Abstract
In healthy individuals measures of 11ß-hydroxysteroid dehydrogenase type 1 (11ß-HSD1) enzyme activity predict the change in bone formation markers in response to therapeutic glucocorticoids. It is unclear whether these measures remain predictive in inflammatory disease. We therefore examined whether 11ß-HSD1 activity predicts changes in bone markers and bone mineral density (BMD) in patients with inflammatory bowel disease (IBD) treated with therapeutic glucocorticoids. Prospective and cross-sectional studies were carried out in patients attending a gastroenterology clinic with active (n = 39) or clinically inactive (n = 34) IBD and healthy controls (n = 51). Urinary corticosteroid metabolite profiles were obtained on a spot urine sample and total corticosteroid metabolite excretion and 11ß-HSD1 activity (measured as the ratio of tetrahydrocortisol to tetrahydrocortisone metabolites, [THF+alloTHF]/THE) determined. Patients with active disease were treated with an 8-week reducing course of oral prednisolone. The (THF+alloTHF)/THE ratio was significantly increased in patients with IBD, even those in clinical remission. The baseline (THF+alloTHF)/THE ratio failed to predict the decrease in bone formation markers or hip BMD. Measures of 11ß-HSD activity do not predict bone loss during glucocorticoid treatment of active IBD, probably due to disease-related increases in 11ß-HSD1 activity. Our observation of elevated 11ß-HSD1 activity in clinically inactive IBD implicates gastrointestinal glucocorticoid activation in the maintenance of disease remission.
Original language | English |
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Pages (from-to) | 246-251 |
Number of pages | 6 |
Journal | Calcified Tissue International |
Volume | 89 |
Issue number | 3 |
DOIs | |
Publication status | Published - Jun 2011 |