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PubMed1990

[Prevention of hypocalcemia in low-birth-weight newborn infants: a comparative clinical study on the efficacy of ergocalciferol (Vit. D2) and calcifediol (Vit. 25(OH)D3)].

During the first week of life, 400 IU per day of 25(OH)D3 were given to 126 preterm and 112 full-term, small for date newborn infants, while 1000 UI per day of Vitamin D2 were given to 18 preterm and 27 full-term, small for date newborn infants, in order to compare their effectiveness for the prevention of neonatal hypocalcemia. 67 preterm and 67 full-term newborns were included in the control group. The incidence of late hypocalcemia was reduced from 16.4% to 0 in full-term babies and from 6% to 2.4% in preterm babies by the 25(OH)D3 but not by Vit. D2 administration. The incidence of early hypocalcemia was not modified at all. The Authors suggest 25(OH)D3 administration to prevent the late hypocalcemia and, together with calcium support, to treat the early hypocalcemia in the low birth weight newborn.

Calcifediol↗
PubMed1983

Prevention of osteonecrosis following renal transplantation by using vitamin D2 (ergocalciferol).

Osteonecrosis is a frequently disabling complication of renal transplantation. Thirty-one of 244 patients (12.7%), who received cadaver renal transplants from 1968 to 1978 developed an osteonecrosis. An analysis of 14 possible risk factors suggested that only the following were significantly more frequent in the osteonecrosis group: greater than 3 pulse doses of 1.2 g prednisolone, serum creatinine greater than 133 mumol/L, steroid-induced diabetes mellitus and second and subsequent transplantation. An important decline in the incidence of osteonecrosis (26.7 per cent to 6.5 per cent) was seen with prophylactic vitamin D2 treatment and the onset of osteonecrosis was on average one year later. Dangerous side effects of the large doses of vitamin D2 were minimal. Hypercalcaemia due to overdosage with vitamin D2 during simultaneous prednisolone therapy was usually mild and returned to normal in a few days by dose reduction.

Ergocalciferols↗
PubMed2001

Effect of 1alpha,25-dihydroxyvitamin D3 and 24R,25-dihydroxyvitamin D3 on metalloproteinase activity and cell maturation in growth plate cartilage in vivo.

Recent studies indicate that 1alpha,25-dihydroxyvitamin D3 (1alpha,25[OH]2D3) and 24R,25-dihydroxyvitamim D3 (24R,25[OH]2D3) differentially regulate proliferation, differentiation, and matrix synthesis of growth plate chondrocytes. To determine whether both metabolites play the same or different roles in vivo, we used the vitamin D-deficient rat as a model. Rickets was induced and then reversed by administering a single dose of ergocalciferol, 1alpha,25(OH)2D3, or 24R,25(OH)2D3 and euthanizing the animals after 4, 24, 48, or 72 h. Growth plates were either processed for histology and histomorphometry or extracted with buffered guanidine-HCl. Neutral metalloproteinase activity in the extracts was measured by use of aggrecan-containing beads, and collagenase activity was determined by use of radioactive type I collagen. The levels of tissue inhibitor of metalloproteinases (TIMP) and plasminogen activator were also determined. The morphology of the growth plate varied as a function of treatment. While 24R,25(OH)2D3 appeared to affect cell maturation and 1alpha,25(OH)2D3 appeared to affect terminal differentiation and calcification, response to ergocalciferol was indicative of the combined responses to the individual metabolites. Enzyme activity was regulated in a differential manner. Treatment with ergocalciferol produced a rapid decline in both neutral metalloproteinase and collagenase activities that was statistically significant by 4 h. By contrast, 1alpha,25(OH)2D3 had no effect on neutral metalloproteinase activity but caused a significant decrease in both active and total collagenase activity by 4 h, while 24R,25(OH)2D3 decreased neutral metalloproteinase activity by 48 h and had no effect on collagenase activity. Ergocalciferol had no effect on TIMP levels at any time examined, whereas 1alpha,25(OH)2D3 caused an increase at 48 and 72 h and 24R,25(OH)2D3 completely blocked TIMP production at 4 and 24 h. By contrast, plasminogen activator activity by ergocalciferol was decreased at 4 h, increased by 1alpha,25(OH)2D3 at 4 and 24 h, and decreased by 24R,25(OH)2D3 at all time points examined. These in vivo results confirm our previous cell culture observations showing that growth plate chondrocytes are differentially regulated by 1alpha,25(OH)2D3 and 24R,25(OH)2D3. Moreover, they show definitively that these two vitamin D metabolites play distinct roles not only in regulating neutral metalloproteinase and collagenase activities in growth plate cartilage but in cell maturation and calcification of this tissue in vivo.

24,25-Dihydroxyvitamin D 3↗
PubMedDate not supplied

Prevalence and correction of 25(OH) vitamin D deficiency in peritoneal dialysis patients.

