Effects of Topical Budesonide Treatment on Glucocorticoid Receptor mRNA Down-Regulation and Cytokine Patterns in Nasal Polyps

Abstract

nasal polyps do not respond with down-regulation of GR mRNA or cytokines following topical corticosteroid treatment. The proposed corticosteroid resistance may be inherent, or induced by a change of local tissue bioavailability.

Effect of intranasal fluticasone propionate and triamcinolone acetonide on basal and dynamic measures of hypothalamic–pituitary–adrenal‐axis activity in healthy volunteers

“…This was confirmed by the fact that serum cortisol concentrations remained within the normal range, and a normal serum cortisol response occurred upon stimulation with ACTH, indicating maintenance of HPA-axis integrity [14]. Interestingly, a more recent study from the same group involved dosing patients at concentrations of up to 800 mg of nasal budesonide, and on this occasion no significant effects on morning serum cortisol were observed [26], confirming our view of the original study. Although oral corticosteroids are well known to have effects on bone density [27], there is now accumulating evidence that intranasal and inhaled corticosteroids at recommended dosages appear to have little effect on bone density and metabolism, as measured by markers of bone resorption and formation, and by techniques used to measure cortical and trabecular bone density [28].…”

Gene profiling reveals increased expression of uteroglobin and other anti-inflammatory genes in glucocorticoid-treated nasal polyps

“…This is in agreement with previous studies of nasal polyps and allergic disease showing either no change or an increase in IFNG after GC treatment. 4,8,25,26,29,30 Little is known about the effects of GCs on antiinflammatory genes in human tissue. Recently, increased expression of the anti-inflammatory gene TGFB was described in GC-treated nasal polyps.…”

In vitro effect of glucocorticoids on nasal polyps

“…However, the success rate of topical GC ranges from 60.9 to 80% 12,13,16 . The anti-inflammatory property of GCs occurs due to their binding to the glucocorticoid receptor (GR); the GC-GR complex inhibits other TF, such as NF-κβ, a phenomenon known as transrepression 4,[17][18][19] .…”