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Primary male osteoporosis is associated with enhanced glucocorticoid availability

Arampatzis, Spyridon ; Pasch, Andreas ; Lippuner, Kurt ; Mohaupt, Markus

In: Rheumatology, 2013, vol. 52, no. 11, p. 1983-1991

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    Titre
    • Primary male osteoporosis is associated with enhanced glucocorticoid availability
    Auteur
    • Arampatzis, Spyridon. Department of Osteoporosis and Department of Nephrology and Hypertension, Inselspital, University Hospital Bern and University of Bern, Berne, Switzerland.
    • Pasch, Andreas. Department of Osteoporosis and Department of Nephrology and Hypertension, Inselspital, University Hospital Bern and University of Bern, Berne, Switzerland.
    • Lippuner, Kurt. Department of Osteoporosis and Department of Nephrology and Hypertension, Inselspital, University Hospital Bern and University of Bern, Berne, Switzerland.
    • Mohaupt, Markus. Department of Osteoporosis and Department of Nephrology and Hypertension, Inselspital, University Hospital Bern and University of Bern, Berne, Switzerland.
    Type de document
    • Postprint
    Identifiant OAI-PMH
    • oai:doc.rero.ch:292772
    Summary
    Objective. While systemic glucocorticoids compromise bone metabolism, altered intracellular cortisol availability may also contribute to the pathogenesis of primary male osteoporosis (MO). The objective of this study was to assess whether intracellular cortisol availability is increased in MO due to a distorted local cortisol metabolism. Methods. Forty-one patients with MO were compared with age- and BMI-matched non-osteoporotic subjects after excluding overt systemic hypercortisolism (N = 41). Cortisol, cortisone and the respective tetrahydro-, 5α-tetrahydro- and total cortisol metabolites were analysed by GC-MS in 24 h urine. Apparent 11β-hydroxysteroid dehydrogenase (11β-HSD) enzyme activities, excretion of cortisol metabolites and calcium, and fractional urinary calcium excretion were assessed and related to BMD. Results. Fractional and total urinary calcium excretion negatively correlated with BMD at all (P < 0.05) and at three of five (P < 0.05) measurement sites, respectively. While systemic cortisol was unchanged, apparent 11β-HSD enzyme activity in MO patients (P < 0.01) suggested increased intracellular cortisol availability. Total and fractional urinary calcium excretion was higher, with apparent 11β-HSD enzyme activities consistent with an enhanced intracellular cortisol availability (P < 0.05). Conclusion. Apparent 11β-HSD enzyme activities consistent with increased intracellular cortisol availability correlated with urinary calcium loss and reduced bone mineral density in MO. The changes in 11β-HSD activity were associated with both the fractional calcium excretion, suggesting altered renal calcium handling, and the absolute urinary calcium excretion. Both mechanisms could result in a marked bone calcium deficiency if insufficiently compensated for by intestinal calcium uptake