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CORTICOSTEROID‐INDUCED OSTEOPENIA AND VITAMIN D METABOLISM. EFFECT OF VITAMIN D 2 , CALCIUM PHOSPHATE AND SODIUM FLUORIDE ADMINISTRATION
Author(s) -
RICKERS H.,
DEDING Å.,
CHRISTIANSEN C.,
RØDBRO P.,
NÆSTOFT J.
Publication year - 1982
Publication title -
clinical endocrinology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.055
H-Index - 147
eISSN - 1365-2265
pISSN - 0300-0664
DOI - 10.1111/j.1365-2265.1982.tb00734.x
Subject(s) - medicine , endocrinology , prednisone , osteopenia , vitamin d and neurology , vitamin , calcium , corticosteroid , sodium fluoride , bone resorption , chemistry , fluoride , bone mineral , osteoporosis , inorganic chemistry
SUMMARY Thirty‐one patients scheduled for long‐term (24 weeks) treatment with prednisone in comparatively high doses were randomly allocated to two further treatment groups. Group A received prednisone plus ‘triple‐treatment’ (vitamin D2 45 000 iu twice weekly, sodium fluoride 50 mg and calcium phosphate 4·5 g daily), group B received only prednisone. The study was undertaken in order to evaluate the effect of prednisone‐ and triple‐treatment upon bone mineral content (BMC) and vitamin D metabolism. The groups were comparable with regard to age, sex and prednisone dose. BMC fell rapidly and similarly in both groups, demonstrating that the triple‐treatment has no preventive effect on corti‐costeroid induced osteopenia. Serum concentrations of 25OHD 2 , 25OHD 3 and 1,25(OH) 2 D were unchanged in group B (without triple‐treatment), whereas in group A 25OHD 2 increased enormously, 25OHD 3 was suppressed possibly by substrate competition for hydroxylation in the liver and 1,25(OH) 2 D was halved. The suppression of 1,25(OH) 2 D may be an effect of raised 25OHD 2 alone, or in combination with corticosteroid excess.

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