Vitamin D Metabolites and Bone Mineralization in Man*

Bordier, P; Rasmussen, Howard; Marie, Pierre J.; Miravet, L; Guéris, J; Ryckwaert, A

doi:10.1210/jcem-46-2-284

Cited by 174 publications

(51 citation statements)

References 22 publications

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“…Our results, therefore, confirm those of Taylor (10) Although results in early studies suggest that 1,25-(OH)2D may be adequate for treating children with vitamin D deficiency (13), results in several other studies are in direct conflict with this concept (11,14). In diseases in which plasma 24,25-(OH)2D and 1,25-(OH)2D concentrations would be very low (vitamin D deficiency and renal osteodystrophy), treatment with 1,25-(OH)2D3 alone did not heal the osteomalacia associated with these diseases (11,14 (11,14) suggested an active role for 24,25-(OH)2D3 in normal bone formation.…”

Section: Introductionsupporting

confidence: 90%

“…In diseases in which plasma 24,25-(OH)2D and 1,25-(OH)2D concentrations would be very low (vitamin D deficiency and renal osteodystrophy), treatment with 1,25-(OH)2D3 alone did not heal the osteomalacia associated with these diseases (11,14 (11,14) suggested an active role for 24,25-(OH)2D3 in normal bone formation. Although untested, response to this dual treatment might be similar in patients with renal osteodystrophy.…”

Section: Introductionmentioning

confidence: 99%

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Impaired 24,25-Dihydroxyvitamin D Production in Anephric Human and Pig

Horst¹,

Littledike²,

Gray³

et al. 1981

J. Clin. Invest.

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A B S T R A C T Plasma progressively rose from 12±4 nglml on day 0 to 705±62 ng/ml on day 10. The 25-OHD3 concentrations in normal pigs rose from 8±2 ng/ml on day 0 to 439±64 ng/ml on day 10. Plasma 25-OHD3 was higher in anephrics throughout the experiment, and concentrations were significantly higher (P < 0.05) on days 9 and 10. Plasma 24,25-(OH)2D3 concentrations declined progressively in anephric pigs from 3.6+0.6 ng/ml on day 0 to 3.2+0.7 ng/ml on day 2.

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Section: Introductionsupporting

confidence: 90%

Section: Introductionmentioning

confidence: 99%

Impaired 24,25-Dihydroxyvitamin D Production in Anephric Human and Pig

Horst¹,

Littledike²,

Gray³

et al. 1981

J. Clin. Invest.

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“…(14) Defective mineralization (M) may result in bone pain and/or fracture. (15)(16)(17)(18) Abnormalities in bone balance will lead to changes in bone volume (V), which result in either osteoporosis or osteosclerosis. (19,20) No up-to-date information is available on with active vitamin D or phosphate binders have not been studied in patients with CKD.…”

Section: Introductionmentioning

confidence: 99%

Renal osteodystrophy in the first decade of the new millennium: Analysis of 630 bone biopsies in black and white patients

Malluche

Mawad

Monier‐Faugere

2010

Journal of Bone and Mineral Research

282

235

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Renal osteodystrophy occurs early during loss of kidney function. There are 26 million American patients with chronic kidney disease (CKD), and almost all patients with CKD stage 5 have abnormal bone histology. Six hundred and thirty bone biopsies from adult CKD-5 patients on dialysis were evaluated by histomorphometry and analyzed using the turnover (T), mineralization (M), and volume (V) classification. There were racial differences; whites exhibited predominantly low turnover (62%), whereas blacks showed mostly normal or high turnover (68%). A mineralization defect was observed in only 3% of patients. In whites, cancellous bone volume was low, normal, or high in approximately the same number of patients, whereas in blacks, cancellous bone volume was high in two-thirds of the patients. More than 80% of blacks and whites with low cancellous bone volume had thin trabeculae owing to low bone formation. Cortical thickness was low in half the whites, whereas it was normal in three-quarters of blacks. Cortical porosity was high in 50% of whites, whereas three-quarters of blacks had high porosity. In summary, the TMV system gives relevant information. It should be expanded to include the architecture of cancellous and cortical bone. There are racial differences. Low bone volume and low bone turnover are more frequent than heretofore appreciated, whereas mineralization defects nowadays are observed rarely in adults. These findings call for an adjustment of the current therapeutic paradigm that takes into consideration race and risk of low bone volume and turnover. The latter have been shown to be associated with increased vascular calcifications. ß

