The physiologically active form of vitamin D. It is formed primarily in the kidney by enzymatic hydroxylation of 25-hydroxycholecalciferol (CALCIFEDIOL). Its production is stimulated by low blood calcium levels and parathyroid hormone. Calcitriol increases intestinal absorption of calcium and phosphorus, and in concert with parathyroid hormone increases bone resorption.
Proteins, usually found in the cytoplasm, that specifically bind calcitriol, migrate to the nucleus, and regulate transcription of specific segments of DNA with the participation of D receptor interacting proteins (called DRIP). Vitamin D is converted in the liver and kidney to calcitriol and ultimately acts through these receptors.
Agents that increase calcium influx into calcium channels of excitable tissues. This causes vasoconstriction in VASCULAR SMOOTH MUSCLE and/or CARDIAC MUSCLE cells as well as stimulation of insulin release from pancreatic islets. Therefore, tissue-selective calcium agonists have the potential to combat cardiac failure and endocrinological disorders. They have been used primarily in experimental studies in cell and tissue culture.
Abnormally elevated PARATHYROID HORMONE secretion as a response to HYPOCALCEMIA. It is caused by chronic KIDNEY FAILURE or other abnormalities in the controls of bone and mineral metabolism, leading to various BONE DISEASES, such as RENAL OSTEODYSTROPHY.
A polypeptide hormone (84 amino acid residues) secreted by the PARATHYROID GLANDS which performs the essential role of maintaining intracellular CALCIUM levels in the body. Parathyroid hormone increases intracellular calcium by promoting the release of CALCIUM from BONE, increases the intestinal absorption of calcium, increases the renal tubular reabsorption of calcium, and increases the renal excretion of phosphates.
Derivatives of ERGOSTEROL formed by ULTRAVIOLET RAYS breaking of the C9-C10 bond. They differ from CHOLECALCIFEROL in having a double bond between C22 and C23 and a methyl group at C24.
Organic substances that are required in small amounts for maintenance and growth, but which cannot be manufactured by the human body.
Two pairs of small oval-shaped glands located in the front and the base of the NECK and adjacent to the two lobes of THYROID GLAND. They secrete PARATHYROID HORMONE that regulates the balance of CALCIUM; PHOSPHORUS; and MAGNESIUM in the body.
Abnormally high level of calcium in the blood.
A non-metal element that has the atomic symbol P, atomic number 15, and atomic weight 31. It is an essential element that takes part in a broad variety of biochemical reactions.
A vitamin that includes both CHOLECALCIFEROLS and ERGOCALCIFEROLS, which have the common effect of preventing or curing RICKETS in animals. It can also be viewed as a hormone since it can be formed in SKIN by action of ULTRAVIOLET RAYS upon the precursors, 7-dehydrocholesterol and ERGOSTEROL, and acts on VITAMIN D RECEPTORS to regulate CALCIUM in opposition to PARATHYROID HORMONE.
Reduction of the blood calcium below normal. Manifestations include hyperactive deep tendon reflexes, Chvostek's sign, muscle and abdominal cramps, and carpopedal spasm. (Dorland, 27th ed)
A basic element found in nearly all organized tissues. It is a member of the alkaline earth family of metals with the atomic symbol Ca, atomic number 20, and atomic weight 40. Calcium is the most abundant mineral in the body and combines with phosphorus to form calcium phosphate in the bones and teeth. It is essential for the normal functioning of nerves and muscles and plays a role in blood coagulation (as factor IV) and in many enzymatic processes.
Decalcification of bone or abnormal bone development due to chronic KIDNEY DISEASES, in which 1,25-DIHYDROXYVITAMIN D3 synthesis by the kidneys is impaired, leading to reduced negative feedback on PARATHYROID HORMONE. The resulting SECONDARY HYPERPARATHYROIDISM eventually leads to bone disorders.
A clinical syndrome associated with the retention of renal waste products or uremic toxins in the blood. It is usually the result of RENAL INSUFFICIENCY. Most uremic toxins are end products of protein or nitrogen CATABOLISM, such as UREA or CREATININE. Severe uremia can lead to multiple organ dysfunctions with a constellation of symptoms.
A mitochondrial cytochrome P450 enzyme that catalyzes the 1-alpha-hydroxylation of 25-hydroxyvitamin D3 (also known as 25-hydroxycholecalciferol) in the presence of molecular oxygen and NADPH-FERRIHEMOPROTEIN REDUCTASE. This enzyme, encoded by CYP27B1 gene, converts 25-hydroxyvitamin D3 to 1-alpha,25-dihydroxyvitamin D3 which is the active form of VITAMIN D in regulating bone growth and calcium metabolism. This enzyme is also active on plant 25-hydroxyvitamin D2 (ergocalciferol).
A condition of abnormally elevated output of PARATHYROID HORMONE (or PTH) triggering responses that increase blood CALCIUM. It is characterized by HYPERCALCEMIA and BONE RESORPTION, eventually leading to bone diseases. PRIMARY HYPERPARATHYROIDISM is caused by parathyroid HYPERPLASIA or PARATHYROID NEOPLASMS. SECONDARY HYPERPARATHYROIDISM is increased PTH secretion in response to HYPOCALCEMIA, usually caused by chronic KIDNEY DISEASES.
