(+)-Vitamin D2

396.65

396.65

200-014-9

2811

DTXSID5020233|DTXSID80746313

Prisms from acetone|White crystals|Colorless crystals

29362900

20.23000

9.56

white to yellowish powder

1.0±0.1 g/cm3

115-118 °C

504.2±29.0 °C at 760 mmHg

14 °C

1.530

soluble in ethanol, water, methanol, dimethylformamide, and dimethyl sulfoxide.H2O: 200 mg/mL, clear to hazy

2-8°C

7 x l0 -7 Pa (20 °C), est.)

82 º (c=3, in acetone 25 ºC)

Odorless

Medications associated with a metallic or bitter taste include ... vitamin D.

Stable in alkaline media. Unstable to light and air, and in acidic media.|Sublimes in very high vacuum (0.0006 mm) without decomposition; not precipitated by digitonin (different from ergosterol)|Hydroxyl radical reaction rate constant = 3.53X10-10 cu cm/molec-sec at 25 °C /Estimated/

No rapid reaction with air. No rapid reaction with water.

Alcohols and Polyols

Flammable and/or toxic gases are generated by the combination of alcohols with alkali metals, nitrides, and strong reducing agents. They react with oxoacids and carboxylic acids to form esters plus water. Oxidizing agents convert them to aldehydes or ketones. Alcohols exhibit both weak acid and weak base behavior. They may initiate the polymerization of isocyanates and epoxides.

II

6.1(a)

UN 2811 6.1/PG 2

3

22-48/25-26-24/25-40-23/24/25-48/22-23-11-20

28-36/37-45-28A-36-26-36/37/39-22-16-7

KE1050000

Xn,T+,T,F

Deterioration of pure crystal is negligible after storage of /9 mo/ in amber evacuated ampuls at refrigerator temperature. /Vitamin D3/

P210-P280-P305 + P351 + P338-P337 + P313-P403 + P235

H225-H319-H373

SRP: The most favorable course of action is to use an alternative chemical product with less inherent propensity for occupational exposure or environmental contamination. Recycle any unused portion of the material for its approved use or return it to the manufacturer or supplier. Ultimate disposal of the chemical must consider: the material's impact on air quality; potential migration in soil or water; effects on animal, aquatic, and plant life; and conformance with environmental and public health regulations.

Manufacturers, packers, and distributors of drug and drug products for human use are responsible for complying with the labeling, certification, and usage requirements as prescribed by the Federal Food, Drug, and Cosmetic Act, as amended (secs 201-902, 52 Stat. 1040 et seq., as amended; 21 U.S.C. 321-392).|Vitamin D2 used as a dietary supplement in food for human consumption is generally recognized as safe when used in accordance with good manufacturing practice.|Vitamin D2 used as a nutrient and/or dietary supplement in animal drugs, feeds, and related products is generally recognized as safe when used in accordance with good manufacturing or feeding practice.

Parfitt AM; Use of Calciferol and its Metabolites and Analogs in Osteoporosis: Current Status. Drugs 36: 513-20 (1988). The rationale for the use of ergocalciferol (calciferol), calcifediol and calcitriol for the treatment of osteoporosis is reviewed.

Shows signs of decomposition when stored for a few days at room temperature. (EPA, 1998)

|Danger|H301: Toxic if swallowed [Danger Acute toxicity, oral]|P260, P264, P270, P271, P280, P284, P301+P310, P302+P352, P304+P340, P310, P312, P314, P320, P321, P322, P330, P361, P363, P403+P233, P405, and P501|H301 (99.31%): Toxic if swallowed [Danger Acute toxicity, oral]|Aggregated GHS information provided by 144 companies from 11 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.

