Endocrine Abstracts (2011) 26 P529

The postprandial response of bone turnover in [beta]-thalassemia major

M Yavropoulou, X Tsekmekidou, K Tomos, E Chasapopoulou, P Chalkia, M Karamouzis & J Yovos

AHEPA University Hospital, Aristotle University of Thessaloniki, Thessaloniki, Greece.

Background: Osteoporosis is considered to be an important cause of morbidity in patients with β-thalassemia major. Despite recent advances in the identification of the molecular pathways involved in the thalassemia-induced osteoporosis, less is known about the responses of the thalassemic skeleton to various physiological and pathological conditions. The aim of the present study was to evaluate the postprandial response of bone turnover, which is an important component of the circadian rhythm of bone remodeling, in thalassemic patients.

Design/methods: Thirty-two adult patients with β-thalassemia major (10 male, 22 female, aged 33.09±7.81 years) and thirty-one healthy individuals matched for age were included in the analysis. Exclusion criteria were concomitant diseases and medication that affect bone metabolism. All participants underwent an oral glucose tolerance test (OGTT) with 75 g of glucose after an overnight fast. Serum carboxy-terminal collagen crosslinks (CTX), procollagen I N-terminal propeptide (S-P1NP) and osteocalcin were assayed. All results are presented as mean±S.E.M.

Results: Baseline values of CTX and P1NP were significantly higher in the patient group compared to control (0.45±0.046 vs 0.34±0.18 μg/l, P=0.049 and 56.42±7.08 vs 40.12±2.80 ng/ml, P=0.039, respectively). At two hours after the glucose load, CTX levels demonstrated a significant reduction compared to baseline values (0.25±0.02 vs 0.45±0.04 μg/l, P<0.001), while markers of bone formation did not change significantly. The postprandial reduction of CTX was comparable to the reduction observed in the control group (43.6±0.02% vs 45.3±0.02%, P=0.684).

Conclusion: Despite the high bone turnover state in thalassemic patients, the postprandial reduction of bone resorption remains unaltered, suggesting that the physiological responses to nutrients are conserved in the thalassemic skeleton.

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