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PubMedDate not supplied

[Effect of thyroid and adrenal hormones on the course of hypervitaminosis A and D].

Tests staged on normal and hypophysectomized rats demonstrated thyroxin to potentiate the general toxic effect of ergocalciferol, with final death of the animals. At the same time, the blood calcium content in animals receiving thyroxin decreases under the effect of the latter. Hydrocortisone, while producing no effect on the high calcium content in the blood of the animals receiving ergocalciferol, attenuates the general toxic action of the latter. These data point to the possibility of dissociating the general toxic action of ergocalciferol and its influence on the blood calcium level, which disproves the existing notion on the correlation between general toxic action of ergocalciferol and hypercalcemia produced by it. Thyroxin and hydrocortisone do not have any effect on the nature of the action exerted by high doses of vitamin A.

Animals↗
PubMed2003

Prevention and treatment of glucocorticoid-induced osteoporosis: a comparison of calcitriol, vitamin D plus calcium, and alendronate plus calcium.

High-dose corticosteroids, used for many medical conditions, are associated with rapid bone loss from sites such as the vertebrae, and compression fractures can be observed within months. Recent trials suggest treatment with bisphosphonates or active vitamin D analogs can reduce bone loss and the risk of fracture associated with glucocorticoids, but few studies have directly compared such agents. We conducted a randomized, multicenter, open-label trial to compare the efficacy of alendronate, calcitriol, and simple vitamin D in prevention and treatment of glucocorticoid-induced bone loss. A total of 195 subjects (134 females and 61 males) commencing or already taking glucocorticoids were randomized to one of three groups: calcitriol, 0.5 to 0.75 microg/day; simple vitamin D (ergocalciferol, 30,000 IU weekly) plus calcium carbonate (600 mg daily); or alendronate, 10 mg/day plus calcium carbonate (600 mg daily). Over 2 years, mean lumbar bone mineral density change was +5.9% with alendronate, -0.5% with ergocalciferol, and -0.7% with calcitriol (p < 0.001). At the femoral neck, there was no significant difference in bone mineral density change between the treatments over 2 years: alendronate (+0.9%), ergocalciferol (-3.2%), and calcitriol (-2.2%). Lumbar bone loss varied according to whether patients were starting or receiving chronic glucocorticoids, and there was a significant treatment x prior glucocorticoid use interaction effect. Six of 66 calcitriol subjects, 1 of 61 ergocalciferol subjects, and 0 of 64 alendronate subjects sustained new vertebral fractures. These data do not suggest any difference between simple vitamin D and calcitriol but do show that alendronate was superior to either treatment for glucocorticoid induced bone loss.

Absorptiometry, Photon↗
PubMed1988

Verhoeff's query: is vitamin D effective against retinoblastoma?

In 1966, Verhoeff suggested that retinoblastomas might be sensitive to vitamin D because they sometimes undergo calcification and spontaneous regression. In recent years, the antineoplastic effect of vitamin D has been established in vitro and in vivo. This study presents evidence that vitamin D2 inhibits the growth of the human retinoblastoma cell line (Y-79) grown in athymic mice. In mice treated with ergocalciferol, the subcutaneous retinoblastomas were smaller and showed increased tumor necrosis and calcification. Unfortunately, the vitamin D caused significant toxic reactions. Further studies that reduce the toxicity of vitamin D will be needed before its use in children with retinoblastomas can be advocated. To our knowledge, this is the first demonstration of the activity of ergocalciferol against a tumor in vivo and it suggests that ergocalciferol or one of its derivatives may be an effective chemotherapeutic agent against retinoblastomas in humans.

Animals↗
PubMed1985

Skeletal challenge: an experimental study of pharmacologically induced changes in bone density in the distal radius, using gamma-ray computed tomography.

