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(Pediatrics in Review. 2007;28:e30-e35.)
© 2007 American Academy of Pediatrics

Inhaled Corticosteroids for Asthma

Edward W. Fong, MD^*
Robert H. Levin, PharmD

^* Pediatric Pulmonologist, Children's Hospital and Research Center Oakland, Oakland, Calif., and California Pacific Medical Center, San Francisco, Calif
Professor Emeritus of Clinical Pharmacy, University of California San Francisco School of Pharmacy, San Francisco, Calif

The first 300 words of the full text of this article appear below.

	Introduction

 
Asthma is an inflammatory disease of the respiratory tract. It is the most common chronic disorder in children and adolescents, with more than 3 million asthma attacks occurring in more than 5% of all children each year. Asthma creates significant morbidity and is the leading cause of school absences. Costs attributed to asthma are in the billions of dollars each year.

All levels of persistent asthma require daily anti-inflammatory treatment, and the safest, most effective treatment for patients who have persistent asthma is inhaled corticosteroids (ICSs). Although steroids may be given orally or parenterally, and numerous nonsteroidal medications are available for treating persistent asthma, ICSs are the treatment of choice. Even when ICSs are given daily over a long period of time, they have less toxicity than oral or parenteral steroids administered only occasionally.

This article reviews the currently available ICSs, devices and techniques for optimal administration, and potential adverse effects. The data and recommendations are based on the National Asthma Education and Prevention Program (NAEPP) guidelines (1991 and 1997) and Update 2002, which are available at http://www.nhlbi.nih.gov/guidelines/asthma.

	Pathophysiology of Asthma

 
Asthma is a complex disorder whose pathogenesis is not fully understood. Current thinking is that susceptible individuals develop asthma because of an imbalance between the T-helper (Th)1 and Th2 lymphocytes. Th1 cells produce interleukin-2 (IL-2) and interferon-gamma, which act as a cellular defense mechanism, and Th2 cells produce cytokines (IL-4, IL-5, IL-6, IL-9, and IL-13), which mediate allergic inflammation. According to this current "hygiene hypothesis," the Th1 cellular defense mechanism is reduced, while Th2 cellular activity increases. This imbalance predisposes the individual to episodes of chronic inflammatory asthma.

Whatever triggers the pathogenesis sets up an inflammatory process in which many cellular components participate, including mast cells, T lymphocytes, eosinophils, neutrophils, and epithelial cells. The result is inflammation, hyperresponsiveness (bronchospasm), and in . . . [Full Text of this Article]

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