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Description Of Calcitirol

Calcitriol should be discontinued if symptoms become severe. Mild pain at the injection site has been noted occasionally as an injection site reaction. Since vitamin D increases the absorption of phosphorus, calcitriol can cause hyperphosphatemia, especially in patients with renal failure. Elevated serum creatinine levels have been observed in about 17% of patients. Calcitriol dosage adjustments may be required for patients receiving aluminum-containing antacids for the treatment of hyperphosphatemia.Calcitriol is a synthetic vitamin D analog which is active in the regulation of the absorption of calcium from the gastrointestinal tract and its utilization in the body. Calcitriol is available as capsules containing 0.25 mcg or 0.5 mcg Calcitriol and as an oral solution containing 1 mcg/mL of Calcitriol. All dosage forms contain butylated hydroxyanisole (BHA) and butylated hydroxytoluene (BHT) as antioxidants. The capsules contain a fractionated triglyceride of coconut oil, and the oral solution contains a fractionated triglyceride of palm seed oil.
Calcitriol is a white, crystalline compound which occurs naturally in ...
... humans. It has a calculated molecular weight of 416.65 and is soluble in organic solvents but relatively insoluble in water. Calcitriol is 9,10- seco(5Z,7E)-5,7,10(19)-cholestatriene-1a, 3ß, 25-triol .The initial transformation of vitamin D3 is catalyzed by a vitamin D3-25-hydroxylase enzyme (25-OHase) present in the liver, and the product of this reaction is 25-hydroxyvitamin D3 [25-(OH)D3]. Hydroxylation of 25-(OH)D3 occurs in the mitochondria of kidney tissue, activated by the renal 25-hydroxyvitamin D3-1 alpha-hydroxylase (alpha-OHase), to produce 1,25-(OH)2D3 (Calcitriol), the active form of vitamin D3. A Calcitriol receptor-binding protein appears to exist in the mucosa of human intestine. Additional evidence suggests that Calcitriol may also act on the kidney and the parathyroid glands. Calcitriol is the most active known form of vitamin D3 in stimulating intestinal calcium transport. In acutely uremic rats Calcitriol has been shown to stimulate intestinal calcium absorption.
Calcitriol treatment is not associated with an accelerated rate of renal function deterioration. No radiographic evidence of extraskeletal calcification has been found in predialysis patients following treatment. The duration of pharmacologic activity of a single dose of Calcitriol is about 3 to 5 days.Calcitriol is rapidly absorbed from the intestine. Peak serum concentrations (above basal values) were reached within 3 to 6 hours following oral administration of single doses of 0.25 to 1.0 mcg of Calcitriol. Following a single oral dose of 0.5 mcg, mean serum concentrations of Calcitriol rose from a baseline value of 40.0±4.4 (SD) pg/mL to 60.0±4.4 pg/mL at 2 hours, and declined to 53.0±6.9 at 4 hours, 50±7.0 at 8 hours, 44±4.6 at 12 hours, and 41.5±5.1 at 24 hours.Calcitriol is approximately 99.9% bound in blood. Calcitriol and other vitamin D metabolites are transported in blood, by an alpha-globulin vitamin D binding protein. There is evidence that maternal Calcitriol may enter the fetal circulation. Calcitriol is transferred into human breast milk at low levels (ie, 2.2±0.1 pg/mL).
Calcitriol is indicated in the management of secondary hyperparathyroidism and resultant metabolic bone disease in patients with moderate to severe chronic renal failure (Ccr 15 to 55 mL/min) not yet on dialysis. Calcitriol is the most potent metabolite of vitamin D available. The administration of Calcitriol to patients in excess of their daily requirements can cause hypercalcemia, hypercalciuria, and hyperphosphatemia. Therefore, pharmacologic doses of vitamin D and its derivatives should be withheld during Calcitriol treatment to avoid possible additive effects and hypercalcemia.Calcitriol increases inorganic phosphate levels in serum. While this is desirable in patients with hypophosphatemia, caution is called for in patients with renal failure because of the danger of ectopic calcification. A nonaluminum phosphate-binding compound and a low-phosphate diet should be used to control serum phosphorus levels in patients undergoing dialysis.
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