24-25-dihydroxyvitamin-d-3 has been researched along with Nephrocalcinosis* in 2 studies
1 review(s) available for 24-25-dihydroxyvitamin-d-3 and Nephrocalcinosis
| Article | Year |
|---|---|
Medical management and complications of X-linked hypophosphatemic vitamin D resistant rickets.
To improve the growth failure, bowed legs, and biochemical and radiological abnormalities in patients with X-linked hypophosphatemic vitamin D resistant rickets (XLH), combined therapy of phosphate and calcitriol is the best therapeutic approach at present. However, the complications involving combined therapy, such as hypercalcemia, nephrocalcinosis and hyperparathyroidism, are not fully solved. To achieve better control, new therapeutic approaches have been reported recently, for example, growth hormone (GH) or new vitamin D analogs. GH improved linear growth, decreased phosphate reabsorption and increased 1-alpha-hydroxylase activity. Furthermore, 24R,25-dihydroxyvitamin D3 (24,25) improved the bone lesions in hypophosphatemic (Hyp) mice, and also in XLH, without the adverse effects such as hypercalcemia or hypercalciuria compared with 1,25-dihydroxyvitamin D3. These new approaches should be considered for the treatment of patients with XLH. Topics: 24,25-Dihydroxyvitamin D 3; Adolescent; Adult; Animals; Child; Child, Preschool; Dwarfism; Female; Human Growth Hormone; Humans; Hyperparathyroidism; Hypophosphatemia, Familial; Infant; Male; Mice; Nephrocalcinosis; Rickets | 1997 |
1 other study(ies) available for 24-25-dihydroxyvitamin-d-3 and Nephrocalcinosis
| Article | Year |
|---|---|
Idiopathic infantile hypercalcemia: rapid response to treatment with calcitonin.
We report on a 7-week-old infant with idiopathic hypercalcemia, hypercalciuria and nephrocalcinosis. At the time of admission, serum concentrations of parathyroid hormone and 1,25(OH)2D3 were found to be inadequately high, and those of calcitonin and 24,25(OH)2D3 too low, relative to the hypercalcemia. Treatment with calcitonin normalized serum calcium concentrations within 4 days, and a 3-week course of thiazides combined with a decreased dietary calcium:phosphorus ratio corrected the hypercalciuria. A repeat profile of the calcium-regulating hormones done at the age of 5.5 months was normal. Based on the clinical course and the hormonal profiles, we hypothesize that the idiopathic infantile hypercalcemia in this patient could have resulted from a generalized maturational delay of calcium homeostasis. Treatment with calcitonin, therefore, seems to be the most appropriate way to control the hypercalcemia. Topics: 24,25-Dihydroxyvitamin D 3; Calcitonin; Calcitriol; Calcium; Female; Homeostasis; Humans; Hypercalcemia; Infant; Nephrocalcinosis; Parathyroid Hormone; Time Factors | 1992 |