ultimately, clinical outcomes, such as new AIDS diagnoses or deaths, will be the measure of efficacy of cART regimens, which requires the follow-up of a very large number of patients over many years.
很少有已发表的研究同时考虑联合抗逆转录病毒疗法(cART)的短期和长期病毒学或免疫学反应以及不同cART策略的影响。
比较2000年1月1日之后开始接受治疗的初治抗逆转录病毒患者,分别使用单一蛋白酶抑制剂(PI;n = 183)、利托那韦增强的PI方案(n = 197)或基于非核苷类逆转录酶抑制剂(NNRTI)的cART方案(n = 447)后,达到初始病毒学(<500拷贝/毫升)或免疫学(CD4细胞增加>200/立方毫米)反应的时间,以及开始cART后3年时缺乏病毒学或免疫学反应的几率。
Cox比例风险模型和逻辑回归。
调整后,与接受NNRTI方案的患者相比,接受单一PI方案的患者病毒载量(VL)<500拷贝/毫升的可能性显著降低(相对风险[RH] 0.74,95%置信区间0.54 - 0.84,p = 0.0005);增强PI方案与NNRTI方案之间无差异(p = 0.72)。开始cART后,各方案在CD4细胞增加>200/立方毫米的风险方面无差异(p > 0.3)。开始cART后3年,接受单一PI方案的患者更有可能未实现病毒学抑制(<500拷贝/毫升;优势比[OR] 1.60,95%置信区间1.06 - 2.40,p = 0.024),而在免疫学反应(增加>200/立方毫米)的几率方面无差异(p > 0.15)。该模型针对开始cART时的CD4和VL、年龄、既往艾滋病诊断、开始cART的年份以及欧洲地区进行了调整。
与开始基于NNRTI方案的患者相比,开始单一PI方案的患者在开始cART后3年时病毒学抑制的可能性较小。由于观察性研究存在潜在偏倚,这些结果应谨慎解读。最终,临床结局,如新发艾滋病诊断或死亡,将是cART方案疗效的衡量标准,这需要对大量患者进行多年的随访。