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Laboratory markers predict bone loss in Crohn's disease: relationship to blood mononuclear cell function and nutritional status

Laboratory markers predict bone loss in Crohn's disease: relationship to blood mononuclear cell function and nutritional status
Laboratory markers predict bone loss in Crohn's disease: relationship to blood mononuclear cell function and nutritional status
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
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
0269-2813
1063-1071
Trebble, T.M.
6fe25566-584d-48fb-8ba2-1b961c9b5e9f
Wootton, S.A.
bf47ef35-0b33-4edb-a2b0-ceda5c475c0c
Stroud, M.A.
1665ae65-0898-4848-bf0d-baec8f2bb078
Mullee, M.A.
fd3f91c3-5e95-4f56-8d73-260824eeb362
Calder, P.C.
1797e54f-378e-4dcb-80a4-3e30018f07a6
Fine, D.R.
ce3d6a77-040e-4aec-a8f5-4c4c22431605
Moniz, C.
d95387e6-7e6c-49f9-a045-209fc703d349
Arden, N.K.
23af958d-835c-4d79-be54-4bbe4c68077f
Trebble, T.M.
6fe25566-584d-48fb-8ba2-1b961c9b5e9f
Wootton, S.A.
bf47ef35-0b33-4edb-a2b0-ceda5c475c0c
Stroud, M.A.
1665ae65-0898-4848-bf0d-baec8f2bb078
Mullee, M.A.
fd3f91c3-5e95-4f56-8d73-260824eeb362
Calder, P.C.
1797e54f-378e-4dcb-80a4-3e30018f07a6
Fine, D.R.
ce3d6a77-040e-4aec-a8f5-4c4c22431605
Moniz, C.
d95387e6-7e6c-49f9-a045-209fc703d349
Arden, N.K.
23af958d-835c-4d79-be54-4bbe4c68077f

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).

Record type: Article

Abstract

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

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Published date: 2004
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

Identifiers

Local EPrints ID: 24531
URI: http://eprints.soton.ac.uk/id/eprint/24531
ISSN: 0269-2813
PURE UUID: ddb3d106-ed41-4401-8703-e7bab2e8763c
ORCID for P.C. Calder: ORCID iD orcid.org/0000-0002-6038-710X

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Date deposited: 31 Mar 2006
Last modified: 09 Jan 2022 02:49

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Contributors

Author: T.M. Trebble
Author: S.A. Wootton
Author: M.A. Stroud
Author: M.A. Mullee
Author: P.C. Calder ORCID iD
Author: D.R. Fine
Author: C. Moniz
Author: N.K. Arden

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