We compared the fractional absorption of calcium (FACa, 6 h, % TD) and the radiocalcium transit (% TD per min) in seven glucocorticoid-treated patients (10-25 mg prednisolone per day) and in seven normal subjects, in the basal state and 12 h after an oral dose of synthetic 1,25-(OH)2D (3 micrograms). In the basal state, the radiocalcium transit was significantly decreased (P less than 0.02) at 15 min in patients treated with prednisolone, but FACa at 6 h was not significantly decreased (51 +/- 5 vs. 60 +/- 5% TD). 12 h after an oral dose of 1,25-(OH)2D which resulted in supraphysiologic plasma levels, FACa increased significantly (P less than 0.02) in both groups but the peak absorption rate of Ca remained lower in the corticoid-treated patients than in controls (P less than 0.02). The results suggest that glucocorticoids decrease the 1,25-(OH)2D-dependent transport of calcium across the proximal small intestine.
Our aim was to investigate the effects of high doses of glucocorticoids on vitamin D metabolism and to evaluate whether these effects play a role in the onset of corticosteroid-induced osteopenia. For that reason, plasma 25 hydroxyvitamin D [25(OH)D] levels and 45 Ca bone uptake were measured in 18 rabbits (group I): Eleven were treated with methylprednisolone (MPT) for 3 weeks and the results were compared to those obtained in 7 controls (C). An additional group of 15 rabbits (group II = 7 MPT and 8 C) received intraperitoneal injections of both 14 C-vitamin D and 3 H-25 (OH)D and plasma concentrations of labelled vitamin D, 25 hydroxyvitamin D [25(OH)D], 24,25dihydroxyvitamin D [24,25(OH)2D] and 1,25-dihydroxyvitamin D [1,25(OH)2 D] were respectively measured 2 and 6 days after 14 C-vitamin D and 3 H-25(OH)D injections. In group I, serum calcium remained unchanged both in MPT and C animals. Plasma 25(OH)D decreased significantly (P< 0.02) in MPT rabbits compared with controls. The bone trabecular volume was correlated positively with the changes in plasma 25(OH)D : r = 0.75, P< 0.01. The results observed in group II showed that less 3 H-25(OH)D remained in circulation in MPT rabbits compared with controls after a 3 H-25(OH)D injection. The present results seem to indicate that the turnover rate of the 25(OH)D is accelerated in MPT animals. This alteration might be due to a disruption of the enterohepatic circulation, since both the 3 H-24,25(OH),D : 3 H-25(OH)D ratio remained unaffected by methylprednisolone and labelled 1,25(OH )2 D were not detectable in plasma of treated animals. However, it seems highly unlikely that the marginal alteration of the 25(OH)D metabolism could explain the profound changes in bone metabolism observed in the present study.
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