Bone density (BD) at the distal end of the radius was measured serially with gamma-ray computed tomography (gamma-CT) in five groups of healthy postmenopausal women. One group comprised untreated controls; women in the other groups were subjected to pharmacologic challenge with putative activators and/or depressors of bone remodeling. The challenge agents, taken orally, were ergocalciferol (vitamin D2) alone and followed by calcium; calcitriol (1,25(OH)2D3), and prednisone. All of the subjects showed changes in BD following challenge; these changes were significant (P less than 0.05) for the groups receiving vitamin D2 and vitamin D2 plus calcium. Responses to ergocalciferol, calcitriol, and prednisone were similar within groups, whereas the group receiving ergocalciferol then calcium comprised two distinct subgroups: bone density transiently increased in one and decreased in the other. For all five groups, the direction of change in bone density in response to the challenge, and its duration and magnitude, were consistent with reported histomorphometric data. We conclude that gamma-CT assessment of change in bone density after pharmacologic challenge provides a useful noninvasive approach to skeletal investigation.

Aged↗
PubMed1982

The effect of vitamin C on the rapid induction of aortic changes in rabbits.

Male rabbits were injected intraperitoneally for five consecutive days with one of the following: (A) 0.3 ml/kg dimethyl ethylene glycol (solvent); (B) 40 mg/kg cholesterol and 8 mg/kg ergocalciferol in solvent; (C) same regimen as B with the addition of 150 mg/kg ascorbic acid in water. Daily blood samples were taken for determination of cholesterol and triglycerides, and for lipoprotein electrophoresis. After 5 days of injections, histological sections were made of the aorta at the arch. After 5 days, group B, as compared with group A, had higher serum cholesterol (150 ng/dl vs. 50 mg/dl, p less than 0.005), higher serum triglycerides (650 mg/dl vs. 150 mg/dl, p less than 0.01), and lower high-density lipoprotein (16% vs. 35%, p less than 0.05). On autopsy, discontinuous elastic fibers and intimal damage were seen in sections of the aortas from group B, but not from group A. After 5 days, group C had control levels of cholesterol (55 mg/dl) and triglycerides (160 mg/dl), and no significant difference from the control lipoprotein profile. Injections of cholesterol alone showed a slight induction of aortic lesions and blood chemistry changes. No alterations in these parameters were induced by ergocalciferol alone. The data indicate a prophylactic effect of vitamin C on the biochemical and histological changes rapidly induced by cholesterol and ergocalciferol.

Animals↗
PubMed1990

Effect of low-dose calcitriol and calcium therapy on bone histomorphometry and urinary calcium excretion in osteopenic women.

We evaluated low-dose calcitriol (0.25 microgram b.i.d.) in combination with 1 g of supplemental calcium therapy as treatment for osteopenic women over 60 years of age (n = 4). Control patients (n = 6) received ergocalciferol (50,000 units twice a week) and 1 g of supplemental calcium. Bone biopsies and CT-determined bone mineral density were done initially and after 1 year of therapy. Bone mineral density increased from 77 +/- 18 to 88 +/- 9 mg/ml (NS) in the calcitriol-treated group and from 87 +/- 13 to 112 +/- 30 mg/ml (NS) in the ergocalciferol-treated group. There was also no significant change in bone volume, as determined by bone biopsy in either group. No compression fractures occurred in either treatment group. After 1 year of therapy, urinary calcium excretion was increased significantly above that observed in age-matched untreated women. Creatinine clearance did not change significantly. Hypercalcemia was rare. In summary, we found calcitriol was not superior to ergocalciferol in preventing progressive bone loss and fractures. Both therapies were associated with significant hypercalciuria.

Bone Density↗
PubMed1990

Effect of ethane-I-hydroxy-I, I-diphosphonate on arterial calcinosis induced by hypervitaminosis D: a morphologic investigation.