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“…Only in one study have at least normal plasma calcitriol levels been continuously maintained between doses (5), but the peak levels exceeded 2,000 pg/ml (10-20 times normal) and growth was retarded, so that the incomplete histologic response in bone most likely resulted from a toxic effect on bone cells. In some patients with vitamin D deficiency who are given calcitriol once daily by mouth, the plasma phosphate rises and osteomalacia heals (34), especially if the plasma calcitriol level is adequately maintained between doses (35), but in other patients neither a rise in plasma phosphate nor healing of osteomalacia are achieved (3,36); these different responses could reflect individual differences in the rate of catabolism of calcitriol.…”

Section: Discussionmentioning

confidence: 99%

“…The question ofwhich of these and possibly other metabolites are responsible for the physiologic actions of vitamin D has been the subject of much research. It is now generally agreed that calcitriol is mainly and perhaps entirely responsible for promoting intestinal calcium and phosphate absorption and calcium release from bone, but some investigators believe that an additional metabolite, either calcidiol (3)(4)(5)(6) or 24,25(OH)2D3 (7)(8)(9)(10)(11)) is necessary for normal growth and mineralization of bone. A partly related issue concerns whether mineralization is controlled entirely by the plasma levels ofcalcium and phosphate or whether some metabolite of vitamin D such as calcidiol or 24,25(OH)2D3 has an additional, more direct effect on bone to promote mineralization (1,2).…”

Section: Introductionmentioning

confidence: 99%

Calcitriol but no other metabolite of vitamin D is essential for normal bone growth and development in the rat.

Parfitt¹,

Mathews²,

Brommage³

et al. 1984

J. Clin. Invest.

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As bstract. To determine the relative importance of different metabolites of vitamin D in bone growth and development, weanling male rat pups suckled by vitamin D-deficient mothers were given either calcitriol (1,25-dihydroxycholecalciferol) by continuous subcutaneous infusion, oral calcidiol (25-hydroxycholecalciferol), or oral 24,24-difluoro-25-hydroxycholecalciferol, a synthetic compound that can undergo 1-hydroxylation but not 24-hydroxylation, as their sole source of vitamin D for 40 d. Pups raised in the same manner, but given no vitamin D, served as controls. The three metabolites compared were given in doses that restored normal plasma calcium levels and normal increments in body weight. After in vivo double tetracycline labeling, bone histomorphometry by standard methods was performed on one femur and one tail vertebra. There were no significant differences between the three metabolite-treated groups in length, periosteal or endosteal diameter, cortical cross-sectional area, cortical porosity, osteoid thickness and volume, appositional rate and bone formation rate in the femur, or in qualitative and quantitative indices of endochondral ossification in the tail vertebra. All three groups differed markedly from the untreated controls with respect to all measurements. Collectively, the data indicate that neither calcidiol nor any 24-hydroxylated metabolite of calcidiol is needed in the rat (other than as a precursor) for longitudinal or transverse bone growth, for normal endochondral ossification, or for normal periosteal and endosteal formation, mineralization, and resorption ofbone. Calcitriol was fully active with respect to each of the indices listed when given in a manner resembling its continuous endogenous production by the kidney, suggesting that previous reports of incomplete skeletal response to calcitriol result from its rapid clearance and infrequent oral administration. We demonstrated that calcitriol is the only metabolite that is both necessary and sufficient for normal bone growth and development in the rat, but our data do not indicate the extent to which its beneficial skeletal effects were mediated by direct action on bone, either of calcitriol itself or of some metabolite thereof, or by restoration of normal plasma levels of calcium and phosphate.

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Vitamin D Metabolites and Bone Mineralization in Man*

Cited by 174 publications

References 22 publications

Impaired 24,25-Dihydroxyvitamin D Production in Anephric Human and Pig

Impaired 24,25-Dihydroxyvitamin D Production in Anephric Human and Pig

Renal osteodystrophy in the first decade of the new millennium: Analysis of 630 bone biopsies in black and white patients

Calcitriol but no other metabolite of vitamin D is essential for normal bone growth and development in the rat.

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