(Non-Specific -- Medicines, n.o.s.) Move container from fire area if you can do so without risk. Spray cooling water on containers that are exposed to flames until well after fire is out. (Non-Specific -- Medicines, n.o.s.) Extinguish with dry chemical, carbon dioxide, water spray, fog, or foam. (EPA, 1998)

Excerpt from ERG Guide 154 [Substances - Toxic and/or Corrosive (Non-Combustible)]: As an immediate precautionary measure, isolate spill or leak area in all directions for at least 50 meters (150 feet) for liquids and at least 25 meters (75 feet) for solids. SPILL: Increase, in the downwind direction, as necessary, the isolation distance shown above. FIRE: If tank, rail car or tank truck is involved in a fire, ISOLATE for 800 meters (1/2 mile) in all directions; also, consider initial evacuation for 800 meters (1/2 mile) in all directions. (ERG, 2016)

(Non-Specific -- Medicines, n.o.s.) Keep unnecessary people away; isolate hazard area and deny entry. Stay upwind; keep out of low areas. Shut off ignition sources; no flares, smoking or flames in hazard area. Keep combustibles (wood, paper, oil, etc.) away from spilled material. Do not touch spilled material. Small spills: absorb with sand or other noncombustible absorbent material and place into containers for later disposal. Large spills: dike far ahead of spill for later disposal. (EPA, 1998)

For emergency situations, wear a positive pressure, pressure-demand, full facepiece self-contained breathing apparatus (SCBA) or pressure- demand supplied air respirator with escape SCBA and a fully-encapsulating, chemical resistant suit. (EPA, 1998)

Releases of CERCLA hazardous substances are subject to the release reporting requirement of CERCLA section 103, codified at 40 CFR part 302, in addition to the requirements of 40 CFR part 355. Ergocalciferol is an extremely hazardous substance (EHS) subject to reporting requirements when stored in amounts in excess of its threshold planning quantity (TPQ) of 1,000/10,000 lbs.

Neither normal nor excessively high intakes of vitamin D are associated with liver injury or liver test abnormalities. Hypervitaminosis D and vitamin D intoxication generally arise with intakes above 50,000 IU daily, but lower doses may induce toxicity in susceptible individuals such as patients with renal osteodystrophy (secondary hyperparathyroidism), and a safer upper limit of recommended intake is 10,000 IU daily. Symptoms of vitamin D intoxication are caused by hypercalcemia and can include dehydration, thirst, polyuria, anorexia, nausea, vomiting, constipation, fatigue, bone pains and muscle cramps. Complications can include renal dysfunction, nephrocalcinosis, decreased consciousness and seizures. Symptoms arise a few weeks to several months after starting excess doses of vitamin D given orally or parenterally. A common cause of hypervitaminosis D is the mislabeling of an over-the-counter or locally prepared nutritional supplement, excessive fortification of milk or foods, and inadvertent prescription or dispensing errors. In clinical descriptions of vitamin D intoxication, typical laboratory findings are hypercalcemia, increase in serum creatinine, and high 25-OH vitamin D levels (usually above 200 ng/mL or 500 nmol/L). Serum aminotransferase and bilirubin levels are typically normal, while alkaline phosphatase levels may actually be lower than normal.

