Studies of Antiricketic Activity in Sera From Patients With Disorders of Calcium Metabolism and Preliminary Observations on the Mode of Transport of Vitamin D in Human Serum*

Wc, Thomas; Hg, Morgan; Tb, Connor; Haddock, L; Ce, Bills; Je, Howard

doi:10.1172/jci103884

Cited by 102 publications

(20 citation statements)

References 28 publications

(31 reference statements)

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“…It is evident from (36)(37)(38)(39), a decrease of these carriers by blood loss likewise might well reduce the proportion of the dose held in the plasma compartment.…”

Section: Resultsmentioning

confidence: 99%

“Activation” of vitamin D by the liver

Ponchon¹,

Kennan²,

DeLuca³

1969

J. Clin. Invest.

361

130

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“…It is evident from (36)(37)(38)(39), a decrease of these carriers by blood loss likewise might well reduce the proportion of the dose held in the plasma compartment.…”

Section: Resultsmentioning

confidence: 99%

“Activation” of vitamin D by the liver

Ponchon¹,

Kennan²,

DeLuca³

1969

J. Clin. Invest.

361

130

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“…3), is biologically active in promoting healing of rachitic bone (Table IV), and is repeatedly found in the blood of normal human subjects (9, 10), patients with familial vitamin D-resistant rickets (10), and in the tissues of rachitic chicks given vitamin D3-3H (8). (23)(24)(25) and man (26)(27). There is general agreement that the vitamin and its metabolite(s) are bound to albumin, a-globulins, and lipoproteins in stable and nonultrafilterable forms.…”

Section: Resultsmentioning

confidence: 99%

The metabolic fate of vitamin D3-3H in chronic renal failure

Avioli¹,

Birge²,

Lee³

et al. 1968

J. Clin. Invest.

161

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A B S TRA CT The absorption and metabolism of vitamin D3-3H was studied in eight patients with chronic renal failure. Although the intestinal absorption of vitamin D8-3H was normal, the metabolic fate of the vitamin was abnormal as characterized by a twofold increase in fractional turnover rate, an abnormal accumulation of biologically inactive lipid-soluble metabolites, and the urinary excretion of both vitamin D3-3H and biologically inactive metabolites. Neither alterations in watersoluble vitamin D. metabolites nor qualitative abnormalities in protein-binding of vitamin D.were observed in the uremic subjects. Although hemodialysis proved ineffectual in reversing the observed abnormalities in vitamin D, metabolism and excretion, renal homotransplantation was completely successful in this regard, These experiments support the conclusion that the resistance to therapeutic doses of vitamin D often seen in patients with chronic renal failure and renal osteodystrophy results from an acquired defect in the metabolism and excretion of vitamin D. INTRODUCTIONThe occurrence of skeletal abnormalities in patients with chronic renal disease (renal osteodystrophy) and the destructive effects of secondary hyperparathyroidism and chronic acidosis on bone in uremia have been well established (1-5). Recent observations by Dent, Harper, and Philpot (2) and Stanbury and Lumb (3,4) suggest that renal

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“…Before the isolation and identification of 25-hydroxycholecalciferol, several studies were conducted to examine the transport of vitamin D in human (15)(16)(17) and in rat (18,19) serum. Human serum proteins were separated by agar-gel electrophoresis by de Crousaz, Blanc, and Antener, who found vitamin D activity, by bioassay, in the albumin and ae-globulin fractions (16).…”

Section: Introductionmentioning

confidence: 99%