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24 - Pulmonary problems

Published online by Cambridge University Press:  23 December 2009

Lauren V. Wood
Affiliation:
National Cancer Institute, Belhesda, MD
Steven L. Zeichner
Affiliation:
National Cancer Institute, Bethesda, Maryland
Jennifer S. Read
Affiliation:
National Institutes of Health, Bethesda, Maryland
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Summary

Introduction

Despite advances in the treatment of HIV disease and the implementation of highly active antiretroviral therapy as the standard of care in resource-rich countries, pulmonary diseases continue to cause significant morbidity and mortality in HIV-infected pediatric patients [1]. Common pulmonary diseases seen in pediatric HIV patients include: (a) lymphoproliferative processes (lymphoid interstitial pneumonitis (LIP), pulmonary lymphoid hyperplasia (PLH)); (b) conventional infectious processes; (c) viral, bacterial, and fungal opportunistic infections pathogens; (d) disorders such as asthma/ reactive airway disease worsened by the immune dysregulation accompanying HIV infection.

Pneumocystis carinii pneumonia (PCP) remains the most common pulmonary complication of pediatric HIV infection in the United States [2]. Pulmonary tuberculosis exceeds recurrent bacterial infections or PCP as the primary clinical manifestation of pediatric HIV disease in tuberculosis-endemic countries [3]. Improvements in prophylaxis and in HIV clinical management have led to a substantial decrease in the incidence of PCP [4]. LIP is the second most common pulmonary complication of pediatric HIV infection [2] and historically has been associated with improved survival in affected patients, including those in developing countries [5].

Recent studies suggest that LIP is a cytokine-mediated process mediated by immune responses against HIV antigens and/or other pathogens (e.g. EBV) [6].

Pediatric HIV patients may develop a variety of immune-related pulmonary disorders. These include T-cell alveolitis due to HIV-specific cytotoxic and NK-like CD8+ CTLs, activated alveolar macrophage accumulation, hyperproduction of macrophage-derived cytokines, pulmonary neutrophilia, and the loss of NK and HIV-specific CTL activities [6].

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Publisher: Cambridge University Press
Print publication year: 2006

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