Cytochrome P-450 monooxygenases (MIXED FUNCTION OXYGENASES) that are important in steroid biosynthesis and metabolism.
The major circulating metabolite of VITAMIN D3. It is produced in the LIVER and is the best indicator of the body's vitamin D stores. It is effective in the treatment of RICKETS and OSTEOMALACIA, both in azotemic and non-azotemic patients. Calcifediol also has mineralizing properties.
The geographic designation for states bordering on or located in the Pacific Ocean. The states so designated are Alaska, California, Hawaii, Oregon, and Washington. (U.S. Geologic Survey telephone communication)
A DNA sequence that is found in the promoter region of vitamin D regulated genes. Vitamin D receptor (RECEPTOR, CALCITRIOL) binds to and regulates the activity of genes containing this element.
Inorganic salts of phosphoric acid.
Derivative of 7-dehydroxycholesterol formed by ULTRAVIOLET RAYS breaking of the C9-C10 bond. It differs from ERGOCALCIFEROL in having a single bond between C22 and C23 and lacking a methyl group at C24.
A condition caused by a deficiency of PARATHYROID HORMONE (or PTH). It is characterized by HYPOCALCEMIA and hyperphosphatemia. Hypocalcemia leads to TETANY. The acquired form is due to removal or injuries to the PARATHYROID GLANDS. The congenital form is due to mutations of genes, such as TBX1; (see DIGEORGE SYNDROME); CASR encoding CALCIUM-SENSING RECEPTOR; or PTH encoding parathyroid hormone.
Disorder caused by an interruption of the mineralization of organic bone matrix leading to bone softening, bone pain, and weakness. It is the adult form of rickets resulting from disruption of VITAMIN D; PHOSPHORUS; or CALCIUM homeostasis.
Therapy for the insufficient cleansing of the BLOOD by the kidneys based on dialysis and including hemodialysis, PERITONEAL DIALYSIS, and HEMODIAFILTRATION.
Excision of one or more of the parathyroid glands.
Phosphorus used in foods or obtained from food. This element is a major intracellular component which plays an important role in many biochemical pathways relating to normal physiological functions. High concentrations of dietary phosphorus can cause nephrocalcinosis which is associated with impaired kidney function. Low concentrations of dietary phosphorus cause an increase in calcitriol in the blood and osteoporosis.
Disorders caused by interruption of BONE MINERALIZATION manifesting as OSTEOMALACIA in adults and characteristic deformities in infancy and childhood due to disturbances in normal BONE FORMATION. The mineralization process may be interrupted by disruption of VITAMIN D; PHOSPHORUS; or CALCIUM homeostasis, resulting from dietary deficiencies, or acquired, or inherited metabolic, or hormonal disturbances.
An inherited condition of abnormally low serum levels of PHOSPHATES (below 1 mg/liter) which can occur in a number of genetic diseases with defective reabsorption of inorganic phosphorus by the PROXIMAL RENAL TUBULES. This leads to phosphaturia, HYPOPHOSPHATEMIA, and disturbances of cellular and organ functions such as those in X-LINKED HYPOPHOSPHATEMIC RICKETS; OSTEOMALACIA; and FANCONI SYNDROME.
A condition of an abnormally low level of PHOSPHATES in the blood.
Carbonic acid calcium salt (CaCO3). An odorless, tasteless powder or crystal that occurs in nature. It is used therapeutically as a phosphate buffer in hemodialysis patients and as a calcium supplement.
A specialized CONNECTIVE TISSUE that is the main constituent of the SKELETON. The principle cellular component of bone is comprised of OSTEOBLASTS; OSTEOCYTES; and OSTEOCLASTS, while FIBRILLAR COLLAGENS and hydroxyapatite crystals form the BONE MATRIX.
Antihistamine drug now withdrawn from the market in many countries because of rare but potentially fatal side effects.
A sulfanilamide that is used as an anti-infective agent.
Vitamin K-dependent calcium-binding protein synthesized by OSTEOBLASTS and found primarily in BONES. Serum osteocalcin measurements provide a noninvasive specific marker of bone metabolism. The protein contains three residues of the amino acid gamma-carboxyglutamic acid (Gla), which, in the presence of CALCIUM, promotes binding to HYDROXYAPATITE and subsequent accumulation in BONE MATRIX.
An enzyme that catalyzes the conversion of an orthophosphoric monoester and water to an alcohol and orthophosphate. EC
A hereditary disorder characterized by HYPOPHOSPHATEMIA; RICKETS; OSTEOMALACIA; renal defects in phosphate reabsorption and vitamin D metabolism; and growth retardation. Autosomal and X-linked dominant and recessive variants have been reported.
The giving of drugs, chemicals, or other substances by mouth.
The end-stage of CHRONIC RENAL INSUFFICIENCY. It is characterized by the severe irreversible kidney damage (as measured by the level of PROTEINURIA) and the reduction in GLOMERULAR FILTRATION RATE to less than 15 ml per min (Kidney Foundation: Kidney Disease Outcome Quality Initiative, 2002). These patients generally require HEMODIALYSIS or KIDNEY TRANSPLANTATION.
