Laboratory markers predict bone loss in Crohn's disease: relationship to blood mononuclear cell function and nutritional status
Trebble, T.M., Wootton, S.A., Stroud, M.A., Mullee, M.A., Calder, P.C., Fine, D.R., Moniz, C. and Arden, N.K. (2004) Laboratory markers predict bone loss in Crohn's disease: relationship to blood mononuclear cell function and nutritional status. Alimentary Pharmacology & Therapeutics, 19, (10), 1063-1071. (doi:10.1111/j.1365-2036.2004.01943.x).
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Background: Crohn's disease is associated with reduced bone density. The power of simple markers of systemic inflammation to identify higher rates of bone loss, in Crohn's disease, is uncertain. This relationship and the role of circulating (peripheral blood) mononuclear cells were investigated in a case-control study.
Methods: Urinary deoxypyridinoline/creatinine and serum osteocalcin concentrations were compared in male and premenopausal females with "active" Crohn's disease (C-reactive protein > or = 10 and/or erythrocyte sedimentation rate > or = 20) (n = 22) and controls with "quiescent" Crohn's disease (C-reactive protein < 10 and erythrocyte sedimentation rate < 20) (n = 21). No patients were receiving corticosteroid therapy. Production of tumour necrosis factor-alpha, interferon-gamma and prostaglandin E(2) by peripheral blood mononuclear cells were measured.
Results Active Crohn's disease was associated with a higher deoxypyridinoline/creatinine (P = 0.02) and deoxypyridinoline/creatinine:osteocalcin ratio (P =0.01) compared with quiescent Crohn's disease, but similar osteocalcin (P = 0.24). These were not explained by vitamin D status, dietary intake or nutritional status. However, production of interferon-gamma by concanavalin A-stimulated peripheral blood mononuclear cells was lower in active Crohn's disease (P = 0.02) and correlated negatively with the deoxypyridinoline/creatinine:osteocalcin ratio (r = -0.40, P = 0.004).
Conclusion: In Crohn's disease, raised C-reactive protein and erythrocyte sedimentation rate may indicate higher rates of bone loss and, if persistent, the need to assess bone mass even where disease symptoms are mild. This may be partly explained by altered production of interferon-gamma by peripheral blood mononuclear cells
|Digital Object Identifier (DOI):||doi:10.1111/j.1365-2036.2004.01943.x|
|Keywords:||necrosis, role, crohn's disease, physiopathology, blood sedimentation, protein, bone mass, physiology, laboratories, bone density, nutrition, serum, inflammation,non-u.s.gov't, metabolism, patients, bone resorption, crohn disease, bone, methods, human, case-control studies, bone remodeling, research support, male, humans,adult, disease, osteocalcin, blood, cytokines, prostaglandins, c-reactive protein, female, therapy, vitamin d, analysis, nutritional status|
|Divisions:||University Structure - Pre August 2011 > School of Medicine > Developmental Origins of Health and Disease
University Structure - Pre August 2011 > School of Medicine > Infection, Inflammation and Repair
University Structure - Pre August 2011 > School of Medicine > Community Clinical Sciences
|Date Deposited:||02 Sep 2008|
|Last Modified:||31 Mar 2016 12:45|
|RDF:||RDF+N-Triples, RDF+N3, RDF+XML, Browse.|
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