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PubMed2003

[Ergocalciferol Reference Standard (Control 031) of National Institute of Health Sciences].

The raw material of ergocalciferol was examined for the preparation of the "Ergocalsiferol Reference Standard (Control 031)", The analytical data obtained were: melting point, 114.5 degrees C; UV spectrum, lambda max of 264.8 nm and specific absorbance in ethanol at 265 nm = 474.7; IR spectrum, same as that of the Ergocalciferol Reference Standard (Control 003); optical rotation, [alpha]20(D) = +104.6 degrees ; thin-layer chromatography, two impurities were detected at 50 micrograms; high-performance liquid chromatography, total amount of impurities estimated to be less than 0.04%. Based on the above results, the raw material was authorized as the Japanese Pharmacopoeia Ergocalciferol Reference Standard (Control 031) of the National Institute of Health Sciences.

Chemical Phenomena↗
PubMedDate not supplied

[Comparative study of the biological activity and toxic effect of 1alpha-hydroxycholecalciferol and ergocalciferol in rats].

Single administration of 0.25 microgram of sunthetic Ialpha-hydroxycholecalciferol (IalphaOHD3) into nephrectomized rats, maintained at D-avitaminous diet, improved the active transport of calcium ions against the concentration gradient in small intestine of these animals, whereas ergocalciferol was biologically inactive under the same conditions. Administration of IalphaOHD3 during 5 days at a dose 0.025 microgram normalized calcium content in blood serum of rats with D-avitaminosis, Increased doses of IalphaOHD3, administered into intact animals, caused transient hyperphosphatemia, hypercalcemia, calcinosis of internal tissues (kidney heart, aorta) as well as death of some animals. IalphaOHD3 exceeded 400-fold the hypercalcemic and calcinose effects of ergocalciferol. LD50 for IalphaOHD3 was equal to 100 microgram/kg, if it was administered during 5 days per os. Tissue calcinosis was developed after administration of a daily dose 10 microgram/kg, moderate hypercalcemia was caused by a daily dose 1 microgram/kg or 0.25 microgram per an animal; this amount is only 10-fold higher as compared with the physiologic requirement. Ergocalciferol caused hypercalcemia and metastatic calcification only at a dose 4000 microgram/kg. Clinical use of IalphaOHD3 at doses, exceeding the physiologic requirements, has to be prohibited due to high activity of the preparation and to toxicity of its increased doses.

Animals↗
PubMed1982

Acute vitamin D2 (ergocalciferol) toxicosis in horses: case report and experimental studies.

Acute accidental vitamin D2 (ergocalciferol) toxicosis was diagnosed in a 6-month-old foal with extensive lesions of soft tissue mineralization. In an experimental study, three 18-month-old horses were given ergocalciferol per os at a rate of 9,300, 22,200, or 47,200 IU/kg of body weight/day for 21 days. Clinical signs or lesions were not seen in horses given the low and intermediate doses, whereas the horse receiving the highest dose developed clinical signs and lesions similar to those noted in the foal. Signs included depression, loss of appetite, weakness, limb stiffness with impaired mobility, and cessation of growth or weight loss. Gross and histologic lesions of mineralization of various soft tissues, especially of the endocardium and wall of large blood vessels, were seen in the foal and the horse given the high dose. Marked, persistent, hyperphosphatemia (7.0 to 13.0 mg of P/dl of serum) developed in each horse. The horse given the intermediate dose remained normocalcemic. Horses given the low and high doses became hypercalcemic (13.6 to 14.5 mg of Ca/dl of serum), but serum calcium concentrations varied from day to day and both horses were normocalcemic at necropsy (12.4 to 12.7 mg of Ca/dl of serum). Distal metacarpal bone ash concentrations of calcium, phosphorus, and magnesium of the foal were mg/g of bone ash) 400.5, 180.5, and 5.30, respectively. In the horses, treatment with ergocalciferol also had no significant effect on serum magnesium (1.88 to 2.18 mg/dl of serum) or distal metacarpal bone ash concentrations of calcium (352.5 to 362.5 mg/g of bone ash), phosphorus (182.5 to 184.0 mg/g of bone ash), or magnesium (5.48 to 6.02 mg/g of bone ash).

Animals↗
PubMed1993

[Ergocalciferol Reference Standard (Control 921) of National Institute of Health Sciences].