A calbindin protein found in many mammalian tissues, including the UTERUS, PLACENTA, BONE, PITUITARY GLAND, and KIDNEYS. In intestinal ENTEROCYTES it mediates intracellular calcium transport from apical to basolateral membranes via calcium binding at two EF-HAND MOTIFS. Expression is regulated in some tissues by VITAMIN D.
An NAPH-dependent cytochrome P450 enzyme that catalyzes the oxidation of the side chain of sterol intermediates such as the 27-hydroxylation of 5-beta-cholestane-3-alpha,7-alpha,12-alpha-triol.
A class of G-protein-coupled receptors that react to varying extracellular CALCIUM levels. Calcium-sensing receptors in the PARATHYROID GLANDS play an important role in the maintenance of calcium HOMEOSTASIS by regulating the release of PARATHYROID HORMONE. They differ from INTRACELLULAR CALCIUM-SENSING PROTEINS which sense intracellular calcium levels.
A nutritional condition produced by a deficiency of VITAMIN D in the diet, insufficient production of vitamin D in the skin, inadequate absorption of vitamin D from the diet, or abnormal conversion of vitamin D to its bioactive metabolites. It is manifested clinically as RICKETS in children and OSTEOMALACIA in adults. (From Cecil Textbook of Medicine, 19th ed, p1406)
Catalyzes reversibly the oxidation of hydroxyl groups of prostaglandins.
9,10-Secoergosta-5,7,10(19),22-tetraene-3,25-diol. Biologically active metabolite of vitamin D2 which is more active in curing rickets than its parent. The compound is believed to attach to the same receptor as vitamin D2 and 25-hydroxyvitamin D3.
Hydroxy analogs of vitamin D 3; (CHOLECALCIFEROL); including CALCIFEDIOL; CALCITRIOL; and 24,25-DIHYDROXYVITAMIN D 3.
Cholecalciferols substituted with two hydroxy groups in any position.
Administration of high doses of pharmaceuticals over short periods of time.
Tumors or cancer of the PROSTATE.
The relationship between the dose of an administered drug and the response of the organism to the drug.
A family of small polypeptide growth factors that share several common features including a strong affinity for HEPARIN, and a central barrel-shaped core region of 140 amino acids that is highly homologous between family members. Although originally studied as proteins that stimulate the growth of fibroblasts this distinction is no longer a requirement for membership in the fibroblast growth factor family.
The calcium salt of gluconic acid. The compound has a variety of uses, including its use as a calcium replenisher in hypocalcemic states.
Disorders in the processing of phosphorus in the body: its absorption, transport, storage, and utilization.
Calcium-binding proteins that are found in DISTAL KIDNEY TUBULES, INTESTINES, BRAIN, and other tissues where they bind, buffer and transport cytoplasmic calcium. Calbindins possess a variable number of EF-HAND MOTIFS which contain calcium-binding sites. Some isoforms are regulated by VITAMIN D.
A diphosphonate which affects calcium metabolism. It inhibits ectopic calcification and slows down bone resorption and bone turnover.
Devices which can substitute for normally functioning KIDNEYS in removing components from the blood by DIALYSIS that are normally eliminated in the URINE.
Injections made into a vein for therapeutic or experimental purposes.
Protein of the annexin family with a probable role in exocytotic and endocytotic membrane events.
Calcium compounds used as food supplements or in food to supply the body with calcium. Dietary calcium is needed during growth for bone development and for maintenance of skeletal integrity later in life to prevent osteoporosis.
Bone loss due to osteoclastic activity.
Excision of kidney.
A carrier or inert medium used as a solvent (or diluent) in which the medicinally active agent is formulated and or administered. (Dictionary of Pharmacy, 1986)
The action of a drug in promoting or enhancing the effectiveness of another drug.
Injections introduced directly into localized lesions.
An anti-inflammatory 9-fluoro-glucocorticoid.
A nonhormonal medication for the treatment of postmenopausal osteoporosis in women. This drug builds healthy bone, restoring some of the bone loss as a result of osteoporosis.
Conditions in which the KIDNEYS perform below the normal level for more than three months. Chronic kidney insufficiency is classified by five stages according to the decline in GLOMERULAR FILTRATION RATE and the degree of kidney damage (as measured by the level of PROTEINURIA). The most severe form is the end-stage renal disease (CHRONIC KIDNEY FAILURE). (Kidney Foundation: Kidney Disease Outcome Quality Initiative, 2002)
Small organic molecules that act as allosteric activators of the calcium sensing receptor (CaSR) in the PARATHYROID GLANDS and other tissues. They lower the threshold for CaSR activation by extracellular calcium ions and diminish PARATHYROID HORMONE (PTH) release from parathyroid cells.

