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Systemic Versus Topical Glucocorticoid Therapy for Acute Asthma

Dr. Rodrigo has eloquently demonstrated that giving 9 mg (i.e., 36 repeated puffs) of inhaled fluticasone over 3 h can improve lung function when compared with 500 mg of intravenous hydrocortisone (1). It has been shown that a single 50-mg dose of oral prednisolone (equivalent transcriptional glucocorticoid activity to 200 mg hydrocortisone), but not 2 mg of inhaled fluticasone, has the additional beneficial effect of upregulating and resensitizing ₂-receptors in patients with asthma after 10 h (2). Moreover, in the setting of acute severe asthma, where airway caliber is greatly reduced, the systemic bioavailability of inhaled fluticasone via a spacer is markedly impaired (3). Such patients will fail to derive the same degree of systemic beneficial glucocorticoid activity that is conferred when administering oral or intravenous corticosteroid. Pointedly, no information was available on outcomes after the 3-h period of follow-up, which may be particularly relevant in terms of the potentially beneficial systemic glucocorticoid effect on the ₂-agonist response, as well as the ongoing transcriptionally regulated systemic anti-inflammatory effect on smaller peripheral airways, where aerosol penetration with fluticasone is likely to be attenuated. The improved initial response to ultra–high dose fluticasone might be attributable to its putative topical nontranscriptional activity, where a very high local concentration would be achieved within the bronchi, in contrast to the much slower onset of the classical transcriptional pathway for its topical anti-inflammatory glucocorticoid effects (4). While we applaud the author for his innovation, we believe that the additional benefit on ₂-receptor function and peripheral airways, as well as the relative ease of administration (particularly when compared with 36 repeated inhaled doses under supervision), will mean that oral prednisolone or intravenous hydrocortisone remain the treatment of choice for acute asthma exacerbations.

Brian J. Lipworth and Daniel Menzies

Ninewells University Hospital, Dundee, United Kingdom

FOOTNOTES

Conflict of Interest Statement: Neither of the authors has a financial relationship with a commercial entity that has an interest in the subject of this manuscript.

REFERENCES

1. Rodrigo GJ. Comparison of inhaled fluticasone with intravenous hydrocortisone in the treatment of adult acute asthma. Am J Respir Crit Care Med 2005;171:1231–1236.[Abstract/Free Full Text]
2. Tan KS, Grove A, Cargill RI, McFarlane LC, Lipworth BJ. Effects of inhaled fluticasone propionate and oral prednisolone on lymphocyte beta 2-adrenoceptor function in asthmatic patients. Chest 1996;109:343–347.[Abstract/Free Full Text]
3. Lee DK, Bates CE, Currie GP, Cowan LM, McFarlane LC, Lipworth BJ. Effects of high-dose inhaled fluticasone propionate on the hypothalamic-pituitary-adrenal axis in asthmatic patients with severely impaired lung function. Ann Allergy Asthma Immunol 2004;93:253–258.[Medline]
4. Lipworth BJ. Therapeutic implications of non-genomic glucocorticoid activity. Lancet 2000;356:87–89.[CrossRef][Medline]

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