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Review
. 2016 Aug 12:9:26.
doi: 10.1186/s40413-016-0117-0. eCollection 2016.

The use of inhaled corticosteroids in pediatric asthma: update

Affiliations
Review

The use of inhaled corticosteroids in pediatric asthma: update

Elham Hossny et al. World Allergy Organ J. .

Abstract

Despite the availability of several formulations of inhaled corticosteroids (ICS) and delivery devices for treatment of childhood asthma and despite the development of evidence-based guidelines, childhood asthma control remains suboptimal. Improving uptake of asthma management plans, both by families and practitioners, is needed. Adherence to daily ICS therapy is a key determinant of asthma control and this mandates that asthma education follow a repetitive pattern and involve literal explanation and physical demonstration of the optimal use of inhaler devices. The potential adverse effects of ICS need to be weighed against the benefit of these drugs to control persistent asthma especially that its safety profile is markedly better than oral glucocorticoids. This article reviews the key mechanisms of inhaled corticosteroid action; recommendations on dosage and therapeutic regimens; potential optimization of effectiveness by addressing inhaler technique and adherence to therapy; and updated knowledge on the real magnitude of adverse events.

Keywords: Adherence; Adverse effects; Asthma; Children; Inhaled corticosteroids.

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Figures

Fig. 1
Fig. 1
Schematic diagram of the complex cellular actions of corticosteroids. Genomic actions are mediated by cytoplasmic receptors, which ultimately alter transcription through A direct DNA binding or B transcription factor inactivation. In contrast, nongenomic actions are mediated by C membrane-bound or D cytoplasmic receptors, or E nonspecific interactions with the cell membrane. cGR: cytoplasmic glucocorticoid receptor; mGR: membrane glucocorticoid receptor; LBD: ligand-binding domain; DBD: DNA-binding domain; Hsp90: heat-shock protein 90; RE: response element; NF-kB: nuclear factor-kB; AP-1: activating protein-1. Quoted with permission from: Horvath, G and Wanner, A. Eur Respir J 2006;27:172–87

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