Vitamin D regulates human ectocervical epithelial cell proliferation and insulin-like growth factor-binding protein-3 level. (1/2474)

The differentiation status of the cervical epithelial cell has an important influence on responsiveness to estrogens and progestins. Several agents, including glucocorticoids and retinoids, are known to influence cervical cell differentiation. However, the effects of vitamin D have not been examined. Vitamin D is known to regulate cell proliferation and gene expression in a variety of epithelial cells. In the present study we investigated the ability of 1alpha25-dihydroxyvitamin D3 (D3) to regulate cell proliferation and expression of insulin-like growth factor-binding protein-3 (IGFBP-3) in human ectocervical epithelial cells. ECE16-1, a non-tumorigenic cervical cell line, was growth inhibited by D3 with maximal inhibition at 1000 nM. IGFBP-3 levels increased in parallel with the growth inhibition. IGFBP-3 levels were half-maximally increased at approximately 10-100 nM and maximally increased (10- to 30-fold) at 1000 nM D3. These studies show that vitamin D regulates cervical epithelial cell gene regulation and cell proliferation and that IGFBP-3 may be an in vivo marker of vitamin D action in the cervix.  (+info)

22-oxacalcitriol suppresses secondary hyperparathyroidism without inducing low bone turnover in dogs with renal failure. (2/2474)

BACKGROUND: Calcitriol therapy suppresses serum levels of parathyroid hormone (PTH) in patients with renal failure but has several drawbacks, including hypercalcemia and/or marked suppression of bone turnover, which may lead to adynamic bone disease. A new vitamin D analogue, 22-oxacalcitriol (OCT), has been shown to have promising characteristics. This study was undertaken to determine the effects of OCT on serum PTH levels and bone turnover in states of normal or impaired renal function. METHODS: Sixty dogs were either nephrectomized (Nx, N = 38) or sham-operated (Sham, N = 22). The animals received supplemental phosphate to enhance PTH secretion. Fourteen weeks after the start of phosphate supplementation, half of the Nx and Sham dogs received doses of OCT (three times per week); the other half were given vehicle for 60 weeks. Thereafter, the treatment modalities for a subset of animals were crossed over for an additional eight months. Biochemical and hormonal indices of calcium and bone metabolism were measured throughout the study, and bone biopsies were done at baseline, 60 weeks after OCT or vehicle treatment, and at the end of the crossover period. RESULTS: In Nx dogs, OCT significantly decreased serum PTH levels soon after the induction of renal insufficiency. In long-standing secondary hyperparathyroidism, OCT (0.03 microg/kg) stabilized serum PTH levels during the first months. Serum PTH levels rose thereafter, but the rise was less pronounced compared with baseline than the rise seen in Nx control. These effects were accompanied by episodes of hypercalcemia and hyperphosphatemia. In animals with normal renal function, OCT induced a transient decrease in serum PTH levels at a dose of 0.1 microg/kg, which was not sustained with lowering of the doses. In Nx dogs, OCT reversed abnormal bone formation, such as woven osteoid and fibrosis, but did not significantly alter the level of bone turnover. In addition, OCT improved mineralization lag time, (that is, the rate at which osteoid mineralizes) in both Nx and Sham dogs. CONCLUSIONS: These results indicate that even though OCT does not completely prevent the occurrence of hypercalcemia in experimental dogs with renal insufficiency, it may be of use in the management of secondary hyperparathyroidism because it does not induce low bone turnover and, therefore, does not increase the risk of adynamic bone disease.  (+info)

