Case Control Study
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World J Gastroenterol. Jul 28, 2014; 20(28): 9534-9540
Published online Jul 28, 2014. doi: 10.3748/wjg.v20.i28.9534
Postprandial response of bone turnover markers in patients with Crohn’s disease
Ioannis Karatzoglou, Maria P Yavropoulou, Maria Pikilidou, George Germanidis, Evangelos Akriviadis, Alexandra Papazisi, Michael Daniilidis, Pantelis Zebekakis, John G Yovos
Ioannis Karatzoglou, Maria Pikilidou, George Germanidis, Michael Daniilidis, Pantelis Zebekakis, 1st Department of Internal Medicine, AHEPA University Hospital, Aristotle University of Thessaloniki, 54636 Thessaloniki, Greece
Maria P Yavropoulou, John G Yovos, Division of Endocrinology and Metabolism, AHEPA University Hospital, Aristotle University of Thessaloniki, 54636 Thessaloniki, Greece
Evangelos Akriviadis, 4th Department of Internal Medicine, Hippokration General Hospital, 54642 Thessaloniki, Greece
Alexandra Papazisi, Department of Nuclear Medicine, AHEPA University Hospital, Aristotle University of Thessaloniki, 54636 Thessaloniki, Greece
Author contributions: Yavropoulou MP and Karatzoglou I contributed equally to this study; Yavropoulou MP and Karatzoglou I designed and performed the research; Germanidis G and Pikilidou M analyzed the data; Akriviadis E and Daniilidis M contributed the analytic tools; Papazisi A performed all assays, and Yavropoulou MP and Yovos JG wrote the paper; Daniilidis M, Zebekakis P, Akriviadis E and Germanidis G revised the final draft.
Correspondence to: Maria P Yavropoulou, MD, PhD, Endocrinologist, Division of Endocrinology and Metabolism, AHEPA University Hospital, Aristotle University of Thessaloniki, 1 S Kyriakidi Street, 54636 Thessaloniki, Greece. margia@med.auth.gr
Telephone: +30-2-310993187 Fax: +30-2-310994608
Received: September 25, 2013
Revised: March 6, 2014
Accepted: April 21, 2014
Published online: July 28, 2014
Abstract

AIM: To investigate the postprandial response of bone turnover markers in patients with Crohn’s disease (CD).

METHODS: Fifty nine patients with CD aged 38 ± 14 years, and 45 healthy individuals matched for age and body mass index were included in the study. All participants underwent an oral glucose tolerance test (OGTT) after an overnight fast and serum levels of the bone resorption marker C-terminal crosslinking telopeptide of type I collagen (CTX-I) and the bone formation marker procollagen type I N propeptide were measured. Activity of the disease was assessed by calculation of the Crohn’s disease activity index (CDAI).

RESULTS: Serum CTX-I was significantly higher in patients compared to controls (CTX-I: 453 ± 21 pg/mL vs 365 ± 25 pg/mL, P = 0.008), and values were significantly correlated with the activity of the disease (r = 0.435, P = 0.001). Results from OGTT-induced suppression of CTX-I showed two different trends. Patients with more active disease (assessed as CDAI > 150) had a more excessive suppression of CTX-I compared to controls (55% vs 43% P < 0.001), while patients on remission (assessed as CDAI < 150) demonstrated an attenuated CTX-I suppression (30% vs 43% P < 0.001). In line with this, CTX-I suppression after oral glucose load was significantly correlated with the activity of the disease (r = 0.913, P < 0.001).

CONCLUSION: The physiological skeletal response of postprandial suppression of bone resorption is maintained in patients with CD and is strongly dependent to the activity of the disease.

Keywords: Crohn’s disease, Bone metabolism, Postprandial bone resorption, Oral glucose tolerance test, C-terminal crosslinking telopeptide of type I collagen

Core tip: Serum C-terminal crosslinking telopeptide of type I collagen is significantly higher in patients with Crohn’s disease (CD) compared to controls and values are significantly correlated with the activity of the disease, reflecting probably the increased osteoclastogenesis induced by the secretion of inflammatory cytokines. Despite higher bone turnover, however, the physiological skeletal response of postprandial suppression of bone resorption is maintained in patients with CD but is strongly dependent to the activity of the disease.