Skeletal Metabolism and Body Composition in Cushing's Syndrome

Aloia, John F.; Roginsky, Martin S.; Ellis, Kenneth J.; Shukla, K.K.; Cohn, S. H.

doi:10.1210/jcem-39-6-981

Cited by 49 publications

(17 citation statements)

References 2 publications

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“…These data are in concert with previous reports from this laboratory as well as others (23,24). However, they are somewhat in contrast to the observations of Klein In response to supplementation with 25-OHD at a mean dose of 40 ,ug/d, intestinal calcium absorption rose to approximately normal levels and serum iPTH was reduced.…”

Section: Discussionsupporting

confidence: 93%

“…Several authors have suggested that glucocorticoids may reduce serum 25-hydroxyvitamin D (25-OHD) concentration either by impairing the hepatic conversion of vitamin D to 25-OHD or by altering subsequent 25-OHD metabolism (19)(20)(21). In contrast, others have reported normal conversion of [3H]vitamin D3 to its active metabolites in cortisone-treated rats (17,22) and normal serum 25-OHD concentrations, measured by competitive-protein binding assay, in steroid-treated patients (23,24). This question remains unresolved; however, it has been reported that administration of vitamin D in doses of 50,000-100,000 U/wk for 12 wk or 0.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Altered mineral metabolism in glucocorticoid-induced osteopenia. Effect of 25-hydroxyvitamin D administration.

Hahn¹,

Halstead²,

Teitelbaum³

et al. 1979

J. Clin. Invest.

378

135

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A B S T R A C T Parameters of mineral and bone metabolism were studied in 17 patients treated chronically with supraphysiologic doses of glucocorticoids. When compared to 15 matched normal subjects, the patient group exhibited similar serum 25-hydroxyvitamin D (25-OHD) levels, decreased intestinal 47Ca absorption, increased serum immunoreactive parathyroid hormone, and decreased forearm bone mass. Iliac crest bone biopsies revealed a decreased bone formation rate and increased osteoclast number. Treatment with 25-OHD (mean dose 40.3 ,ug/d) and calcium (500 mg/d) in nine patients produced a 46% increase in 47Ca absorption (P < 0.001) and a 54% decrease in serum immunoreactive parathyroid hormone (P <0.001) by 3 mo. In addition, by 12 mo the treatment group exhibited (a) a 13.2+5.1% increase in metaphyseal (P < 0.001) and a 2.1+0.4% increase in diaphyseal (P < 0.05) forearm bone mass, and (b) significant decreases in cortical and endosteal osteoclast number. Biochemical and bone mass changes persisted through 18 mo. No significant changes in any parameter occurred in eight control patients administered calcium 100 mgld. It is concluded that treatment with 25-OHD and calcium can significantly improve parameters of mineral and bone metabolism in patients with glucocorticoid-induced osteopenia.

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Section: Discussionsupporting

confidence: 93%

Section: Introductionmentioning

confidence: 99%

Altered mineral metabolism in glucocorticoid-induced osteopenia. Effect of 25-hydroxyvitamin D administration.

Hahn¹,

Halstead²,

Teitelbaum³

et al. 1979

J. Clin. Invest.

378

135

View full text Add to dashboard Cite

show abstract

“…In patients undergoing either short-or long-term treat-ments with glucocorticoids, plasma levels of 25-hydroxycholecalciferol (25OHD) have been reported to be either substantially reduced [12,16,18,19,34,35] or normal [13,18,22,[36][37][38]. In some patients, the low 25OHD 3 levels depended on the dose and duration of therapy [12].…”

Section: Discussionmentioning

confidence: 99%

Effects of prednisone and deflazacort on mineral metabolism and parathyroid hormone activity in humans

et al. 1984

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The effects of two different glucocorticoids, prednisone and deflazacort, (an oxazoline derivative of prednisolone) on bone metabolism were analyzed in 10 patients with disorders that required glucocorticoid therapy. Significant elevations in blood immunoreactive parathyroid hormone, alkaline phosphatase and urinary calcium, phosphate, hydroxyproline and nephrogenous cyclic AMP were observed during prednisone therapy in addition to an increase in the exchangeable calcium pool as estimated by 47Ca-kinetic analyses. In contrast to these changes, deflazacort therapy induced minimal, and in some instances, no changes in these indices. In fact, in studies wherein prednisone therapy was followed by deflazacort alterations in bone metabolism, iPTH, and nephrogenous cAMP observed during prednisone were reversed. The data are consistent with the fact that the skeletal effects of prednisone therapy are mediated, at least in part, by increased parathyroid hormone activity, and that deflazacort is less potent in this regard.

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“…This action, often called 'anti-vitamin D effect', was thought to be mediated by alterations of the vitamin D metabolism [22], but the primarily reported low levels of 25-OH-vitamin Dj levels [23] were not confirmed by others [24,25], More over. plasma 25-OH-vitamin D3 levels cor related with vitamin D intake, independently of the concomitant intake of glucocorticoste roids.…”

Section: Pathophysiologymentioning

confidence: 99%

Corticosteroids and Bone: a Review

Burckhardt¹

1984

Horm Res

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Skeletal Metabolism and Body Composition in Cushing's Syndrome

Cited by 49 publications

References 2 publications

Altered mineral metabolism in glucocorticoid-induced osteopenia. Effect of 25-hydroxyvitamin D administration.

Altered mineral metabolism in glucocorticoid-induced osteopenia. Effect of 25-hydroxyvitamin D administration.

Effects of prednisone and deflazacort on mineral metabolism and parathyroid hormone activity in humans

Corticosteroids and Bone: a Review

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