IL-6 may modulate the skeletal response to glucocorticoids during exacerbations of inflammatory bowel disease

Kriel, Muhammed, Sayers, Adrian, Fraser, William D., Williams, Amanda M., Koch, Alexander, Zacharowski, Kai, Probert, Chris S. and Tobias, Jonathan H. (2010) IL-6 may modulate the skeletal response to glucocorticoids during exacerbations of inflammatory bowel disease. Calcified Tissue International, 86 (5). pp. 375-381. ISSN 0171-967X

Full text not available from this repository. (Request a copy)

Abstract

Whether inflammatory cytokines affect the skeletal response to glucocorticoid (GC) treatment is unclear. Our objectives were to (1) identify the cytokine(s) elevated during exacerbations of inflammatory bowel disease (IBD); (2) determine whether the cytokine(s) identified in this way is related to systemic GC sensitivity; and (3) examine whether cytokines and/or measures of GC sensitivity are related to changes in bone formation or resorption following GC therapy. We designed a combined cross-sectional and prospective study, including patients with active (n = 31) and inactive (n = 34) IBD as well as controls (n = 29). We assessed circulating concentrations of cytokines, PINP and βCTX, as well as GC sensitivity in peripheral blood mononuclear cells. IL-6 was the only cytokine increased in active IBD, 2.35 (2.63) versus 1.64 (1.21) versus 1.31 (2.79) pg/μl active IBD, inactive IBD, and controls, respectively (median [interquartile range]) (P = 0.03, ANOVA). IL-6 was positively related to magnitude of GC sensitivity (beta = 0.02, 95% CI 0.008–0.04, P = 0.005). Following treatment with GC in active IBD, PINP decreased (P < 0.001), whereas βCTX showed no significant change (P = 0.2). Subsequently, multiple regression analyses revealed that plasma IL-6 concentrations were inversely related to the extent of PINP suppression following GC (beta = 3.3, 95% CI 0.2–6.4, P = 0.04, adjusted for baseline PINP and duration of GC treatment), while no association was observed with GC sensitivity. In conclusion, IL-6 is elevated in active IBD and may protect against GC-induced suppression of bone formation via a mechanism which appears to be independent of systemic GC sensitivity.

Item Type:	Article
Faculty \ School:	Faculty of Medicine and Health Sciences > Norwich Medical School
Depositing User:	Rhiannon Harvey
Date Deposited:	11 May 2011 09:20
Last Modified:	22 Dec 2022 15:31
URI:	https://ueaeprints.uea.ac.uk/id/eprint/30187
DOI:	10.1007/s00223-010-9345-4

Actions (login required)

View Item