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Response to changes in antiretroviral therapy after genotyping in human immunodeficiency virus-infected children


The Pediatric Infectious Disease Journal: July 2002 - Volume 21 - Issue 7 - p 647-653
Original Studies

Background. HIV genotyping has been beneficial when choosing salvage regimens in adults failing highly active antiretroviral therapy (HAART). Our objectives were to evaluate the usefulness of genotyping in HIV-infected children failing HAART and to determine whether the presence of resistance mutations was associated with previous antiretroviral therapy.

Methods. We followed the progress of pediatric patients who had HIV genotyping performed after HAART failure. Charts were reviewed at 3-month intervals for 1 year after genotyping for changes in viral load and CD4+ cell percentage. Patients whose antiretroviral therapy was changed after genotyping were compared with those whose medications were not changed. We also compared the proportion of patients with genotypic mutations according to antiretroviral exposure at time of genotyping.

Results. Eighteen pediatric patients were eligible for inclusion. None of 10 patients who had antiretroviral therapy changed after genotyping had a decrease in viral load at 12 months after genotyping. One of 8 patients who had no changes in antiretroviral therapy had a sustained decrease in viral load at 12 months. Two-thirds of patients had resistance mutations to antiretrovirals without prior exposure to that drug.

Conclusions. This study did not demonstrate substantial clinical benefit to HIV genotyping in antiretroviral agent-experienced pediatric patients with high viral loads. These results contrast with favorable short term clinical and virologic responses to therapeutic changes after genotyping in HIV-infected adults. However, medication history alone does not appear to be an adequate alternative to genotyping in choosing salvage regimens in antiretroviral agent-experienced children.

From the Department of Pediatrics, University of Chicago Hospitals, Chicago, IL.

Accepted for publication Feb. 20, 2002.

This paper was presented in part at the 38th Annual Meeting of the Infectious Diseases Society of America. 22

Reprints not available.

© 2002 Lippincott Williams & Wilkins, Inc.