The effect of calcitriol (1,25-dihydroxyvitamin D3) on the conversion of ergocalciferol (vitamin D2) to 25-hydroxyvitamin D in 20 normal subjects receiving 2 separate doses of ergocalciferol, one with and one without concomitant administration of calcitriol is described. The concurrent administration of the 2 drugs made no difference to serum calcitriol concentrations.|The effects of glutethimide therapy, 500 mg/day, on the metabolism of vitamin D in a 77 yr old female patient who had taken an overdose of vitamin D2 are reported. Hypercalcemia in this patient was associated with raised serum concentrations of total 25-hydroxyvitamin D and total 1,25-dihydroxyvitamin D. Eight days after administration of glutethimide, plasma gamma-glutamyltransferase activity rose above the upper limit of normal, peaking at 90 IU/L on days 18-22 of therapy. The plasma calcium concentration fell to within the normal range on day 13. The serum concentration of 1,25-dihydroxyvitamin D began to fall within 4 days, and after 8 days it was near the lower limit of the reference range, at 70 pmol/L. The serum concentration of total 25-hydroxyvitamin D did not change appreciably until hepatic enzymes were induced; thereafter it fell gradually. Although the 25-hydroxyvitamin D concentration remained high, the concentration of 1,25-dihydroxyvitamin D did not rise again but remained within the lower part of the normal range.|The effect of a high cholesterol diet and corticosteroids on the toxicity of vitamin D2 in rats was studied. Vitamin D2 was administered orally at the dosage of 5X10+4 to 60X10+4 IU/kg, once daily for 4 days. Animals fed cholesterol showed a decrease in mortality due to vitamin D2 treatment. Dietary cholesterol inhibited toxic responses such as a diminished growth rate following anorexia, elevated serum calcium level and calcium deposition in tissues, which were produced by a sublethal dose of vitamin D2 (20X10+4 IU/kg, once daily for 4 days). Animals pretreated with the high cholesterol diet from 2 wk before the first vitamin D2 administration showed much more symptomatic relief than those given this diet after the first vitamin D2 administration. On the other hand, dexamethasone as well as corticosterone remarkably increased the mortality due to vitamin D2. The degree of vitamin D2 toxicity, enhanced by dexamethasone, was correlated with the degree of hypercalcemia and tissue calcification. Therefore, the inhibitory effect of cholesterol is not likely to be due to activation of the cholesterol corticosterone system in the adrenal gland.|The effect of short term treatment with pharmacological doses of vitamin D2 or vitamin D3 on the serum concentration of 1,25(OH)2D metabolites was examined in epileptic patients on chronic anticonvulsant drug therapy. Nine patients were studied before and after treatment with vitamin D2 4000 IU daily for 24 wk and 10 before and after treatment with vitamin D3 in the same dose. Before treatment the serum concentrations of 1,25(OH)2D and 25(OH)D were significantly lower in epileptics than in normal subjects (p< 0.01). Vitamin D2 treatment increased the serum concentration of 1,25(OH)2D2, but a corresponding decrease in 1,25(OH)2D3 resulted in an unchanged serum concentration of total 1,25(OH)2D. The serum concentration of 25(OH)D2 and 25(OH)D increase significantly, whereas there was a small decrease in 25(OH)D3. Vitamin D3 treatment did not change the serum concentration of 1,25(OH)2D3 whereas serum 25(OH)D3 increased significantly. The correlation between the serum ratio of 1,25(OH)2D2/1,25(OH)2D3 and 25(OH)D2/25(OH)D3 estimated on vitamin D2 treated epileptic patients and normal subjects was highly significant (p< 0.01). The data indicate that the serum concentration of 1,25(OH)2D2 and 1,25(OH)2D3 are directly proportional to the amount of their precursors 25(OH)D2 and 25(OH)D3 and that the concentration of total 1,25(OH)2D is tightly regulated.|Vitamin D analogs should be administered with caution in patients receiving cardiac glycosides, because hypercalcemia in these patient may result in cardiac arrhythmias. Vitamin D analogs should also be used with caution in patients with increased sensitivity to these drugs. /Vitamin D analogs/

A plant sterol widely distributed in nature.

Vitamin D is a fat soluble vitamin important in the regulation of calcium metabolism and bone health and deficiency of which cause rickets, a disease marked by lack of mineralization of bone. Conventional doses of vitamin D are well tolerated without appreciable adverse effects. High doses of vitamin D can be toxic, leading to a constellation of signs and symptoms but not liver injury or jaundice.

Vitamins

MEDICATION (VET): ... Recommended for prophylaxis of milk fever in cows. ... Prevent atrophic rhinitis in pigs. ... Aid fracture healing in cats and dogs.|MEDICATION (VET): To be effective ... supplementation with Ca & PO4. ... Fish meals & irradiated yeast may be used as supplemental ... source. ... Diets are routinely supplemented ... 1400-1600 IU/kg. Therapy for rickets ... Level 10-20 times daily requirement, alternate days for 1 wk. /Vitamin D/|In adults and children with nutritional rickets or osteomalacia and normal GI absorption, oral administration of ... ergocalciferol daily results in normal serum calcium and phosphate concentrations in about 10 days, radiographic evidence of healing of bone within 2-4 wk, and complete healing in about 6 months. ... Diet should be corrected and, after healing has occurred, supplemental doses of ergocalciferol may be discontinued in patients with normal GI absorption. In adults with severe malabsorption and vitamin D deficiency, /daily/ dosages ... have been given to correct osteomalacia. In children with malabsorption, oral ergocalciferol dosages ... have been recommended. In vitamin D-deficient infants with tetany and rickets, calcium should be administered orally or iv to control tetany. Vitamin D deficiency is then treated orally with /a daily dose/ of ergocalciferol ... until the bones have healed, ... .|In adults with Fanconi syndrome, oral ergocalciferol .. have been given along with treatment of acidosis. In children with Fanconi syndrome oral ergocalciferol ... have been used.|For more Therapeutic Uses (Complete) data for VITAMIN D2 (11 total), please visit the HSDB record page.