The raw material for ergocalciferol was tested for preparation of the "Ergocalciferol Reference Standard (Control 921)". Analytical data obtained were as follows: melting point, 118.1 degrees C; UV and infrared spectra, the same as those for the JP Ergocalciferol Reference Standard; specific absorbance, E1%1 cm = 457.5 (265 nm); thin-layer chromatography and high-performance liquid chromatography (HPLC), no impurities were detected; assay, 101.0% by HPLC. Based on the above results, the raw material was authorized as the Japanese Pharmacopoeia Reference Standard (Control 921).

Chromatography, High Pressure Liquid↗
PubMed1976

High-performance liquid chromatographic analysis of vitamins I: quantitation of cholecalciferol or ergocalciferol in presence of photochemical isomers of the provitamin and application to cholecalciferol resins.

A high-performance liquid chromatographic (HPLC) procedure was developed for the quantitative determination of cholecalciferol or ergocalciferol in the presence of the photochemical isomers of the provitamin. Separation is also achieved from various common reaction products encountered in the vitamin synthesis as well as other fat-soluble vitamins. The method was applied to the routine analysis of cholecalciferol resins, and experimental data are set forth. A comparison of the HPLC method to the AOAC biological and chemical procedures shows that the HPLC method most closely approximates the antirachitic activity of a cholecalciferol sample. The specificity, sensitivity, and reproducibility of the method make it applicable to various vitamin samples containing cholecalciferol or ergocalciferol.

Biological Assay↗
PubMed1980

Bone response to phosphate salts, ergocalciferol, and calcitriol in hypophosphatemic vitamin D-resistant rickets.

We treated 11 children with vitamin D-resistant rickets with a phosphate mixture either alone (1.2 to 3.6 g per day) or combined with ergocalciferol (vitamin D2, to 50 x 103 IU per day) or with calcitriol (1,25-dihydroxyvitamin D3, 0.25 to 1 microgram per day). Serum calcitriol concentrations were normal in all patients. Calcitriol therapy circulating levels of the hormone to values above normal and increased intestinal phosphate absorption. In some patients this regimen decreased the need for phosphate supplements. None of the treatment regimens corrected the renal phosphate leak. Radiologic studies and bone histomorphometric analyses showed that phosphate (alone or with ergocalciferol) induced the mineralization of the growth plate but not of the endosteal bone surface. Combined calcitriol and phosphate therapy for a total of 2850 patient-days greatly improved the mineralization of trabecular bone. Short-term episodes of hypercalcemia were easily controlled by changes in calcitriol dosage. The data indicate that the combined calcitriol and phosphate regimen is useful in the treatment of vitamin D-resistent rickets.

Adolescent↗
PubMed1976

Effects of ergosterol on bone mineralisation in chicks given cholecalciferol or ergocalciferol.

Groups of chicks were given diets containing cholecalciferol or ergocalciferol supplemented with 0, 0-1, 1 or 10 g ergosterol/kg. 2. Ergosterol had no significant effect on growth, on the plasma concentration of calcium or on the content of bone-ash, indicating that it did not impair the absorption of either form of vitamin D. 3. An explanation is given for the apparent disagreement in the published findings on the relative anti-rachitic potencies of ergocalciferol and cholecalciferol in the chick.

Animals↗
PubMed2006

The case against ergocalciferol (vitamin D2) as a vitamin supplement.

Supplemental vitamin D is available in 2 distinct forms: ergocalciferol (vitamin D2) and cholecalciferol (vitamin D3). Pharmacopoeias have officially regarded these 2 forms as equivalent and interchangeable, yet this presumption of equivalence is based on studies of rickets prevention in infants conducted 70 y ago. The emergence of 25-hydroxyvitamin D as a measure of vitamin D status provides an objective, quantitative measure of the biological response to vitamin D administration. As a result, vitamin D3 has proven to be the more potent form of vitamin D in all primate species, including humans. Despite an emerging body of evidence suggesting several plausible explanations for the greater bioefficacy of vitamin D3, the form of vitamin D used in major preparations of prescriptions in North America is vitamin D2. The case that vitamin D2 should no longer be considered equivalent to vitamin D3 is based on differences in their efficacy at raising serum 25-hydroxyvitamin D, diminished binding of vitamin D2 metabolites to vitamin D binding protein in plasma, and a nonphysiologic metabolism and shorter shelf life of vitamin D2. Vitamin D2, or ergocalciferol, should not be regarded as a nutrient suitable for supplementation or fortification.

Biomarkers↗
PubMed2007

Prevalence of vitamin D deficiency and the safety and effectiveness of monthly ergocalciferol in hemodialysis patients.

