Arampatzis, Spyridon; Pasch, Andreas; Lippuner, Kurt; Mohaupt, Markus (2013). Primary male osteoporosis is associated with enhanced glucocorticoid availability. Rheumatology, 52(11), pp. 1983-1991. Oxford: Oxford University Press 10.1093/rheumatology/ket228
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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.
Item Type: |
Journal Article (Original Article) |
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Division/Institute: |
04 Faculty of Medicine > Department of Orthopaedic, Plastic and Hand Surgery (DOPH) > Clinic of Osteoporosis 04 Faculty of Medicine > Department of Dermatology, Urology, Rheumatology, Nephrology, Osteoporosis (DURN) > Clinic of Nephrology and Hypertension |
UniBE Contributor: |
Arampatzis, Spyridon, Pasch, Andreas, Lippuner, Kurt, Mohaupt, Markus |
Subjects: |
600 Technology > 610 Medicine & health |
ISSN: |
1462-0324 |
Publisher: |
Oxford University Press |
Language: |
English |
Submitter: |
Markus Georg Mohaupt |
Date Deposited: |
04 Oct 2013 14:42 |
Last Modified: |
05 Dec 2022 14:13 |
Publisher DOI: |
10.1093/rheumatology/ket228 |
PubMed ID: |
23882110 |
Uncontrolled Keywords: |
11β-hydroxysteroid dehydrogenase, bone mineral density, cortisol, gas chromatography–mass spectrometry, idiopathic osteoporosis, male |
BORIS DOI: |
10.7892/boris.17466 |
URI: |
https://boris.unibe.ch/id/eprint/17466 (FactScience: 225246) |
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