... Ergocalciferol should be administered with extreme caution, if at all, to patients with impaired renal function and with extreme caution in patient with heart disease, renal stones, or arterioscleroses.|Initial signs and symptoms ... consists of weakness, fatigue, lassitude, headache, nausea, vomiting, and diarrhea. Obtundation and coma may develop. Early impairment of renal function from hypercalcemia is manifest by polyuria, polydipsia, nocturia, decreased urinary concentration ability, and proteinuria.

Both vitamin D2 & vitamin D3 are absorbed from the small intestine, although vitamin D3 may be absorbed more efficiently. The exact portion of the gut that is most effective in vitamin D absorption reflects the vehicle in which the vitamin is dissolved. Most of the vitamin appears first within chylomicrons in lymph.|The presence of bile is required for absorption of ergocalciferol and the extent of GI absorption may be decreased in patients with hepatic, biliary, or GI disease (e.g., Crohn's disease, Whipple's disease, sprue).|A longitudinal, randomized, double blind, placebo controlled study was conducted for 6 months to monitor ultraviolet B light exposure in human milk-fed infants both with and without supplemental vitamin D2, and to measure longitudinally the bone mineral content, growth, and serum concentrations of calcium, phosphorus, 25-hydroxyvitamin D3, 25-hydroxyvitamin D2, 1,25-dihydroxyvitamin D, and parathyroid hormone. Sequential sampling was performed of 46 human milk-fed white infants; 24 received 400 IU/day of vitamin D2, and 22 received placebo. An additional 12 patients were followed who received standard infant formula. 83% of patients completed a full 6 months of the study. Ultraviolet B light exposure and measurements of growth did not differ between groups. At 6 months, the human milk groups did not differ significantly in bone mineral content or serum concentrations of parathyroid hormone or 1,25-dihydroxyvitamin D, although total 25-hydroxyvitamin D values were significantly less in the unsupplemented human milk group (23.53 + or - 9.94 vs 36.96 + or - 11.86 ng/ml; p< 0.01). However, 25-hydroxyvitamin D3 serum concentrations were significantly higher in the unsupplemented human milk-fed group compared with the supplemented group (21.77 + or - 9.73 vs 11.74 + or - 10.27 ng/ml, p< 0.01) by 6 months of age. It was concluded that unsupplemented, human milk-fed infants had no evidence of vitamin D deficiency during the first 6 months of life.|A comparison was made of the ability of ergocalciferol and cholecalciferol to elevate plasma concentrations of vitamin D and 25-hydroxyvitamin D in cats. Cholecalciferol, given as an oral bolus in oil, resulted in a rapid elevation of plasma concentration of cholecalciferol followed by a rapid decline. In contrast, 25-hydroxyvitamin D concentration in plasma increased until day 3 after administration and remained elevated for a further 5 days. When 337 microg of both cholecalciferol and ergocalciferol in oil were given as an oral bolus to 10 cats, the peak plasma concentrations of cholecalciferol and ergocalciferol occurred at 8 or 12 h after administration. Peak concentrations of cholecalciferol were over twice those of ergocalciferol (570 +/- 80 vs. 264 +/- 42 nmol/l). The area under the curve 0-169 h for cholecalciferol was also more than twice that for ergocalciferol. When ergocalciferol and cholecalciferol were administered in a parenteral oil-based emulsion, higher concentrations of 25-hydroxyvitamin D3 than 25-hydroxyvitamin D2 were maintained in plasma. When both vitamins were included in the diet in the nutritional range, plasma concentrations of 25-hydroxyvitamin D2 were 0.68 of those of 25-hydroxyvitamin D3. Discrimination against ergocalciferol by cats appears to result from differences in affinity of the binding protein for the metabolites of the two forms of vitamin D. These results indicate that cats discriminate against ergocalciferol, and use it with an efficiency of 0.7 of that of cholecalciferol to maintain plasma 25-hydroxyvitamin D concentration.|Osteoporosis diminishes the quality of life in adults with cystic fibrosis (CF). Vitamin D deficiency resulting from malabsorption may be a factor in the etiology of low bone mineral density (BMD) in patients with CF. OBJECTIVE: Absorption of oral ergocalciferol (vitamin D2) and the consequent response of 25-hydroxyvitamin D in 10 adults with CF and exocrine pancreatic insufficiency was compared with that of 10 healthy control subjects. DESIGN: In this pharmacokinetic study, CF patients and control subjects were pair-matched on age, sex, and race. Each subject consumed 2500 microg oral vitamin D2 with a meal. The CF group also took pancreatic enzymes that provided > or = 80000 U lipase. Blood samples were obtained at baseline and at 5, 10, 24, 30, and 36 h after vitamin D2 consumption to measure serum vitamin D2 and 25-hydroxyvitamin D concentrations. RESULTS: Vitamin D2 concentrations in all subjects were near zero at baseline. CF patients absorbed less than one-half the amount of oral vitamin D2 that was absorbed by control subjects (P < 0.001). Absorption by the CF patients varied greatly; 2 patients absorbed virtually no vitamin D2. The rise in 25-hydroxyvitamin D in response to vitamin D2 absorption was significantly lower over time in the CF group than in the control group (P = 0.0012). CONCLUSIONS: Vitamin D2 absorption was significantly lower in CF patients than in control subjects. These results may help explain the etiology of vitamin D deficiency in CF patients, which may contribute to their low BMD.