Serum levels of 1,25-dihydroxyvitamin D, 24,25-dihydroxyvitamin D, and 25-hydroxyvitamin D in nondialyzed patients with chronic renal failure. (3/2474)

BACKGROUND: In patients with chronic renal failure (CRF), abnormalities in vitamin D metabolism are known to be present, and several factors could contribute to the abnormalities. METHODS: We measured serum levels of three vitamin D metabolites, 1,25(OH)2D, 24, 25(OH)2D and 25(OH)D, and analyzed factors affecting their levels in 76 nondialyzed patients with CRF (serum creatinine> 1.6 and < 9.0 mg/dl), 37 of whom had diabetes mellitus (DM-CRF) and 39 of whom were nondiabetic (nonDM-CRF). RESULTS: Serum levels of 1,25(OH)2D were positively correlated with estimated creatinine clearance (CCr; r = 0.429; P < 0.0001), and levels of 24,25(OH)2D were weakly correlated with CCr (r = 0.252, P < 0.05); no correlation was noted for 25(OH)D. Serum levels of all three vitamin D metabolites were significantly and positively correlated with serum albumin. Although there were no significant differences in age, sex, estimated CCr, calcium and phosphate between DM-CRF and nonDM-CRF, all three vitamin D metabolites were significantly lower in DM-CRF than in nonDM-CRF. To analyze factors influencing vitamin D metabolite levels, we performed multiple regression analyses. Serum 25(OH)D levels were significantly and independently associated with serum albumin, presence of DM and serum phosphate (R2 = 0.599; P < 0.0001). 24,25(OH)2D levels were significantly and strongly associated with 25(OH)D (beta = 0.772; R2 = 0.446; P < 0.0001). Serum 1,25(OH)2D levels were significantly associated only with estimated CCr (R2 = 0. 409; P < 0.0001). CONCLUSIONS: These results suggest that hypoalbuminemia and the presence of DM independently affect serum 25(OH)D levels, probably via diabetic nephropathy and poor nutritional status associated with diabetes, and that 25(OH)D is actively catalyzed to 24,25(OH)2D in CRF, probably largely via extrarenal 24-hydroxylase. Serum levels of 1,25(OH)2D were significantly affected by the degree of renal failure. Thus, this study indicates that patients with CRF, particularly those with DM, should receive supplements containing the active form of vitamin D prior to dialysis.  (+info)

1,25-Dihydroxyvitamin D3 enhances the susceptibility of breast cancer cells to doxorubicin-induced oxidative damage. (4/2474)

