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The clinical course after glucocorticoid treatment in patients with inflammatory bowel disease is linked to suppression of the hypothalamic-pituitary-adrenal axis: a retrospective observational study
Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Medicin.
Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Medicin.
Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Medicin.
Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Medicin.
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2017 (Engelska)Ingår i: Therapeutic Advances in Gastroenterology, ISSN 1756-283X, E-ISSN 1756-2848, Vol. 10, nr 11, s. 829-836Artikel i tidskrift (Refereegranskat) Published
Abstract [en]

Background: Adrenal insufficiency (AI) secondary to treatment with glucocorticoids (GCs) is common in patients with inflammatory bowel disease (IBD), but little is known about the relationship between AI and the clinical course in IBD. The aim of the study was to compare the clinical course in IBD patients with normal adrenal function versus patients with subnormal adrenal function.

Methods: A retrospective observational study on 63 patients with IBD who had performed a low-dose short Synacthen test (LDSST) (1 μg) immediately (1-7 days) after a standard course of GCs. A subnormal LDSST was defined as serum cortisol <550 nmol/L. Outcomes were time to next flare and fecal calprotectin levels.

Results: Sixty-three percent (n = 40) of the IBD patients had a subnormal LDSST. Patients who were steroid-free (n = 41) after the LDSST were observed for 3 years. Patients with a peak serum cortisol <400 nmol/L immediately after GC treatment had significantly longer time until the next flare-up of their IBD and tended to use a lower cumulative prednisolone dose during the study period in comparison to the other subgroups. Fecal calprotectin levels were significantly lower in patients with a peak s-cortisol <550 nmol/L versus patients with peak s-cortisol ⩾550 nmol/L (median 336 µg/g (IQR 521) versus 955 µg/g (IQR 1867); p = 0.012).

Conclusions: GC-induced AI is common in patients with IBD and is associated with lower disease activity. This suggests a link between responsiveness to GC treatment and suppression of the hypothalamic-pituitary-adrenal axis in IBD.

Ort, förlag, år, upplaga, sidor
London: Sage Publications, 2017. Vol. 10, nr 11, s. 829-836
Nyckelord [en]
Crohn’s disease, adrenal insufficiency, clinical pharmacology, immunosuppression, inflammatory bowel disease, ulcerative colitis
Nationell ämneskategori
Gastroenterologi
Identifikatorer
URN: urn:nbn:se:umu:diva-142067DOI: 10.1177/1756283X17730748ISI: 000414470200002PubMedID: 29147134OAI: oai:DiVA.org:umu-142067DiVA, id: diva2:1158361
Tillgänglig från: 2017-11-20 Skapad: 2017-11-20 Senast uppdaterad: 2018-06-09Bibliografiskt granskad

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Ibrahim, AghilDahlqvist, PerOlsson, TommyLundgren, DavidWerner, MårtenSuhr, Ole B.Karling, Pontus

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