Vitamin D ... is hydroxylated at the 25 position in liver to produce 25-hydroxy-vitamin D3 which is the major metabolite circulating in the plasma. The metabolite is further hydroxylated in the kidney to 1,25-dihydroxy-vitamin D3, the most active metabolite in initiating intestinal transport of calcium & phosphate & mobilization of mineral from bone.|A polar, biologically active metabolite of vitamin D2, 25-hydroxyergocalciferol, which is about 1.5 times more active in curing rickets in rats, has been isolated from pig plasma.|Dihydrotachysterol is a vitamin D analog that may be regaurded as a reduction product of vitamin D2 ... Dihydrotachysterol is about 1/450 as active as vitamin D in the antirachitic assay, but at high doses it is much more effective than vitamin D in mobilizing bone mineral.

19 to 48 hours (however, stored in fat deposits in body for prolonged periods).

The mechanism of action of calcitriol, the activated form of vitamin D, resembles that of the steroid and thyroid hormones. Thus, calcitriol binds to cytosolic receptors within target cells, and the receptor-hormone complex interacts with the DNA of certain genes to either enhance or inhibit their transcription. Structural analysis of the calcitriol receptor indicates that it belongs to the same supergene family as the steroid receptors. Calcitriol also appears to exert a few effects that occur too rapidly to be explained by genomic actions. /Calcitriol/|The mechanisms responsible for mobilization of bone salts have been only partially defined, and the interaction of multiple factors appears to be involved. Paradoxically, the cells responsible for bone resorption (osteoclasts) are not directly acted upon by calcitriol and do not appear to contain calcitriol receptors. Instead, calcitriol causes an increase in the number of osteoclasts available to resorb bone; this may result from an action upon myeloid hematopoietic precursor cells that are induced to differentiate toward functional osteoclasts. The cells responsible for bone formation (osteoblasts) do contain receptors, and calcitriol causes them to elaborate several proteins, including osteocalcin, a vitamin K-dependent protein that contains gamma-carboxyglutamic acid residues. The exact role of this protein is not known, but other unidentified substances are also elaborated that appear to stimulate the function of osteoclasts. In addition, calcitriol acts synergistically with gamma-interferon to increase the production of interleukin-1, a lymphokine that promotes bone resorption.

