Predictors of a viral response and subsequent virological treatment failure in patients with HIV starting a protease inhibitor

被引:131
作者
Mocroft, A
Gill, MJ
Davidson, W
Phillips, AN
机构
[1] UCL, Royal Free & Univ Coll London Med Sch, Royal Free Ctr HIV Med, London NW3 2PF, England
[2] UCL, Royal Free & Univ Coll London Med Sch, Dept Primary Care & Populat Sci, London NW3 2PF, England
[3] Univ Calgary, Dept Med, Calgary, AB, Canada
[4] Univ Calgary, So Alberta HIV Clin, Calgary, AB, Canada
关键词
viral load; protease inhibitors; undetectability; progression;
D O I
10.1097/00002030-199816000-00011
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Objectives: 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. Subjects and methods: 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. Results: At 24 weeks after first exposure to a protease inhibitor, 52.8% of the patients [95% confidence interval (CI), 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% CI, 0.35-0.70; P < 0.0001], whereas those starting more new drugs (RH per new drug, 1.53; 95% CI, 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% CI, 0.53-1.00; P = 0.049), as was treatment with indinavir (versus any other protease inhibitor RH, 0.17; 950/;, CI, 0.03-0.86; P = 0.033). Conclusions: 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. (C) 1998 Lippincott Williams & Wilkins
引用
收藏
页码:2161 / 2167
页数:7
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