The present study was undertaken to examine changes in vascular ultrastructure of rats subjected to hypervitaminosis D with or without treatment with ethane-I-hydroxy-I, I-diphosphonate (EHDP). Five groups of rats were studied. Untreated rats were given 0.9% NaCl i.p. Sham-treated rats were given vehicle (corn oil). Treated rats were given ergocalciferol (75,000 IU i.p.) dissolved in vehicle with or without EHDP (5 mM/100 g body-weight i.p.). Rats which had been given ergocalciferol without EHDP developed hypercalcemia and demonstrated significant arterial calcinosis. A similar degree of calcinosis was not observed in rats given ergocalciferol with EHDP. EHDP appeared to inhibit arterial calcinosis; however, it did not affect plasma calcium levels. This suggests that EHDP might delay calcium influx into the cell and thereby prevent calcium overload. Our findings support the suggestion that EHDP therapy can be an effective treatment for the inhibition of dystrophic arterial calcinosis.

Animals↗
PubMedDate not supplied

[Effects of cadmium on vitamin D function involved in the regulation of phosphorus-calcium metabolism].

The role of vitamin D in regulation of phosphoric-calcium metabolism was evaluated in conditions of experimental cadmium intoxication induced by daily dietetic intake (100 micrograms/kg for 8 months) of cadmium in parallel with intake of calcium in diverse amounts. Daily requirements in vitamin D were provided in different groups of animals either with ergocalciferol (D2) or 24,25-dihydroxycholecalciferol (0.25 microgram per animal). The results of the trial suggested that despite regular supply of ergocalciferol, renal damage induced by cadmium intoxication was associated with phosphoric-calcium metabolic derangement which is likely to result from defects in renal synthesis of active vitamin D form. This was confirmed by the fact that the change of ergocalciferol for 24,25-dihydroxycholecalciferol did not produce any noticeable shifts in the phosphoric-calcium metabolism.

24,25-Dihydroxyvitamin D 3↗
PubMed1980

The effect of various cholecalciferol-related substances on the biosynthesis of the cholecalciferol-dependent calcium-binding protein in the small intestine of the rachitic chick and its relation to rickets.

Rachitic chicks were injected with different dose-levels of cholecalciferol and several cholecalciferol-related substances, i.e., dihydrotachysterol 3, ergocalciferol, 5,6-transcholecalciferol and 25-hydroxycholecalciferol. The response to treatment was assayed by the amount of cholecalciferol-dependent calcium-binding protein produced in the mucosa of the small intestine. The biological activity of these substances in the healing of rickets in the rat was also estimated except for ergocalciferol. The relative potencies in stimulating calcium-binding protein production were: 25-hydroxycholecalciferol > cholecalciferol > 5,6-trans-cholecalciferol > ergocalciferol > dihydrotachysterol 3.

Animals↗
PubMed1980

Supranormal 25-hydroxyvitamin D and subnormal 1,25-dihydroxyvitamin D: their role in X-linked hypophosphatemic rickets.

Serum 25-hydroxyvitamin D (25-OH-D) and 1,25-dihydroxyvitamin D (1,25-(OH)2D) and bone mineral content by the photon-absorption technique were determined in eight patients with X-linked hypophosphatemic rickets treated for at least 24 months with oral sodium phosphate and high-dosage ergocalciferol (vitamin D2). Mean 25-OH-D2 level was 129.5 +/- 67.5 ng/mL (mean +/- SD); the level of 25-OH-D3 was 10.5 +/- 5.8 ng/mL. These values were significantly higher than in normal subjects (total 25-OH-D mean of 27 +/- 10 ng/mL). Serum 1,25-(OH)2D was 16.9 +/- 8.5 pg/mL (mean +/- SD) in the eight patients, significantly lower than 47 +/- 16 pg/mL in 27 age-matched controls. Values indicative of significant demineralization were found in seven of the eight phsophate-treated patients, who had no radiologic evidence of rickets. These results suggest that any theory of the pathogenesis of this disorder must account for inappropriate renal vitamin D metabolism and for renal hyperphosphaturia. The failure of high-dosage oral phosphate and ergocalciferol to fully correct demineralization may suggest a role for calcitriol (1,25-(OH)2D3) as a therapeutic agent.