Ergocalciferol poisoning disturbs calcium metabolism and causes kidney damage. Ergocalciferol in a single acute ingestion presents no toxic hazards. Daily ingestion in excess of 5000 units/day in children or 7500 units/day in adults will produce toxic symptoms associated with hypervitaminosis D. Those with hypercalcemia are at a greater risk. (EPA, 1998)

Note: Emesis, activated charcoal, and cathartics are seldom necessary with acute ingestion unless extremely large amounts are ingested (more than 100 times the Recommended Daily Allowance for Vitamin D2). Signs and Symptoms of Acute Ergocalciferol Exposure: Signs and symptoms of acute exposure to ergocalciferol may include the following: thirst, itching, fatigue, muscular weakness, nervousness, headache, nausea, vomiting, and diarrhea. Excessive urination, kidney impairment, and hypertension (high blood pressure) may be noted. Emergency Life-Support Procedures: Acute exposure to ergocalciferol may require decontamination and life support for the victims. Emergency personnel should wear protective clothing appropriate to the type and degree of contamination. Air-purifying or supplied-air respiratory equipment should also be worn, as necessary. Rescue vehicles should carry supplies such as plastic sheeting and disposable plastic bags to assist in preventing spread of contamination. Inhalation Exposure: 1. Move victims to fresh air. Emergency personnel should avoid self-exposure to ergocalciferol. 2. Evaluate vital signs including pulse and respiratory rate, and note any trauma. If no pulse is detected, provide CPR. If not breathing, provide artificial respiration. If breathing is labored, administer oxygen or other respiratory support. 3. Obtain authorization and/or further instructions from the local hospital for administration of an antidote or performance of other invasive procedures. 4. Transport to a health care facility. Dermal/Eye Exposure: 1. Remove victims from exposure. Emergency personnel should avoid self-exposure to ergocalciferol. 2. Evaluate vital signs including pulse and respiratory rate, and note any trauma. If no pulse is detected, provide CPR. If not breathing, provide artificial respiration. If breathing is labored, administer oxygen or other respiratory support. 3. Remove and isolate contaminated clothing as soon as possible. 4. If eye exposure has occurred, eyes must be flushed with lukewarm water for at least 15 minutes. 5. Wash exposed skin areas thoroughly with water. 6. Obtain authorization and/or further instructions from the local hospital for administration of an antidote or performance of other invasive procedures. 7. Transport to a health care facility. Ingestion Exposure: 1. Evaluate vital signs including pulse and respiratory rate, and note any trauma. If no pulse is detected, provide CPR. If not breathing, provide artificial respiration. If breathing is labored, administer oxygen or other respiratory support. 2. Obtain authorization and/or further instructions from the local hospital for administration of an antidote or performance of other invasive procedures. 3. Vomiting may be induced with syrup of Ipecac. If elapsed time since ingestion of ergocalciferol is unknown or suspected to be greater than 30 minutes, do not induce vomiting and proceed to Step 4. Ipecac should not be administered to children under 6 months of age. Warning: Syrup of Ipecac should be administered only if victims are alert, have an active gag-reflex, and show no signs of impending seizure or coma. If ANY uncertainty exists, proceed to Step 4. The following dosages of Ipecac are recommended: children up to 1 year old, 10 mL (1/3 oz); children 1 to 12 years old, 15 mL (1/2 oz); adults, 30 mL (1 oz). Ambulate (walk) the victims and give large quantities of water. If vomiting has not occurred after 15 minutes, Ipecac may be readministered. Continue to ambulate and give water to the victims. If vomiting has not occurred within 15 minutes after second administration of Ipecac, administer activated charcoal. 4. Activated charcoal may be administered if victims are conscious and alert. Use 15 to 30 g (1/2 to 1 oz) for children, 50 to 100 g (1-3/4 to 3-1/2 oz) for adults, with 125 to 250 mL (1/2 to 1 cup) of water. 5. Promote excretion by administering a saline cathartic or sorbitol to conscious and alert victims. Children require 15 to 30 g (1/2 to 1 oz) of cathartic; 50 to 100 g (1-3/4 to 3-1/2 oz) is recommended for adults. 6. Transport to a health care facility. (EPA, 1998)

Emergency and supportive measures: Treat fluid loses caused by gastroenteritis with intravenous crystalloid solutions. Treat vitamin ... D induced hypercalcemia if /it/ occurs.|Recommended treatment includes the following: Hypervitaminosis D is treated by withdrawal of the vitamin, low-calcium diet, and generous fluid intake. If hypercalcemia persists, prednisone may be started. Severe hypercalcemia may be treated with calcitonin, etidronate, pamidronate, or gallium nitrate. Hypercalcemic crisis requires vigorous hydration with intravenous saline to increase calcium excretion, with or without a loop diuretic. Cardiac arrhythmias may be treated with small doses of potassium with continuous cardiac monitoring. Therapy may be reinstituted at a lower dose when serum calcium concentrations return to normal. Serum or urinary calcium levels should be obtained twice weekly after dosage changes. / Vitamin D and analogs/

