24-25-dihydroxyvitamin-d-3 and Hypocalcemia

Topics: 24,25-Dihydroxyvitamin D 3; Absorption; Adrenal Cortex Hormones; Anticonvulsants; Calcifediol; Calcitriol; Calcium; Chemical Phenomena; Chemistry; Chronic Kidney Disease-Mineral and Bone Disorder; Digestive System Diseases; Dihydroxycholecalciferols; Fanconi Syndrome; Female; Humans; Hydroxycholecalciferols; Hypocalcemia; Hypoparathyroidism; Hypophosphatemia, Familial; Infant, Newborn; Kidney Diseases; Kinetics; Liver Diseases; Menopause; Neoplasms; Osteomalacia; Osteoporosis; Rickets; Vitamin D

Topics: 24,25-Dihydroxyvitamin D 3; 25-Hydroxyvitamin D3 1-alpha-Hydroxylase; Adolescent; Adult; Alopecia; Animals; Bone and Bones; Calcitriol; Calcium; Cell Nucleus; Cells, Cultured; Child; Child, Preschool; Cytochrome P-450 Enzyme System; Dihydroxycholecalciferols; Drug Resistance; Female; Fibroblasts; Humans; Hypocalcemia; Hypophosphatemia, Familial; Male; Pregnancy; Steroid Hydroxylases; Vitamin D3 24-Hydroxylase

Effects of 1,25(OH)2D3 or 24,25(OH)2D3 on plasma PTH were examined following induced hypocalcemia with EGTA. EGTA infusions caused an elevation of plasma PTH within 10 min. Sixty min after the start of EGTA infusions, 1,25(OH)2D3 or 24,25(OH)2D3 were IV administered. Transient (within 5 min) elevations in plasma PTH were observed in two of five animals following the administration of 1,25(OH)2D3 or of 24,25(OH)2D3. Neither secosterol had an effect on the induced elevations in plasma PTH during the remaining 60 min of the EGTA infusions. Twenty-two hr following 24,25(OH)2D3 administration, plasma PTH, ionized and total calcium, inorganic phosphate, and magnesium were normal, while plasma 24,25(OH)2D was elevated. The plasma PTH response to EGTA-induced hypocalcemia was not significantly altered from that observed prior to the administration of 24,25(OH)2D3. Animals, which were IV injected with 1,25(OH)2D3 received the same amount IM 60 min later. Twenty-two h following IM 1,25(OH)2D3, plasma 1,25(OH)2D, ionized and total calcium, and plasma inorganic phosphate were elevated. Plasma PTH and magnesium were lowered. The PTH response to EGTA-induced hypocalcemia was significantly reduced in these animals. A similar reduction in the PTH response to induced hypocalcemia was observed in animals receiving 7 hr IV infusions of calcium chloride. The findings suggest that the blunted response was, in part, the consequence of the preceding hypercalcemia. These results indicate that 1,25(OH)2D3 does not directly regulate plasma PTH secretion and that 24,25(OH)2D3 has no effect on plasma PTH during induced hypocalcemia in the bovine species.

Topics: 24,25-Dihydroxyvitamin D 3; Animals; Calcitriol; Cattle; Cattle Diseases; Dihydroxycholecalciferols; Egtazic Acid; Hypocalcemia; Magnesium; Male; Parathyroid Hormone; Phosphates

The plasma concentrations of 25-hydroxyvitamin D (OHD), 1,25-(OH)2D and 24,25-(OH)2D were determined in 28 healthy premature infants (median gestational age 33, range 28-36 wk; and median birth weight 1880, range 900-2350 g) during the first 5-10 wk of life, and in a reference group of 17 young adults. The infants received a vitamin D supplement of 500 IU/d and a diet low in calcium (Ca) and phosphorus (P) compared with that of corresponding intrauterine accretion rates. The median 25-OHD concentration increased from 11 (range 6-30) ng/ml at 1 d to 27 (range, 15-41) ng/ml by 5-10 wk of age (P less than 0.01). 1,25-(OH)2D concentrations at age 1 d were similar to the adult levels (median 37, range 8-64 versus 35, range 18-58 pg/ml), but increased significantly within 1 wk to 48 (26-156) pg/ml (P = 0.01), and between 1 and 3-4 wk of age to 104 (58-203) pg/ml (P less than 0.01). The levels at 5-10 wk were similar to the 3-4 wk value. 24,25-(OH)2D concentrations were persistently low compared with the adult levels (medians 0.4-0.5, range less than 0.3-2.1 versus 1.7, range 0.4-2.0 ng/ml, P less than 0.01). The relative concentrations, expressed as the ratio of 24,25-(OH)2D to 25-OHD, were comparable to those of the adults at birth, but decreased significantly within 2 wk. The data demonstrate that healthy premature infants can produce high plasma levels of 1,25-(OH)2D.

Topics: 24,25-Dihydroxyvitamin D 3; Adult; Aging; Calcifediol; Calcitriol; Dihydroxycholecalciferols; Humans; Hypocalcemia; Infant, Newborn; Infant, Premature

Severe hypokinesia of rats given the diet with a ratio of Ca:P = 1:0.5-1:3 was accompanied by hypocalcemia, development of osteoporosis, and some intensification of renal calcinosis. The decrease of phosphorus consumption (Ca:P = 1:0.5-1:1) prevented a development of these changes in intact animals and increased bone mineralization in hypokinetic ones. Excessive phosphorus consumption (Ca:P = 1:3) produced hypocalcemia, hyperphosphatemia, and some osteoporotic changes in the bones of intact animals and intensified these changes with hypokinesia. Administration of 24,25-dihydroxycholecalciferol, an active metabolite of vitamin D3, at a dose of 1.25 micrograms/d prevented a development of bone disorders, thus effectively stimulating diaphyses and epiphyses mineralization and correcting hypocalcemia in hypokinetic rats. 24,25(OH)2D3 at the same dose did not intensify nephocalcinosis and produced no toxic symptoms with hypokinetic animals.

Topics: 24,25-Dihydroxyvitamin D 3; Alkaline Phosphatase; Animals; Bone and Bones; Bone Diseases; Calcinosis; Calcium; Diet; Dihydroxycholecalciferols; Hypocalcemia; Kidney; Male; Osteoporosis; Phosphorus; Rats; Rats, Inbred Strains; Restraint, Physical