25-26-dihydroxycholecalciferol and Hypercalcemia

24R,25(OH)2D3, one of the endogenous active metabolites of vitamin D3, showed suppressive effects on the proliferation of various tumor cells in vitro, and showed a suppressive effect on the growth of human osteosarcoma transplanted in nude mice. 24R,25(OH)2D3 increased bone strength lowered by the tumor burden which causes abnormal calcium metabolism and results in hypercalcemia.

Topics: Animals; Antineoplastic Agents; Bone and Bones; Carcinoma; Cell Division; Dihydroxycholecalciferols; Humans; Hypercalcemia; Lung Neoplasms; Male; Mice; Mice, Inbred BALB C; Mice, Inbred C57BL; Mice, Nude; Neoplasm Transplantation; Osteosarcoma; Rats; Stress, Mechanical; Transplantation, Heterologous; Tumor Cells, Cultured

Lewis lung carcinoma was found to cause hypercalcemia in tumor-bearing mice. 24R,25(OH)2D3 (K-DR, prepared by Kureha Chemical Ind.) significantly prolonged the survival time of mice with Lewis lung carcinoma. K-DR exhibited an antimetastatic effect on Lewis lung carcinoma, and also had an analgesic effect in mice with Lewis lung carcinoma.

Topics: Analgesics; Animals; Antineoplastic Agents; Calcium; Carcinoma; Dihydroxycholecalciferols; Hypercalcemia; Lung Neoplasms; Male; Mice; Mice, Inbred C57BL; Mice, Inbred ICR; Neoplasm Metastasis

Metabolites of vitamin D were measured in plasma from 83 patients with idiopathic infantile hypercalcaemia syndrome who were mentally handicapped but had normal calcium values at the time of the study. No significant difference was detected in the mean plasma concentrations of 25-hydroxyvitamin D2, 1,25-dihydroxyvitamin D, 24,25-dihydroxyvitamin D3, or 25,26-dihydroxyvitamin D3 between patients and age matched controls. The mean plasma concentration of 25-hydroxyvitamin D3 was significantly lower in patients than controls but this may be a secondary phenomenon related to less sunlight exposure. In addition, two hypercalcaemic patients with this syndrome were studied during the first year of life, and were found to have normal concentrations of vitamin D metabolites. These findings do not support a role for abnormal vitamin D metabolism in the pathogenesis of this syndrome.

Topics: 24,25-Dihydroxyvitamin D 3; 25-Hydroxyvitamin D 2; Adolescent; Calcitriol; Calcium; Child; Dihydroxycholecalciferols; Ergocalciferols; Female; Humans; Hydroxycholecalciferols; Hypercalcemia; Infant; Intellectual Disability; Male; Syndrome; Vitamin D

A 9-month-old boy who had the mild form of idiopathic infantile hypercalcemia was observed for 18 months. During the initial hypercalcemic stage, the serum concentration of 25-hydroxyvitamin D was normal. Urinary levels of cyclic adenosine monophosphate (cAMP) were low, and the serum concentrations of the dihydroxyl metabolites of vitamin D were appropriate to the high serum calcium concentration, with low 1,25-dihydroxyvitamin D and relatively high 24,25- and 25,26-dihydroxyvitamin D levels. Throughout the study period, there was a close positive correlation between the magnitude of the urinary cAMP excretion and the serum level of 1,25-dihydroxyvitamin D. The results indicate that excessive vitamin D intake leading to high serum levels of 25-hydroxyvitamin D are not decisive factors in the pathogenesis of idiopathic infantile hypercalcemia.

Topics: 24,25-Dihydroxyvitamin D 3; 25-Hydroxyvitamin D 2; Calcitriol; Cyclic AMP; Dihydroxycholecalciferols; Ergocalciferols; Humans; Hypercalcemia; Infant; Male; Phosphates; Phosphorus; Vitamin D