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OBJECTIVE: To determine the relationship between inflammation and glucocorticoid metabolism in vivo, in a clinical study of patients with inflammatory arthritis treated with anti-TNFα therapy. METHODS: Urine samples were collected from patients with rheumatoid arthritis (RA) and psoriatic arthritis (PsA) as part of a multicentre study assessing responses to infliximab and etanercept. Systemic measures of glucocorticoid metabolism were assessed by gas chromatography/mass spectrometry at weeks 0 (baseline), 4 and 12 after anti-TNFα therapy. Clinical data including DAS28 and C-reactive protein were also collected. RESULTS: Systemic measures of 11β-HSD1 activity in patients with inflammatory arthritis decreased significantly following anti-TNFα therapy in patients with RA and PsA. Additionally, the activity of the glucocorticoid inactivating enzyme 5α-reductase appeared to increase significantly. CONCLUSIONS: This study demonstrates, for the first time, that the increased 11β-HSD1 activity seen in patients with inflammatory arthritis is mediated through TNFα. Furthermore, the changes in related glucocorticoid metabolising enzymes suggest that there is a coordinated change in glucocorticoid metabolism which promotes higher tissue glucocorticoid levels.

Original publication

DOI

10.1136/annrheumdis-2013-203926

Type

Journal article

Journal

Ann rheum dis

Publication Date

02/2015

Volume

74

Pages

464 - 469

Keywords

Anti-TNF, Corticosteroids, Psoriatic Arthritis, Rheumatoid Arthritis, Adult, Aged, Antibodies, Monoclonal, Antirheumatic Agents, Arthritis, Psoriatic, Arthritis, Rheumatoid, Etanercept, Female, Gas Chromatography-Mass Spectrometry, Humans, Hydrocortisone, Immunoglobulin G, Infliximab, Male, Middle Aged, Receptors, Tumor Necrosis Factor, Tumor Necrosis Factor-alpha