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Timing of Antiretroviral Therapy Initiation and its Impact on Disease Progression in Perinatal Human Immunodeficiency Virus-1 Infection

Sturt, Amy S. MD*,†; Halpern, Meira S. PhD; Sullivan, Barbara RN; Maldonado, Yvonne A. MD

Pediatric Infectious Disease Journal: January 2012 - Volume 31 - Issue 1 - p 53–60
doi: 10.1097/INF.0b013e31823515a2
HIV Reports

Objective: Treatment with highly active antiretroviral therapy (HAART) reduces overall perinatal human immunodeficiency virus (HIV) type 1–related mortality. The effect of timing of HAART initiation on reduction of morbidity is not well defined. We evaluated the association of timing of HAART initiation on progression to moderate or severe disease.

Methods: Retrospective, population-based study of 196 perinatally HIV-infected children followed from birth in northern California from 1988 to 2009.

Results: Of 196 children, 58% received HAART and were followed for a median of 6.2 years after HAART initiation. HAART use was associated with improved survival to the age of 5 years: no HAART, 50% versus HAART, 88%; P < 0.0001. However, the advantage of initial HAART over mono or dual therapy transitioning to HAART was small and not statistically significant (P = 0.23). Starting HAART before the development of moderate or severe disease delayed the median age of diagnosis of moderate disease from 0.4 years (interquartile range, [0.3–0.8]) without HAART to 3.0 years ([interquartile range, 1.9–5.8]; P < 0.0001) with HAART. HAART initiation after progression to moderate or severe disease was associated with decreased progression to severe disease or death, respectively (moderate to severe: 8% [3/36] with HAART vs. 84% [70/83] with no HAART, P < 0.0001; severe to death: 9% [6/68] with HAART vs. 73% [49/67] with no HAART, P < 0.0001).

Conclusions: In perinatal HIV infection, HAART is associated with delayed progression and reduced mortality regardless of disease severity at HAART initiation. This finding reinforces US guidelines regarding HAART initiation at >1 year of age if children present with most clinical category B diagnoses, regardless of CD4 measurements or plasma HIV RNA level.

From the *Department of Medicine, Division of Infectious Diseases and Geographic Medicine, Stanford University, Stanford, CA; †Department of Medicine, Division of AIDS Medicine, Santa Clara Valley Medical Center, San Jose, CA; and ‡Department of Pediatrics, Infectious Diseases Division, Santa Clara Valley Medical Center, San Jose, CA.

Accepted for publication August 16, 2011.

Presented (data from the same cohort) at the Infectious Diseases Society of America Meeting in a poster entitled “Relationship of Pediatric HIV CDC Category B Diagnoses to Progression to Category C Disease and Death”; October 2010; Vancouver, British Columbia, Canada.

Conflicts of interest and sources of funding: A.S.S. supported by NIH training grant “Applied Genomics in Infectious Diseases,” T32 AI 07502–13 and T32 AI 07502–14 and received a travel grant from Pfizer to attend the 2010 Infectious Diseases Society of America national meeting for work unrelated to this publication. Y.A.M. is on vaccine advisory boards for Merck and Novartis. The authors have no other funding or conflicts of interest to disclose.

Address for correspondence: Amy S. Sturt, MD, Santa Clara Valley Medical Center, Ira Greene PACE Clinic, 751 S Bascom Ave, Ste 316, San Jose, CA 95128. E-mail: Amy.Sturt@hhs.sccgov.org.

© 2012 Lippincott Williams & Wilkins, Inc.