Institutional members access full text with Ovid®

Share this article on:

Efficacy of and adherence to highly active antiretroviral therapy in children infected with human immunodeficiency virus type 1


The Pediatric Infectious Disease Journal: August 1999 - Volume 18 - Issue 8 - p 682-689
Original Studies

Background. Clinical trials in adults have demonstrated the efficacy of highly active antiretroviral therapy (HAART) to suppress replication of HIV-1 to nondetectable levels, but lower success rates have been observed in practice. We sought to determine the efficacy of HAART in our population of HIV-1-infected children and to identify determinants of efficacy, especially the role of adherence to prescribed antiretrovirals.

Methods. The viral load and CD4+ T cell responses of 72 children with perinatally acquired HIV-1 treated with HAART including a protease inhibitor for at least 90 days were examined retrospectively in relation to adherence, as measured by pharmacy records for the first 180 days of HAART.

Results. Patients were defined as adherent if ≥75% of protease inhibitors and ≥75% of all antiretroviral prescriptions were filled. Of the 42 patients (58%) who were adherent, nondetectable viral loads were achieved and maintained in 22 (52%). A Kaplan-Meier plot showed a drop-off in patients maintaining a nondetectable viral load after 200 days. Higher initial viral load was the only pretreatment factor that identified adherent patients at risk for treatment failure. Only 3 (10%) nonadherent patients maintained a viral load of <400 copies/ml. The adherent group had a prompt and sustained increase in CD4+ T cell counts.

Conclusions. HAART can achieve control of viral replication in HIV-1-infected children who adhere to therapy. However, treatment failure is likely unless there is a high level of adherence. Nonadherence to therapy is common and might be the major impediment to successful treatment of children infected with HIV-1.

From the Division of Pediatric Immunology, Department of Pediatrics, University of Maryland School of Medicine, Baltimore, MD.

Accepted for publication April 15, 1999.

Address for reprints: Douglas C. Watson, M.D., Division of Pediatric Immunology, University of Maryland School of Medicine, 120 Penn Street, Baltimore, MD 21201. Fax 410-706-0031; E-mail

© 1999 Lippincott Williams & Wilkins, Inc.