1,25-Dihydroxycholecalciferol AND 1α-Hydroxycholecalciferol IN HYPOPARATHYROIDISM

Russell, R. G. G.; Walton, R. J.; Smith, Roger; Preston, Christopher J.; Basson, Rosemary; Henderson, R. G.; Norman, Anthony W.

doi:10.1016/s0140-6736(74)91348-8

Cited by 88 publications

(12 citation statements)

References 10 publications

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“…Hypocalcemia in these patients was responsive to 1,25(OH) 2 D 3 given by mouth in doses of 14-20 /xg/day. In most states with deficiency or abnormal metabolism of vitamin D, hypocalcemia is corrected with doses of 1,25(OH) 2 D 3 between 0.5-1.0 /xg/day (25)(26)(27)(28). In the presence of active skeletal disease, dosage requirements may initially be higher.…”

Section: Discussionmentioning

confidence: 99%

A Familial Syndrome of Decrease in Sensitivity to 1,25-Dihydroxyvitamin D*

Marx

Spiegel

Brown

et al. 1978

The Journal of Clinical Endocrinology & Metabolism

134

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Typical features of hereditary vitamin D-dependent (pseudovitamin D-deficient) rickets were observed beginning at ages 20 and 5 months in a brother and sister. Both had calcium malabsorption correctable with high doses of 25-hydroxyvitamin D. During periods of hypocalcemia they both manifested secondary hyperparathyroidism with hypophosphatemia and high serum concentrations of endogenously produced 1,25-dihydroxyvitamin D. In each, normalization of serum calcium concentration and resolution of osteomalacia were obtained with continuous administration of high doses of ergocalciferol or high doses of 1,25-dihydroxycholecalciferol. Chemical features of vitamin D deficiency were corrected in the presence of high circulating concentrations of 1,25-dihydroxyvitamin D2, produced endogenously, or of 1,25-dihydroxyvitamin D3, administered by mouth. Serum concentrations of 25-hydroxyvitamin D2, 25-hydroxyvitamin D3, 24,25-dihydroxyvitamin D, and 1,25-dihydroxyvitamin D were normal in five first degree relatives. We conclude that in these five first degree relatives. We conclude that in these siblings, rickets and osteomalacia resulted from a hereditary decreased sensitivity to 1,25-dihydroxyvitamin D at the intestine and perhaps other vitamin D target tissues.

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Section: Discussionmentioning

confidence: 99%

A Familial Syndrome of Decrease in Sensitivity to 1,25-Dihydroxyvitamin D*

Marx

Spiegel

Brown

et al. 1978

The Journal of Clinical Endocrinology & Metabolism

134

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“…In idiopathic hypoparathyroidism and pseudohypoparathyroidism, plasma 1,25(OH)2D is low (19)(20)(21) due to the lack of PTH or to the unresponsiveness of the kidney to PTH (22)(23)(24), and active vitamin D3(1 ,25(OH)2D3 or I aOHD3) are administered (25)(26)(27)(28) as the treatment. Several reports proved that serum osteocalcin is low in hypoparathyroidism (7,29).…”

mentioning

confidence: 99%

Effects of active vitamin D3 and parathyroid hormone on the serum osteocalcin in idiopathic hypoparathyroidism and pseudohypoparathyroidism.

Mizunashi¹,

Furukawa²,

Miura³

et al. 1988

J. Clin. Invest.

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Serum osteocalcin was measured in patients with idiopathic hypoparathyroidism or pseudohypoparathyroidism, before or during the treatment with active vitamin D3 (1,25(OH)2D3 or lcaOHD3).Serum osteocalcin and plasma 1,25(OH)2D were decreased in 11 patients with idiopathic hypoparathyroidism before treatment (2.8±1.27 ng/ml, P < 0.001 and 14.3±4.27 pg/ml, P <0.001, respectively). In 24 patients with idiopathic hypoparathyroidism during the treatment, serum osteocalcin and plasma 1,25(OH)2D were within the normal range (4.5+0.74 ng/ml and 25.7±5.69 pg/ml, respectively).In five patients with pseudohypoparathyroidism before treatment, plasma 1,25(OH)2D was decreased (15.6±10.6 pg/ml, P < 0.001) but serum osteocalcin was normal (7.8±1.6 ng/ml). In nine patients with pseudohypoparathyroidism during the treatment with active vitamin D3, serum osteocalcin and plasma 1,25(0H)21) H3ere iormal (6.8±1.47 ng/ml and 27.2±6.0 pg/ml, respectively). Serum P'I in pseudohypoparathyroidism was increased before treatment (0.70±0.34 ng/ml? P < 0.05) and was normal during the treatment (0.50±0.13 ng/ml).In idiopathic hypoparathyroidism, the active vitamin D3 increased serum osteocalcin without PTH. In pseudohypoparathyroidism, PT1I may increase serum osteocalcin or modulate the effect of active vitamin D3 on serum osteocalcin.

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“…The reason for this has become clear recently as the control of vitamin D metabolism has been elucidated. It is likely that in the absence of PTH the production of 1,25-dihydroxycholecalciferol is impaired; this view is supported by recent reports of a response to small doses of 1,2S-dihydroxycholecalciferol or of lehydroxycholecalciferol by patients with hypoparathyroidism (Russell et al, 1974).…”

Section: Treatmentmentioning

confidence: 77%

Hypocalcaemia: Differential Diagnosis and Investigation

Paterson

1976

Ann Clin Biochem

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Hypocalcaemia accounts for many of the telephone inquiries made to the Department of Biochemical Medicine in Dundee. About half of these cases can be explained by hypoalbuminaemia; the causes of “true” hypocalcaemia are given in Table 1. Chronic renal failure is probably the most frequent cause of hypocalcaemia in Britain. In the world as a whole it is likely that vitamin D deficiency, causing rickets in children and osteomalacia in adults, is the commonest cause of hypocalcaemia.

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1,25-Dihydroxycholecalciferol AND 1α-Hydroxycholecalciferol IN HYPOPARATHYROIDISM

Cited by 88 publications

References 10 publications

A Familial Syndrome of Decrease in Sensitivity to 1,25-Dihydroxyvitamin D*

A Familial Syndrome of Decrease in Sensitivity to 1,25-Dihydroxyvitamin D*

Effects of active vitamin D3 and parathyroid hormone on the serum osteocalcin in idiopathic hypoparathyroidism and pseudohypoparathyroidism.

Hypocalcaemia: Differential Diagnosis and Investigation

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