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PubMed2001

Topical corticosteroids in nasal polyposis.

Nasal polyps are the common end-point of a number of conditions characterised by inflammation and are rarely 'curable' in its true sense. After consideration of the underlying aetiology and confirmation of the diagnosis, they are normally managed by a combination of medical and surgical interventions. Of these, topical corticosteroids have proved to be the medical treatment of choice. The objectives of the medical management are to eliminate or reduce the size of polyps, re-establish nasal airway and nasal breathing, improve or restore the sense of smell, and prevent recurrence of nasal polyps. The mechanism of action of corticosteroids may be by a multifactorial effect on various aspects of the inflammatory reaction, the effect being initiated by their binding to a specific cytoplasmic glucocorticoid receptor. At a cellular level, there is a reduction in the number of antigen-presenting cells, in the number and activation of T cells, in the number of mast cells, and in the number and activation of eosinophils. When polyps are large (grade 3) topical medication is difficult to instil in a very blocked nose and surgery or short term systemic corticosteroids may be required. Topical corticosteroids are of use in the primary treatment of nasal polyps when they are of a small or medium size (grades 1 and 2) and in the maintenance of any therapeutic improvement. The efficacy of topical corticosteroids such as betamethasone sodium phosphate nose drops, beclomethasone dipropionate, fluticasone propionate and budesonide nasal sprays in reducing polyp size and rhinitis symptoms has been demonstrated in several randomised, placebo-controlled trials. Beclomethasone dipropionate, flunisolide and budesonide sprays have also been shown to delay the recurrence of polyps after surgery. Placebo-controlled studies of agents that have shown a significant clinical effect in the management of nasal polyposis are reviewed.

Administration, Topical↗
PubMed1994

Histamine-induced airway mucosal exudation of bulk plasma and plasma-derived mediators is not inhibited by intravenous bronchodilators.

Experimental data suggest the possibility that common bronchodilators, such as the xanthines and beta 2-adrenoceptor agonists, may produce microvascular anti-permeability effects in the subepithelial microcirculation of the airways. In this study, we have examined the effect of bronchodilators given intravenously on exudation of different-sized plasma proteins (albumin and fibrinogen) and the generation of plasma-derived peptides (bradykinins) in human nasal airways challenged with histamine. In a double-blind, crossover, placebo-controlled and randomised trial, 12 normal volunteers were given i.v.infusions of terbutaline sulphate, theophylline and enprofylline to produce therapeutic drug levels. The effect of topical nasal provocation with histamine was closely followed by frequently nasal lavage with saline. The lavage fluid levels of albumin, fibrinogen and bradykinins increased significantly after each histamine provocation. The ratio of albumin-to-fibrinogen in plasma and the lavage fluid was 24 and 56, respectively, indicating that topical histamine provocation induced a largely non-sieved flux of macromolecules across the endothelial-epithelial barriers. The systemically administered drugs did not affect the nasal symptoms (sneezing, secretion and blockage), nor did they significantly reduce the levels of plasma proteins and plasma-derived mediators in the nasal lavage fluids. The present data suggest that systemic xanthines and beta 2-adrenoceptor agonists, at clinically employed plasma levels, may not affect the microvascular (and epithelial) exudative permeability and the bradykinin forming capacity of human airways.

Adolescent↗