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Actions of Calcibest in details
Pharmacology: Calcibest is the active form of vitamin D3 (cholecalciferol). The natural or endogenous supply of vitamin D in man mainly depends on ultraviolet light for conversion of 7-dehydrocholesterol to vitamin D3 in the skin. Vitamin D3 must be metabolically activated in the liver and the kidney before it is fully active on its target tissues. The initial transformation is catalyzed by a vitamin D3-25-hydroxylase enzyme present in the liver, and the product of this reaction is 25-(OH)D3 (calcifediol). The latter undergoes hydroxylation in the mitochondria of kidney tissue and this reaction is activated by the renal 25-hydroxyvitamin D3-1-α-hydroxylase to produce 1,25-(OH)2D3(Calcibest), the active form of vitamin D3.
The known sites of action of Calcibest are intestine, bone, kidney and parathyroid gland. Calcibest is the most active known form of vitamin D3 in stimulating intestinal calcium transport. In acutely uremic rats, Calcibest has been shown to stimulate intestinal calcium absorption. In bone, Calcibest, in conjunction with parathyroid hormone (PTH), stimulates resorption of calcium; and in the kidney, Calcibest increases the tubular reabsorption of calcium. In vitro and in vivo studies have shown that Calcibest directly suppresses secretion and synthesis of PTH. A vitamin D-resistant state may exist in uremic patients because of the failure of the kidney to adequately convert precursors to the active compound, Calcibest.
Calcibest when administered by bolus injection is rapidly available in the bloodstream. Vitamin D metabolites are known to be transported in blood, bound to specific plasma proteins. The pharmacologic activity of an administered dose of Calcibest is about 3-5 days. Two metabolic pathways for Calcibest have been identified, conversion to 1,24,25-(OH)3D3 and to calcitroic acid.
Toxicology: Preclinical Safety Data: Carcinogenesis, Mutagenesis, Impairment of Fertility: Long-term studies in animals have not been performed to evaluate the carcinogenic potential of Calcibest. There was no evidence of mutagenicity as studied by the Ames method. No significant effects of Calcibest on fertility were reported using oral Calcibest.
How should I take Calcibest?
Take this medication exactly as prescribed by your doctor. Do not take it in larger amounts or for longer than recommended. Follow the directions on your prescription label.
Your doctor may occasionally change your dose to make sure you get the best results from this medication.
Measure liquid medicine with a special dose-measuring spoon or cup, not a regular table spoon. If you do not have a dose-measuring device, ask your pharmacist for one.
Drink plenty of fluids unless your doctor has told you to restrict your fluid intake.
Call your doctor if you have ongoing vomiting or diarrhea, or if you are sweating more than usual. You can easily become dehydrated while taking this medication, which can lead to a serious electrolyte imbalance.
To be sure this medicine is helping your condition and is not causing harmful effects, your blood will need to be tested often. Visit your doctor regularly.
Calcibest is only part of a complete program of treatment that may also include a special diet. It is very important to follow the diet plan created for you by your doctor or nutrition counselor. You should become very familiar with the list of foods you must eat or avoid to help control your condition.
If you need to be on bed-rest or have any type of surgery, your dose or testing needs may change. Follow your doctor's instructions.
Store at room temperature away from moisture, light, and heat.
Use exactly as prescribed by your doctor. Do not use in larger or smaller amounts or for longer than recommended. Follow the directions on your prescription label.
Calcibest topical is usually applied once in the morning and once in the evening. Follow your doctor's instructions.
Do not share this medication with other people, even if they have the same symptoms you have.
Wash your hands before and after applying this medicine.
Apply a thin layer of the medication and rub it in completely.
Do not cover treated skin areas unless your doctor has told you to.
Calcibest topical is for use only on areas of psoriasis. Avoid getting it on healthy skin areas.
Calcibest topical should not be applied to the face or the vaginal area.
Store at room temperature away from moisture and heat. Do not allow the medicine to freeze.
Man's natural supply of vitamin D depends mainly on exposure to the ultraviolet rays of the sun for conversion of 7-dehydrocholesterol in the skin to vitamin D3 (cholecalciferol). Vitamin D3 must be metabolically activated in the liver and the kidney before it is fully active as a regulator of calcium and phosphorus metabolism at target tissues. 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 (Calcibest), the active form of vitamin D3. Endogenous synthesis and catabolism of Calcibest, as well as physiological control mechanisms affecting these processes, play a critical role regulating the serum level of Calcibest. Physiological daily production is normally 0.5 to 1.0 mcg and is somewhat higher during periods of increased bone synthesis (eg, growth or pregnancy).