BACKGROUND: Vitamin D deficiency is common in CKD and dialysis patients. Studies suggest a physiologic autocrine and/or paracrine role for 1,25(OH)D produced via 1alpha-hydroxylase in tissues such as vascular smooth muscle, breast, prostate, and bone marrow. Studies have not yet defined the optimal dose and duration of vitamin D necessary to replete and maintain stores in dialysis patients, or whether it is safe or beneficial. METHODS: We performed a review of the prevalence of vitamin D deficiency and the safety and effectiveness of ergocalciferol oral supplementation (vitamin D(2), 50,000 IU monthly) given to hemodialysis patients during dialysis May to October 2005 in St. Louis (latitude 38 degrees ). RESULTS: Among the 119-patient cohort present for the entire 6 months, 25(OH)D was (mean +/- SD) 16.9 +/- 8.5 ng/ml, (91% < 30 ng/ml) and increased to 53.6 +/- 16.3 ng/ml (p < 0.001), (95% > 30 ng/ml, and none > 100 ng/ml). Initial versus 6 mo. serum calcium (9.1 +/- 0.56 vs. 9.2 +/- 0.70), phosphorus (5.25 +/- 1.38 vs. 5.11 +/- 1.31), Ca x P, and paricalcitol dose (10.3 +/- 9.6 vs. 11.3 +/- 9.2 mcg/week) were not significantly different. No hypercalcemia could be attributed to supplementation. Mean hemoglobin did not change significantly (11.96 +/- 1.4 vs. 11.69 +/- 1.4, p = 0.124), but most patients experienced a reduced weekly epoetin dose. Epoetin dose decreased in 64% of patients, and increased in 28%. CONCLUSIONS: We conclude that the vast majority of hemodialysis patients are vitamin D-deficient; monthly ergocalciferol 50,000 IU is safe and effective in normalizing serum 25(OH)D levels and may have an epoetin-sparing effect.

Adult↗
PubMed1977

An improved procedure for the isolation of suprasterol2 I and II from a photochemical reaction mixture of ergocalciferol (vitamin D2).

An improved procedure for the isolateion suprasterol2 I and II from a photochemical reaction mixture of ergocalciferol (vitamin D2) and their spectral data are described in this paper. When a solution of ergocalciferol in ethanol was irradiated by UV light from a high-pressure mercury lamp, the reaction mixture gave six spots, including suprasterol2 I and II, on the thin-layer chromatogram, while the peaks corresponding to pyro-D2, isopyro-D2,5,b-trans-D2, suprasterol 2 I and II were observed in the gas chromatogram obtained from a capillary column GLC (Suprasterol2 I and II were main peaks). After purifying the mixture by column chromatography on silica gel containing 12% alumina as an absorbent, two main fractins were isolated. The data of their spectra, TLC and GLC showed that the former fraction was suprasterol2 II while the latter was suprasterol2 I and that the both fractions contained the respective compound only. Both suprasterol2 were crystallized as the 3,5-dinitro-benzoates.

Cyclosteroids↗
PubMed1991

[Ergocalciferol Reference Standard (Control 901) of the National Institute of Hygienic Sciences].

Ergocalciferol Reference Standard for the Japanese Pharmacopoeia (JP RS) was prepared. The following analytical data were obtained: melting point 118.4 degrees C; UV and IR spectra were in agreement with both of the previous JP RS and USP RS of ergocalciferol; absorptivity at 265nm E1%lcm = 467; optical rotation [alpha]20D = 103 degrees; no impurities were detected by TLC and HPLC analyses; assay 100.1% by HPLC against the USP RS. Based on the above results, the raw material was authorized as the Reference Standard of the National Institute of Hygienic Sciences.

Chromatography, High Pressure Liquid↗
PubMed1989

[Ergocalciferol Reference Standard (Control 871) of National Institute of Hygienic Sciences].

The Ergocalciferol Reference Standard (Control 871) for the Japanese Pharmacopoeia was prepared. The following analytical data were obtained: melting point, 115.9 degrees C; infrared spectrum, same as the Japanese Pharmacopoeia Standard "Ergocalciferol Standard (Control 851)"; absorbance, E1%1cm (265 nm) = 464.8; optical rotation, [alpha]20D = +104.7 degrees; thin-layer chromatography, same as the Japanese Pharmacopoeia Standard; high-performance liquid chromatography, contaminants were not detected; assay, 101.2%. On the basis of those results, this material was authorized as the Japanese Pharmacopoeia Standard (control 871).