BACKGROUND: Peritoneal dialysis (PD) patients are at risk for 25(OH) vitamin D deficiency due to effluent loss in addition to traditional risk factors. OBJECTIVES: To measure 25(OH) vitamin D deficiency in prevalent PD patients, to evaluate a replacement dose, and to determine the effects of correction. METHODS: 25(OH) vitamin D levels were drawn on prevalent PD patients. Patients deficientin 25(OH) vitamin D were given ergocalciferol, 50000 IU orally once per week for 4 weeks. Patients scored muscle weakness, bone pain, and fatigue on a scale of 0 (none) to 5 (severe). Serum calcium, phosphate, parathyroid hormone (PTH), and 25(OH) vitamin D, and 1,25(OH)2 vitamin D levels were obtained before and after treatment. RESULTS: 25(OH) vitamin D levels were measured in 29 PD patients. Deficiency (<15 ng/mL) was found in 28/29 (97%); 25/29 (86%) had undetectable levels (<7 ng/mL). One course of ergocalciferol corrected the deficiency in all but 1 patient, who required a second course. Scores for muscle weakness and bone pain fell from pre- to posttreatment (p < 0.001). 1,25(OH)2 vitamin D levels rose post ergocalciferol (from 20 to 26 pg/mL, n = 20, p = 0.09). Serum calcium, phosphate, and PTH levels did not change with ergocalciferol. CONCLUSIONS: Most PD patients had marked 25(OH) vitamin D deficiency, which was readily and safely corrected with one course of 50000 IU ergocalciferol, having no effect on serum calcium, phosphorus, or PTH, but complaints of muscle weakness and bone pain decreased. A prospective, placebo-controlled double-blinded study is needed to determine whether replacement of 25(PH) vitamin D is beneficial in PD patients.

Administration, Oral↗
PubMed1988

Metabolic bone disease of total parenteral nutrition: course after changing from casein to amino acids in parenteral solutions with reduced aluminum content.

Bone disease with total parenteral nutrition (TPN) has been attributed to aluminum loading or vitamin D therapy. We studied 17 patients who first received TPN containing casein hydrolysate with high Al and ergocalciferol (25 micrograms/d) for 6-72 mo followed by TPN containing amino acids with reduced Al and ergocalciferol (5 micrograms/d) for 9-58 mo. We also did a cross-sectional study of 22 patients receiving casein and ergocalciferol (25 micrograms/d) compared with 46 patients receiving amino acids and ergocalciferol (5 micrograms/d) for 6-58 mo. Bone formation was higher and osteoid area, bone-surface stainable Al and total bone Al were lower with amino acid TPN than with casein TPN. Bone formation varied inversely with both plasma Al and bone-surface Al, suggesting that plasma or bone-surface Al, acquired during TPN, can reduce bone formation and lead to patchy osteomalacia. Serum levels of iPTH and 1,25-dihydroxyvitamin D were higher with amino acid TPN.

Aluminum↗
PubMed2005

All-trans retinoic acid antagonizes the action of calciferol and its active metabolite, 1,25-dihydroxycholecalciferol, in rats.

An antagonistic interaction between retinol and calciferol has been established. However, the mechanism by which this antagonism occurs is unclear. One possibility is that retinol affects the metabolism of calciferol. To investigate this hypothesis, retinol- and calciferol-depleted rats were given various amounts of ergocalciferol, cholecalciferol, 1alpha,25-dihydroxycholecalciferol [1,25(OH)2D3], or 24,24-difluoro-1alpha,25-dihydroxycholecalciferol [24-F2-1,25(OH)2D3] in combination with various amounts of retinyl acetate or all-trans retinoic acid (ATRA) in a series of studies. Rats administered 1720 or 3440 microg retinyl acetate once every 3 d for 33 d in combination with 25.8 ng ergocalciferol or 25 ng cholecalciferol every 3 d had lower serum calcium and greater serum phosphorus concentrations than rats fed 0 or 11.4 mug retinyl acetate every 3 d. In addition, rats fed 400 microg ATRA/d in combination with 25.8 ng ergocalciferol every 3 d, 25 ng cholecalciferol every 3 d, 2-5 ng 1,25(OH)2D3/d, or 0.5-1 ng 24-F2-1,25(OH)2D3/d had significantly lower serum calcium and higher serum phosphorus concentrations than rats not given ATRA in the diet. Therefore, both retinyl acetate and ATRA are able to antagonize the action of ergocalciferol and cholecalciferol in vivo. Additionally, ATRA antagonizes the in vivo action of 1,25(OH)2D3 and an analog, 24-F2-1,25(OH)2D3, that cannot be 24-hydroxylated. Together, these results suggest that retinol does not antagonize the action of calciferol by altering the metabolism of calciferol or 1,25(OH)2D3, but does so by another mechanism.

Animals↗