Absorption↗
PubMed1982

Vitamin D metabolism in hypophosphatemic rickets.

Vitamin D metabolites were measured in 21 patients with hypophosphatemic osteomalacia of juvenile onset. In eight patients who had not received any antirachitic treatment, serum 25-hydroxyvitamin D(25-OH-D) and 1,25-dihydroxyvitamin D (1,25-[OH]2D) values were normal, whereas serum 24,25-dihydroxyvitamin D (24,25-[OH]2D) values were lower than in normal subjects. In 13 patients who were receiving ergocalciferol and oral elemental phosphorus, serum 25-OH-D and 24,25-(OH)2D concentrations were elevated and serum 1,25-(OH)2D values were low. The findings in untreated patients supported the hypothesis that vitamin D metabolism is abnormal in hypophosphatemic rickets/osteomalacia. The reduction of serum 1,25-(OH)2D levels with ergocalciferol and phosphate therapy gives further support to a therapeutic role for 1,25-(OH)2D in this disorder.

24,25-Dihydroxyvitamin D 3↗
PubMed2005

Fracture prevention with vitamin D supplementation: a meta-analysis of randomized controlled trials.

CONTEXT: The role and dose of oral vitamin D supplementation in nonvertebral fracture prevention have not been well established. OBJECTIVE: To estimate the effectiveness of vitamin D supplementation in preventing hip and nonvertebral fractures in older persons. DATA SOURCES: A systematic review of English and non-English articles using MEDLINE and the Cochrane Controlled Trials Register (1960-2005), and EMBASE (1991-2005). Additional studies were identified by contacting clinical experts and searching bibliographies and abstracts presented at the American Society for Bone and Mineral Research (1995-2004). Search terms included randomized controlled trial (RCT), controlled clinical trial, random allocation, double-blind method, cholecalciferol, ergocalciferol, 25-hydroxyvitamin D, fractures, humans, elderly, falls, and bone density. STUDY SELECTION: Only double-blind RCTs of oral vitamin D supplementation (cholecalciferol, ergocalciferol) with or without calcium supplementation vs calcium supplementation or placebo in older persons (> or =60 years) that examined hip or nonvertebral fractures were included. DATA EXTRACTION: Independent extraction of articles by 2 authors using predefined data fields, including study quality indicators. DATA SYNTHESIS: All pooled analyses were based on random-effects models. Five RCTs for hip fracture (n = 9294) and 7 RCTs for nonvertebral fracture risk (n = 9820) met our inclusion criteria. All trials used cholecalciferol. Heterogeneity among studies for both hip and nonvertebral fracture prevention was observed, which disappeared after pooling RCTs with low-dose (400 IU/d) and higher-dose vitamin D (700-800 IU/d), separately. A vitamin D dose of 700 to 800 IU/d reduced the relative risk (RR) of hip fracture by 26% (3 RCTs with 5572 persons; pooled RR, 0.74; 95% confidence interval [CI], 0.61-0.88) and any nonvertebral fracture by 23% (5 RCTs with 6098 persons; pooled RR, 0.77; 95% CI, 0.68-0.87) vs calcium or placebo. No significant benefit was observed for RCTs with 400 IU/d vitamin D (2 RCTs with 3722 persons; pooled RR for hip fracture, 1.15; 95% CI, 0.88-1.50; and pooled RR for any nonvertebral fracture, 1.03; 95% CI, 0.86-1.24). CONCLUSIONS: Oral vitamin D supplementation between 700 to 800 IU/d appears to reduce the risk of hip and any nonvertebral fractures in ambulatory or institutionalized elderly persons. An oral vitamin D dose of 400 IU/d is not sufficient for fracture prevention.

Aged↗
PubMed1989

Effects of vitamin D derivatives on soft tissue calcification in neonatal and calcium mobilization in adult rats.

