Privational and malabsorption metabolic bone disease: Plasma vitamin D metabolite concentrations and their relationship to quantitative bone histology

J. E. Compston, S. Vedi, A. L. Merrett, Thomas Clemens, J. L H O'Riordan, J. S. Woodhead

Research output: Contribution to journalArticle

Abstract

Plasma 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] and 25-hydroxyvitamin D (250HD) concentrations were measured in twenty patients with metabolic bone disease due either to privational causes (10 patients) or malabsorption (10 patients). Abnormally low plasma 1,25(OH)2D3 levels were found in eleven patients, six with privational and five with malabsorption bone disease. Normal plasma 1,25(OH)2D3 concentrations were found in the remaining nine patients; of these, five were either receiving anticonvulsant therapy or had been hospitalised prior to investigation. In the absence of either of these factors, normal plasma 1,25(OH)2D3 levels were only found in patients with malabsorptionassociated bone disease. Plasma 250HD levels were below normal in eleven patients; six had malabsorption and five had privational bone disease. In the fifteen patients not receiving anticonvulsants there were significant inverse correlations between plasma 1,25(OH)2D3 levels and the osteoid volume, surface and seam thickness index. This study indicates that plasma 1,25(OH)2D3 concentrations are low in privational osteomalacia in the absence of anticonvulsant therapy or hospitalisation, although normal levels may occur in malabsorption metabolic bone disease uncomplicated by these factors. The plasma 1,25(OH)2D3 concentration appears to be inversely related to the histological severity of bone disease in patients not receiving anticonvulsant therapy.

Original languageEnglish (US)
Pages (from-to)165-170
Number of pages6
JournalMetabolic Bone Disease and Related Research
Volume3
Issue number3
DOIs
StatePublished - 1981
Externally publishedYes

Fingerprint

Metabolic Bone Diseases
Vitamin D
Histology
Bone and Bones
Bone Diseases
Anticonvulsants
Osteomalacia
Calcitriol
Hospitalization
Therapeutics

Keywords

  • Malabsorption
  • Metabolic Bone Disease
  • Osteomalacia
  • Plasma 1,25-dihydroxyvitamin D
  • Plasma 25-hydroxyvitamin D
  • Quantitative Bone Histology

ASJC Scopus subject areas

  • Endocrinology, Diabetes and Metabolism
  • Surgery

Cite this

Privational and malabsorption metabolic bone disease : Plasma vitamin D metabolite concentrations and their relationship to quantitative bone histology. / Compston, J. E.; Vedi, S.; Merrett, A. L.; Clemens, Thomas; O'Riordan, J. L H; Woodhead, J. S.

In: Metabolic Bone Disease and Related Research, Vol. 3, No. 3, 1981, p. 165-170.

Research output: Contribution to journalArticle

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AB - Plasma 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] and 25-hydroxyvitamin D (250HD) concentrations were measured in twenty patients with metabolic bone disease due either to privational causes (10 patients) or malabsorption (10 patients). Abnormally low plasma 1,25(OH)2D3 levels were found in eleven patients, six with privational and five with malabsorption bone disease. Normal plasma 1,25(OH)2D3 concentrations were found in the remaining nine patients; of these, five were either receiving anticonvulsant therapy or had been hospitalised prior to investigation. In the absence of either of these factors, normal plasma 1,25(OH)2D3 levels were only found in patients with malabsorptionassociated bone disease. Plasma 250HD levels were below normal in eleven patients; six had malabsorption and five had privational bone disease. In the fifteen patients not receiving anticonvulsants there were significant inverse correlations between plasma 1,25(OH)2D3 levels and the osteoid volume, surface and seam thickness index. This study indicates that plasma 1,25(OH)2D3 concentrations are low in privational osteomalacia in the absence of anticonvulsant therapy or hospitalisation, although normal levels may occur in malabsorption metabolic bone disease uncomplicated by these factors. The plasma 1,25(OH)2D3 concentration appears to be inversely related to the histological severity of bone disease in patients not receiving anticonvulsant therapy.

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