PREDICTORS OF A VIRAL RESPONSE AND SUBSEQUENT VIROLOGICAL TREATMENT FAILURE IN PATIENTS WITH HIV STARTING A PROTEASE INHIBITOR

Citation
A. Mocroft et al., PREDICTORS OF A VIRAL RESPONSE AND SUBSEQUENT VIROLOGICAL TREATMENT FAILURE IN PATIENTS WITH HIV STARTING A PROTEASE INHIBITOR, AIDS, 12(16), 1998, pp. 2161-2167
Citations number
33
Categorie Soggetti
Immunology,"Infectious Diseases",Virology
Journal title
AIDSACNP
ISSN journal
02699370
Volume
12
Issue
16
Year of publication
1998
Pages
2161 - 2167
Database
ISI
SICI code
0269-9370(1998)12:16<2161:POAVRA>2.0.ZU;2-C
Abstract
Objectives: To investigate the factors related to viral load becoming undetectable among patients from Southern Alberta who started a protea se inhibitor for the first time, and to determine the factors related to subsequent re-emergence of detectable viral load amongst those pati ents whose viral load initially became undetectable. Subjects and meth ods: A total of 243 patients from the Southern Alberta Clinic had star ted a protease inhibitor for the first time and had been followed up f or a median time of 32 weeks. Standard survival techniques including K aplan-Meier techniques and Cox proportional hazards models were used t o determine which factors were related to viral load becoming undetect able. Results: At 24 weeks after first exposure to a protease inhibito r, 52.8% of the patients [95% confidence interval (CI), 45.2-56.6] had achieved an undetectable viral load. In a multivariate analysis, thos e with a higher initial viral load were less likely to become undetect able [relative hazard (RH), 0.50; 95% CI, 0.35-0.70; P < 0.0001], wher eas 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 undetec table viral load. Amongst 111 patients whose viral load became undetec table, Kaplan-Meier analysis indicated that 15.5% of patients experien ced 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 pr otease inhibitor RH, 0.17; 950/;, CI, 0.03-0.86; P = 0.033). Conclusio ns: A significant proportion of patients in a routine clinic setting a chieved an undetectable viral load measurement after first starting a protease inhibitor; viral load in patients with a higher CD4 cell coun t was more likely to become and stay undetectable. There was no eviden ce that patients who were drug-naive experienced significantly worse v irological effects than drug-experienced patients, as long as the same number of new drugs was started at the date of first exposure to a pr otease 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