The activity of 18 vitamin D analogs on soft tissue calcification and growth impairment in neonatal rats and their effect on bone calcium mobilization, intestinal calcium absorption and binding to intestinal 1,25-dihydroxyvitamin D3 receptors in adult rats were compared. Depending on the chemical modification of the vitamin D parent compounds, they could be separated into active and inactive analogs. Cholecalciferol and ergocalciferol were similarly active, but epimerization of ergocalciferol at carbon 23 caused loss of activity. Hexafluorination at carbon 26 and 27 and the introduction of a double bond at carbon 22 or 23 had no or little effect on the activity. The loss of activity was caused by the introduction of a triple bond at carbon 23 and by hydroxylation at carbon 23, 26 or 28. The differentiation of human promyelocytic leukemia cells (HL-60) induced by these derivatives was used as a parameter for antitumour activity. All six analogs, which markedly affected calcium metabolism, were highly active in HL-60 cells. However, at least three derivatives were highly active in the antitumour test but failed to induce hypercalcemia. Thus, these results indicate that it could be possible to develop medically useful vitamin D derivatives devoid of hypercalcemic side-effects.

Animals↗
PubMed1969

Investigations on metabolites of vitamin D in rat bile. Separation and partial identification of a major metabolite.

1. Young rats with cannulated bile ducts were given 0.34mg. of [1alpha-(3)H]cholecalciferol or 0.54mg. of [(14)C]ergocalciferol by intravenous infusion. Of the radioactivity in the dose of [1alpha-(3)H]cholecalciferol 31% was recovered in bile within 24hr. 2. The metabolites in bile were separated by gradient-elution column chromatography on silicic acid into five components, all more polar than cholecalciferol or 25-hydroxycholecalciferol. [(14)C]Ergocalciferol gave a similar pattern of metabolites in bile. 3. The three most polar metabolites were shown to be ionic. The major component has been identified as a glucuronide conjugate, which was not identical with synthetic cholecalciferyl glucuronide.

Animals↗
PubMed1997

Subclinical vitamin D deficiency in neonates: definition and response to vitamin D supplements.

To determine the biological criteria for neonatal vitamin D deficiency, serum 25-hydroxyvitamin D (calcidiol), parathyroid hormone (PTH), calcium, phosphates, and alkaline phosphatase (ALP) activity were measured during the winter-spring period in 80 healthy neonates and their mothers 3-6 d after delivery. A longitudinal 3-mo survey of the serum biology of 52 of these neonates consuming formula was also performed to test the influence of their neonatal vitamin D status on the effects of two oral ergocalciferol supplements (500 and 1000 IU or 12.5 and 25 micrograms/d). At birth, 63.7% of the infants had calcidiol concentrations < or = 30 nmol/L. Most of them had no other biological sign evocative of vitamin D deficiency, but 14 neonates had low calcidiol concentrations and serum PTH concentrations > 60 ng/L, the upper limit of the adult normal range. They also had a significantly lower mean serum calcium concentration than did neonates with calcidiol concentrations > 30 nmol/L. On the basis of the association of low calcidiol concentrations (< or = 30 nmol/L) and high PTH concentrations (> 60 ng/L) as criteria for vitamin D deficiency, 24% of the neonates born to unsupplemented mothers were found to be vitamin D-deficient. Neonatal vitamin D status influenced the response of the infants to vitamin D supplements. Neonates with no sign of vitamin D deficiency showed similar changes in their serum calcidiol, calcium, phosphate, and PTH concentrations and ALP activity and no toxic effect (hypercalcemia or highly elevated calcidiol concentration) was observed whatever their vitamin D intake. In contrast, neonates with subclinical vitamin D deficiency had normalized serum PTH within 1 mo only when they were given 1000 IU ergocalciferol (25 micrograms)/d in addition to their formula.

Adult↗
PubMed1999

Bioavailability of vitamin D from wild edible mushrooms (Cantharellus tubaeformis) as measured with a human bioassay.

