The mechanism of action of oral corticosteroids in relation to short- and long-term-burst therapy

Abstract

Corticosteroids, potent anti-inflammatory agents, are broadly used in various inflammatory and immune-dependent pathologies, which include asthma. Through non-genomic and genomic mechanisms of action, corticosteroids reduce pro-inflammatory mediators while promoting anti-inflammatory molecule expression. Furthermore, in the context of asthma treatment, they also promote the expression of β2 adrenergic receptors which increase the therapeutic potential of β2-receptor agonists to promote bronchodilation. However, corticosteroids also precipitate a variety of adverse events which reduce the quality of life of patients and predispose them to further pathological alterations. Given the ubiquitous expression of the glucocorticoid receptor, alongside the non-genomic and genomic mechanisms of corticosteroids, a myriad interconnecting physiological processes are altered upon receptor modulation. Both long- and short-course treatment has been linked to immune suppression, metabolic and cardiovascular disease, cerebrovascular accidents, osteoporosis, ophthalmic disorders, pneumonia and mood disorders. Consequently, clinical decision-making should consider the potential risks involved in short- and long-term use of corticosteroids because pathophysiological changes may be precipitated in both.