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Albert Einstein Medical Center, Temple University School of Medicine Philadelphia, Pennsylvania 19141
University of Pennsylvania Philadelphia, Pennsylvania 19104
National Animal Disease Center Ames, Iowa 50010
Address all correspondence and requests for reprints to: Sol Epstein, M.D., Division of Endocrinology and Metabolism, Albert Einstein Medical Center, York and Tabor Roads, Philadelphia, Pennsylvania 19141.
Abstract
Glucocorticoid excess is associated with alterations in the vitamin D endocrine system. The aim of this study was to assess change in serum bone Gla protein (BGP) after low and high dose cortisone acetate treatment and to assess whether these alterations are altered or attenuated by 1,25-dihydroxyvitamin D3[1,25-(OH)2D3] administration. Five groups of rats were studied and compared to a control group [cortisone acetate in doses of 0.2, 3.3, and 5.0 mg/100 g BW; 1,25-(OH)2D3 in a dose of 100 ng/100 g BW; and a combination of 1,25-(OH)2D3 (100 ng/100 g BW) plus cortisone acetate (3.3 mg/100 g BW)]. Each animal received daily sc injections for 27 days. BGP decreased significantly by day 7 in the two groups receiving high doses of cortisone acetate compared to control group values (65.20 ± 4.38 vs. 150.18 ± 6.13 ng/ml in the intermediate dose group and 91.57 ± 5.30 vs. 150.18 ± 6.13 ng/ml in the high dose group; P < 0.01); this effect persisted until day 28. Histomorphometry revealed decreased formation and resorption in the two high dose cortisone acetate groups, whereas low dose cortisone acetate produced no histological change. The combination therapy lessens any change in BGP until day 28 when BGP was lower than the control value (P < 0.01); histomorphometry showed that combination therapy prevents the effect of cortisone acetate by increasing bone formation and resorption.
The data demonstrate that high doses of cortisone acetate suppress bone formation and that this is reflected in the low serum BGP values. Thus, BGP may be a marker of glucocorticoid- induced bone disease. 1,25-(OH)2D3 protects against glucocorticoid- induced bone disease and the normal BGP level reflects this. (Endocrinology 120: 531–536, 1987)
Received September 26, 1986.
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