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Journal of Clinical Endocrinology & Metabolism Vol. 67, No. 5 1025-1030
doi:10.1210/jcem-67-5-1025
Copyright © 1988 by the Endocrine Society.
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The Effect of Single Oral Doses of Prednisone on the Circadian Rhythm of Serum Osteocalcin in Normal Subjects*

HENNING KASPERSEN NIELSEN, PEDER CHARLES and LEIF MOSEKILDE

Department of Clinical Physiology and Nuclear Medicine, Århus Kommunehospital (H.K.N.) Århus, Denmark
The Department of Medical Endocrinology, Århus Amtssygehus (P.C., L.M.) Århus, Denmark

Address all correspondence and requests for reprints to: Henning Kaspersen Nielsen, M.D., Department of Clinical Physiology and Nuclear Medicine, ÅRHUS KOMMUNEHOSPITAL, DK 8000 Århus C, Denmark.

Serum osteocalcin (OC), which is a sensitive marker of bone formation, is reduced during chronic glucocorticoid treatment in accordance with the finding of reduced bone formation, and even short term glucocorticoid treatment reduces serum OC. In a double blind placebo-controlled study, we measured the effects of 2.5 and 10 mg prednisone, orally, on the circadian variation of serum OC in 15 normal subjects (8 women and 7 men), aged 22–46 yr. All subjects were studied twice at an interval of 1 week. Blood samples were collected every 60 min from 1630 until 1700 h the following day. Prednisone or placebo was given at 2000 h. Serum OC was measured by an in-house RIA. After placebo administration serum OC increased from 2230 h to a peak value around 0230 h, followed by a gradual decline to a nadir around 1500 h. Both doses of prednisone inhibited and even reversed the nocturnal rise in serum OC levels; the inhibition occurred within 3–4 h. There was no significant difference in the time from prednisone ingestion to maximal decrease (7.2 h vs. 9.8 h) or in the maximal decrease (52% vs. 54%). However, the duration of the inhibition was significantly snorter after 2.5 mg than after 10 mg prednisone (~ 6 h vs. 12 h; (p < 0.01). We conclude that serum OC is sensitive to small doses of prednisone, and that serial serum OC measurements may be a sensitive marker of the effect of exogenous glucocorticoids on osteoblastic activity in vivo.

* This work was supported by grants from the Danish Medical Research Council (12-6096 and 5.52.19.37, stastical consultant), P. Carl Pedersen’s Foundation, Dir. Madsen and Wife’s Foundation, and C. Otto Hansen’s Foundation.

Received February 4, 1988.




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