BACKGROUND: The bioavailability of vitamin D from mushrooms in humans is unknown. OBJECTIVE: We investigated the bioavailability of vitamin D from wild edible mushrooms (Cantharellus tubaeformis) using the increase in serum 25-hydroxyvitamin D concentrations as a measure of vitamin D bioavailability. DESIGN: Twenty-seven volunteers with serum 25-hydroxyvitamin D concentrations <60 nmol/L (mean : 38.5 nmol/L; range: 15-60 nmol/L) were randomly divided into 3 groups of 9 persons each. For 3 wk, excluding Saturdays and Sundays, group 1 received mushrooms (C. tubaeformis) providing 14 microg ergocalciferol/d with their lunch, group 2 (control) received an ergocalciferol supplement providing 14 microg/d, and group 3 (also a control) received no supplementation. RESULTS: At the beginning of the study, mean serum 25-hydroxyvitamin D concentrations did not differ significantly among the groups (P = 0.280). When all 3 groups were considered, serum 25-hydroxyvitamin D concentrations showed different time-related changes among the groups during the study: group (P = 0.388), time (P = 0.000), and group x time (P = 0.001). When groups 1 and 2 were compared with group 3, serum 25-hydroxyvitamin D concentrations at 3 wk differed significantly between groups 1 and 3 (P = 0.032) as well as between groups 2 and 3 (P = 0.004). Serum 25-hydroxyvitamin D concentrations at 3 wk did not differ significantly between groups 1 and 2 (P = 0.317). CONCLUSIONS: We showed for the first time that ergocalciferol was well absorbed from lyophilized and homogenized mushrooms in humans and that vitamin D bioavailability can be studied in humans with such an experimental protocol.

25-Hydroxyvitamin D 2↗
PubMed1981

Occurrence of vitamin D sulfate in human milk whey.

Following reports that vitamin D sulfate is the major source of vitamin D activity in human milk, we investigated the presence of this compound in milk whey using a modification of techniques for the determination of vitamin D metabolites in plasma. Synthetic cholecalciferol sulfate, ergocalciferol sulfate an [3H]cholecalciferol sulfate were prepared by reacting radioactive cholecalciferol or nonradioactive cholecalciferol or ergocalciferol with sulfamic acid in pyridine. The products were purified sequentially by Sephadex LH-20 and high pressure liquid chromatography. The purified products were chromatographically homogeneous, exhibited an ultraviolet absorption spectrum identical to that of standard cholecalciferol, demonstrated a sulfonate ester linkage and upon saponification yielded the parent vitamin. Milk whey was extracted with methanol:methylene chloride (1:2 v/v) using [3H]cholecalciferol sulfate to estimate recovery of the compound. The extract was purified by chromatography on silica cartridges an reverse phase high pressure liquid chromatography and was quantitated by ultraviolet absorption (UV). Although added cholecalciferol sulfate was readily detected in human milk whey samples, no endogenous vitamin D sulfate was found (detection limit 1 ng/ml). The results indicate that vitamin D sulfate is not a major source of vitamin D activity in human milk.

Cholecalciferol↗
PubMed1999

[The balance of elastase and its inhibitors in the vascular tissues of rabbits of different ages in the early stages of experimental Mönckeberg-type arteriosclerosis].

The role of the elastolytic system in pathogenesis of vascular diseases was investigated on adult and one-month old rabbits in experimental ergocalciferol-induced media calcinosis depending on age aspect. The obtained results indicate that elastase activity was increased in aortic homogenates of one-month old rabbits but not in adult animals. The level of alpha 1-proteinase inhibitor is reduced in one-month old rabbits, and decrease of the alpha 2-macroglobulin content in arterial walls occurs in adults. A higher level of antielastase proteins in both groups of animals in venous vessels is determined. After effect of ergocalciferol in the veins of one-month-old rabbits, differs from the adults, a significant increase of the inhibitor content is observed. The presented results confirm the importance of balance between elastase and it inhibitors in pathogenesis of arteriosclerosis.

Aging↗