Chemical Phenomena↗
PubMed1995

[Ergocalciferol reference standard (Control 941) of the National Institute of Health Sciences].

The raw material for ergocalciferol was tested for preparation of the "Ergocalciferol Reference Standard (Control 941)". Analytical data obtained were as follows: melting point, 117.6 degrees C; UV and infrared spectra, the same as those for JP Cholecalciferol Reference Standard; specific absorbance, E1%1cm = 458 (265 nm); thin-layer chromatography and high-performance liquid chromatography (HPLC), no impurities were detected, respectively; assay, 100.6% by HPLC. Based on the above results, the candidate raw material was authorized as the Japanese Pharmacopoeia Reference Standard (Control 941).

Chemical Phenomena↗
PubMed1993

A study of the photostability of ergocalciferol (vitamin d(2)) in organic solvents.

The photolysis of ergocalciferol (vitamin D(2)) in several organic solvents has been studied to determine the influence of solvent dielectric constant and viscosity on the rate of reaction. Ergocalciferol degrades by zero-order kinetics and the rate constants vary from 0.74x10(-5) mol 1(-1) (methanol) to 1.56x10(-5) mol 1(-1) (chloroform). The rates appear to be a linear function of the reciprocal of dielectric constant and viscosity of the medium in the range studied.

Journal Article↗
PubMed1984

Degradation of crystalline ergocalciferol [vitamin D2, (3 beta,5Z,22E)-9,10-secoergosta-5,7,10(19),22-tetra en-3-ol].

The products of the degradation of crystalline ergocalciferol were investigated. These studies showed that numerous acidic and neutral oxidation products were formed resulting in the complete destruction of the triene functionality. Separation of the neutral products by preparative TLC led to material identified as the Windaus ketone IIa, 2,3,3a,4,5,6,7,7a beta-octahydro-7a alpha-methyl-1R-(1 alpha,1R,4R,5-trimethyl-2E-hexenyl)-4H-inden-4-one.

Chromatography, Thin Layer↗
PubMed1993

A large dose of ergocalciferol does not cause deficient blood coagulation but is extremely toxic to rats.

Male Jcl:SD rats were fed vitamin D2 (ergocalciferol) at levels of 0 (control), 0.39, 0.63 and 1.00% or 0 (control), 0.0195, 0.0315 and 0.050% in the diet for 7 days. All rats of the 0.39-1.00% groups expired on days 2 and 3, while some rats of the 0.0195-0.050% groups died on days 3-6. LD50 (median lethal 7-day cumulative dose calculated from food intake) is 110.5 mg/kg (0.0354% dietarily). In expired and surviving treated rats, several organs (kidney, heart, etc.) were found to be mineralized; there were also renal tubular injuries and pulmonary bleeding. Centrilobular necrosis of liver was detected only in dead rats. Treatment also caused hypercalcemia but did not decrease blood coagulation factors. These results suggest that vitamin D does not have the effect of impeding blood coagulation but that it is extremely toxic, probably due to the hypercalcemia it causes.

Animals↗
PubMed2006

Severe hypercalcemia after transition from calcium carbonate to calcium citrate in an elderly woman treated with ergocalciferol 50,000 IU per day.

BACKGROUND: Absorption of calcium carbonate in the fasting state has been reported to be significantly compromised in subjects with achlorhydria. Although calcium carbonate malabsorption in the fasting state cannot be predicted, it might be corrected if the compound is administered with meals. However, administering calcium carbonate with meals is logistically challenging in long-term care facilities. OBJECTIVE: The aim of this study was to report the case of a woman who was transitioned to calcium citrate and subsequently experienced symptomatic severe hypercalcemia. METHODS: An 89-year-old female resident of the Wisconsin Veterans Home, a skilled nursing facility in King, Wisconsin, was receiving long-term treatment with ergocalciferol (vitamin D2) 50,000 IU/d. The patient also was receiving calcium carbonate supplements in the morning, and she rarely ate breakfast (fasting state). The patient was transitioned from 2000 mg/d of elemental calcium as carbonate to 1230 mg/d as citrate. RESULTS: After being switched from calcium carbonate to calcium citrate, the patient developed severe symptomatic hypercalcemia (16.8 mg/dL), the primary cause of which was the administration of an inappropriately high dose of vitamin D. CONCLUSIONS: We report a case of symptomatic severe hypercalcemia in a skilled nursing facility resident treated with an inappropriately high daily dose of vitamin D. Hypercalcemia manifested when calcium carbonate was replaced with calcium citrate.

Aged, 80 and over↗