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Endocrine Abstracts (2014) 34 OC6.1 | DOI: 10.1530/endoabs.34.OC6.1

SFEBES2014 Oral Communications Clinical (6 abstracts)

Adverse outcome in glucocorticoid induced adrenal suppression; an analysis of short synacthen tests in 2782 patients

Matthew Chapman 1 , Nicola Argese 2 , Dhanasekaran Mani 3 , Vijay Dabhi 3 , Christopher Boot 4 , Rachel Crowley 1 , Paul Stewart 5 & Jeremy Tomlinson 1


1School of Clinical and Experimental Medicine, Institute of Biomedical Research, Centre for Endocrinology, Diabetes and Metabolism, University of Birmingham, Birmingham, UK; 2Faculty of Medicine and Psychology, Endocrinology, Sant’Andrea Hospital, ‘Sapienza’ University of Rome, Rome, Italy; 3Health Informatics Department, Queen Elizabeth Hospital, University Hospitals Birmingham, NHS Foundation Trust, Birmingham, UK; 4Regional Endocrine Laboratory, Queen Elizabeth Hospital, University Hospitals Birmingham, NHS Foundation Trust, Birmingham, UK; 5School of Medicine, University of Leeds, Leeds, UK.


2–3% of the UK population are prescribed glucocorticoid (GC) therapy and their adverse effects contribute to a significant health burden. Suppression of endogenous GC secretion is a recognized complication of therapy, but the magnitude of the problem, together with its clinical consequences have not been determined. We conducted a retrospective study across all specialties in a large secondary–tertiary care center identifying 2782 patients who underwent 3666 250 μg short Synacthen tests (SST) between 2008–2013. Patients were grouped according to indication and clinical and biochemical assessments made prior to SST were analyzed; a 30-min cortisol of ≥550 nmol/l was considered indicative of adequate adrenal reserve.

497 (17.9%) patients failed the SST; failure rates were highest in those patients with underlying adrenal disease (60.8%). 693 patients had pituitary disease and 21.5% (n=142) failed the SST. 408 patients were taking oral, topical, intranasal or inhaled GC therapy (excluding those with pituitary, adrenal and central nervous system pathology) and 32.8% (n=134) of these patients failed. In this group, 30-min cortisol response was positively associated with systolic blood pressure (P<0.05), and those patients with the highest cortisol response had fewest elective hospital admissions in the preceding 2 years (0.8±0.2 vs 0.3±0.1, P<0.05). In those patients taking inhaled corticosteroids (those with oral co-administration were excluded), Fluticasone treatment was associated with the highest SST failure rates (26.1%). However, in patients taking either inhaled fluticasone or beclometasone, there was a dose-dependent effect upon the cortisol response across the SST; those patients on the highest doses having both decreased basal and 30-min cortisol values (e.g. Fluticasone 30-min cortisol, <400 vs >400 μg/day, 880±72 vs 737±34 nmol/l, P<0.05).

Suppression of adrenal reserve due to GC administration (oral, topical or inhaled) is both common and associated with adverse outcome. Future prospective studies need to define appropriate interventional strategies and determine their impact upon clinical outcome.

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