The two known sites of action of Calcibest are intestine and bone. A Calcibest receptor-binding protein appears to exist in the mucosa of human intestine. Additional evidence suggests that Calcibest may also act on the kidney and the parathyroid glands. Calcibest is the most active known form of vitamin D3 in stimulating intestinal calcium transport. In acutely uremic rats Calcibest has been shown to stimulate intestinal calcium absorption. The kidneys of uremic patients cannot adequately synthesize Calcibest, the active hormone formed from precursor vitamin D. Resultant hypocalcemia and secondary hyperparathyroidism are a major cause of the metabolic bone disease of renal failure. However, other bone-toxic substances which accumulate in uremia (eg, aluminum) may also contribute.
The beneficial effect of Calcibest in renal osteodystrophy appears to result from correction of hypocalcemia and secondary hyperparathyroidism. It is uncertain whether Calcibest produces other independent beneficial effects. Calcibest 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 Calcibest is about 3 to 5 days.
Calcibest 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 Calcibest. Following a single oral dose of 0.5 mcg, mean serum concentrations of Calcibest 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.
Following multiple-dose administration, serum Calcibest levels reached steady-state within 7 days.
Calcibest is approximately 99.9% bound in blood. Calcibest and other vitamin D metabolites are transported in blood, by an alpha-globulin vitamin D binding protein. There is evidence that maternal Calcibest may enter the fetal circulation. Calcibest is transferred into human breast milk at low levels (ie, 2.2±0.1 pg/mL).
In vivo and in vitro studies indicate the presence of two pathways of metabolism for Calcibest. The first pathway involves the 24-hydroxylase as the first step in catabolism of Calcibest. There is definite evidence of 24-hydroxylase activity in the kidney; this enzyme is also present in many target tissues which possess the vitamin D receptor such as the intestine. The end product of this pathway is a side chain shortened metabolite, calcitroic acid. The second pathway involves the conversion of Calcibest via the stepwise hydroxylation of carbon-26 and carbon-23, and cyclization to yield ultimately 1α, 25R(OH)2-26, 23S-lactone D3. The lactone appears to be the major metabolite circulating in humans, with mean serum concentrations of 131±17 pg/mL. In addition, several other metabolites of Calcibest have been identified: 1α, 25(OH)2-24-oxo-D3; 1α, 23,25(OH)3-24-oxo-D3; 1α, 24R,25(OH)3D3; 1α, 25S,26(OH)3D3; 1α, 25(OH)2-23-oxo-D3; 1α, 25R,26(OH)3-23-oxo-D3; 1α, (OH)24,25,26,27-tetranor-COOH-D3.
Enterohepatic recycling and biliary excretion of Calcibest occur. The metabolites of Calcibest are excreted primarily in feces. Following intravenous administration of radiolabeled Calcibest in normal subjects, approximately 27% and 7% of the radioactivity appeared in the feces and urine, respectively, within 24 hours. When a 1-mcg oral dose of radiolabeled Calcibest was administered to normal subjects, approximately 10% of the total radioactivity appeared in urine within 24 hours. Cumulative excretion of radioactivity on the sixth day following intravenous administration of radiolabeled Calcibest averaged 16% in urine and 49% in feces. The elimination half-life of Calcibest in serum after single oral doses is about 5 to 8 hours in normal subjects.
The steady-state pharmacokinetics of oral Calcibest were determined in a small group of pediatric patients (age range: 1.8 to 16 years) undergoing peritoneal dialysis. Calcibest was administered for 2 months at an average dose of 10.2 ng/kg (SD 5.5 ng/kg). In this pediatric population, mean Cmax was 116 pmol/L, mean serum half-life was 27.4 hours, and mean clearance was 15.3 mL/hr/kg.1
No studies have examined the pharmacokinetics of Calcibest in geriatric patients.
Controlled studies examining the influence of gender on Calcibest have not been conducted.
Controlled studies examining the influence of hepatic disease on Calcibest have not been conducted.
Lower predose and peak Calcibest levels in serum were observed in patients with nephrotic syndrome and in patients undergoing hemodialysis compared with healthy subjects. The elimination half-life of Calcibest increased by at least twofold in chronic renal failure and hemodialysis patients compared with healthy subjects. Peak serum levels in patients with nephrotic syndrome were reached in 4 hours. For patients requiring hemodialysis peak serum levels were reached in 8 to 12 hours; half-lives were estimated to be 16.2 and 21.9 hours, respectively.
- DailyMed. "CALCITRIOL: DailyMed provides trustworthy information about marketed drugs in the United States. DailyMed is the official provider of FDA label information (package inserts).". https://dailymed.nlm.nih.gov/dailyme... (accessed September 17, 2018).
- NCIt. "Calcitriol: NCI Thesaurus (NCIt) provides reference terminology for many systems. It covers vocabulary for clinical care, translational and basic research, and public information and administrative activities.". https://ncit.nci.nih.gov/ncitbrowser... (accessed September 17, 2018).
- EPA DSStox. "Calcitriol: DSSTox provides a high quality public chemistry resource for supporting improved predictive toxicology.". https://comptox.epa.gov/dashboard/ds... (accessed September 17, 2018).
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Information checked by Dr. Sachin Kumar, MD Pharmacology