/HUMAN EXPOSURE STUDIES/ There is a relationship between excess maternal vitamin D intake or extreme sensitivity to the vitamin and nonfamilial congenital supravalvular aortic stenosis. In infants, this anomaly is often found in association with other stigmata of hypercalcemia. /Vitamin D/|/HUMAN EXPOSURE STUDIES/ Serious toxicity may result from excessive ingestion of vitamin, and even as little as 1800 USP units per day in infants may lead to possible inhibition of growth. /Vitamin D/|/HUMAN EXPOSURE STUDIES/ Maternal hypercalcemia may also result in suppression of parathyroid function in the newborn with resultant hypocalcemia, tetany, and seizures. /Vitamin D/

Ergocalciferol capsules usually consist of the drug in an edible oil solution encapsulated with gelatin. Commercially available ergocalciferol solution is a clear solution of the drug in an edible vegetable oil or in propylene glycol. Ergocalciferol injection is a sterile solution of the drug in sesame oil.|Ergocalciferol is also commercially available in combination with other vitamins and minerals, analgesic-antipyretics, amino acids, infant formulas, laxatives, and protein supplements.|Parenteral: Injection (for IM use only): 12.5 mg (500,000 units) per mL, Calciferol (in oil), (Schwarz)|Ergocalciferol (calciferol; Drisdol) is pure vitamin D2. ... Available in capsules or tablets that contain 1.25 mg (50,000 USP units) each. An oral solution (8,000 units/mL) of the vitamin in propylene glycol is also available. An injection in oil (500,000 units/mL) is available for im administration. ... Dihydrotachysterol (DHT; hytakerol) is the pure crystalline compound obtained by reduction of vitamin D2 ... Available as tablets (0.125 to 0.4 mg), capsules (0.125 mg), an oral soln (0.2 mg/mL) & a soln in oil (0.2 mg/mL).|For more Formulations/Preparations (Complete) data for VITAMIN D2 (7 total), please visit the HSDB record page.

Cyclohexanol, 4-methylene-3-[(2E)-2-[(1R,3aS,7aR)-octahydro-7a-methyl-1-[(1R,2E,4R)-1,4,5-trimethyl-2-hexen-1-yl]-4H-inden-4-ylidene]ethylidene]-, (1S,3Z)-: ACTIVE|Information available in 2004 indicated that Ergocalciferol was used in the manufacture of pharmaceutical preparations in the following countries: Argentina, Australia, Austria, Brazil, Canada, Chile, Czech Republic, Denmark, Ecuador, Finland, France, Germany, Greece, Hong Kong, Ireland, Israel, Italy, Luxembourg, Malaysia, Mexico, Norway, Portugal, Romania, Slovakia, South Africa, Spain, Switzerland, Thailand, United Kingdom, USA (1,2)|International & USP units of vitamin D are equivalent in activity to 0.025 ug of crystalline vitamin D2.|Ergosterol, which is present in plants, is provitamin for vitamin D2 (calciferol). ... Vitamin D2 is active constituent in a number of commercial vitamin preparations as well as in irradiated bread & irradiated milk.|Vitamin D2 crystals have a potency of 40 units of vitamin D (USP)/ug.|Because of vitamin D2's sensitivity to oxygen and light, USP allows traces of antioxidants in crystalline compound.

HPLC separation and identification of vitamins D2 and D3 in presence of fat soluble vitamins in dosage forms. As little as 2 ng each of vitamin D2 & D3 can be separated & identified.|A GC method is described for the determination of vitamin D2 (ergocalciferol) in capsules & injections.|GLC procedure to determine vitamin D2 & D3 in infant feedings.|A GLC procedure for determination of vitamin D2.|For more Analytic Laboratory Methods (Complete) data for VITAMIN D2 (15 total), please visit the HSDB record page.

Determination of vitamin D2 & D3 in milk by using reverse phase HPLC.