1,25-Dihydroxyvitamin D3 (1,25(OH)2D3), the hormonal form of vitamin D, has anticancer activity in vivo and in vitro. Doxorubicin exerts its cytotoxic effect on tumor cells mainly by two mechanisms: (a) generation of reactive oxygen species (ROS); and (b) inhibition of topoisomerase II. We studied the combined cytotoxic action of 1,25(OH)2D3 and doxorubicin on MCF-7 breast cancer cells. Pretreatement with 1,25(OH)2D3 resulted in enhanced cytotoxicity of doxorubicin. The average enhancing effect after a 72-h pretreatment with 1,25(OH)2D3 (10 nM) followed by a 24-h treatment with 1 microg/ml doxorubicin was 74+/-9% (mean +/- SE). Under these experimental conditions, 1,25(OH)2D3 on its own did not affect cell number or viability. 1,25(OH)2D3 also enhanced the cytotoxic activity of another ROS generating quinone, menadione, but did not affect cytotoxicity induced by the topoisomerase inhibitor etoposide. The antioxidant N-acetylcysteine slightly reduced the cytotoxic activity of doxorubicin but had a marked protective effect against the combined action of 1,25(OH)2D3 and doxorubicin. These results indicate that ROS are involved in the interaction between 1,25(OH)2D3 and doxorubicin. 1,25(OH)2D3 also increased doxorubicin cytotoxicity in primary cultures of rat cardiomyocytes. Treatment of MCF-7 cells with 1,25(OH)2D3 alone markedly reduced the activity, protein, and mRNA levels of the cytoplasmic antioxidant enzyme Cu/Zn superoxide dismutase, which indicated that the hormone inhibits its biosynthesis. This reduction in the antioxidant capacity of the cells could account for the synergistic interaction between 1,25(OH)2D3 and doxorubicin and may also suggest increased efficacy of 1,25(OH)2D3 or its analogues in combination with other ROS-generating anticancer therapeutic modalities.  (+info)

Convergence of transforming growth factor-beta and vitamin D signaling pathways on SMAD transcriptional coactivators. (5/2474)

Cell proliferation and differentiation are regulated by growth regulatory factors such as transforming growth factor-beta (TGF-beta) and the liphophilic hormone vitamin D. TGF-beta causes activation of SMAD proteins acting as coactivators or transcription factors in the nucleus. Vitamin D controls transcription of target genes through the vitamin D receptor (VDR). Smad3, one of the SMAD proteins downstream in the TGF-beta signaling pathway, was found in mammalian cells to act as a coactivator specific for ligand-induced transactivation of VDR by forming a complex with a member of the steroid receptor coactivator-1 protein family in the nucleus. Thus, Smad3 may mediate cross-talk between vitamin D and TGF-beta signaling pathways.  (+info)

Regulation of PiT-1, a sodium-dependent phosphate co-transporter in rat parathyroid glands. (6/2474)

A cDNA encoding an Na+-Pi co-transporter, termed rat PiT-1, has now been isolated from rat parathyroid. Expression of rat PiT-1 in Xenopus oocytes revealed that it possesses Na+-dependent Pi co-transport activity. The amount of PiT-1 mRNA in the parathyroid of vitamin D-deficient rats was reduced compared with that in normal animals, and increased markedly after administration of 1,25-dihydroxyvitamin D3. Furthermore, the abundance of PiT-1 mRNA in the parathyroid was much greater in rats fed a low-Pi diet than in those fed a high-Pi diet. Thus, rat PiT-1 may contribute to the effects of Pi and vitamin D on parathyroid function.  (+info)

Regulation of vitamin D action. (7/2474)

The control of gene transcription by vitamin D compounds is initiated by binding to the VDR, which enhances the receptor's ability to heterodimerize to RXR, interact with response elements in target genes and attract components of the transcriptional initiation complex. A number of factors are capable of influencing this process, including (i) the rate of uptake and catabolism of the ligand, (ii) the nature of the conformational change induced by a specific ligand, (iii) the cellular content of the VDR, (iv) post-translational modifications of the VDR and (v) the availability of other transcriptional components. Vitamin D analogues may affect these factors differently to 1,25(OH)2D3 to produce unique biological profiles that can be exploited for therapeutic use.  (+info)

Topical psoriasis therapy. (8/2474)

Psoriasis is a common dermatosis, affecting from 1 to 3 percent of the population. Until recently, the mainstays of topical therapy have been corticosteroids, tars, anthralins and keratolytics. Recently, however, vitamin D analogs, a new anthralin preparation and topical retinoids have expanded physicians' therapeutic armamentarium. These new topical therapies offer increased hope and convenience to the large patient population with psoriasis.  (+info)

TY - JOUR. T1 - Direct inhibitory effect of calcitriol on parathyroid function (sigmoidal curve) in dialysis. AU - Dunlay, R.. AU - Rodriguez, M.. AU - Felsenfeld, A. J.. AU - Llach, F.. PY - 1989/1/1. Y1 - 1989/1/1. N2 - The effect of intravenous calcitriol on parathyroid function was evaluated in nine chronic hemodialysis patients with secondary hyperparathyroidism. Two micrograms of calcitriol were administered intravenously after dialysis thrice weekly for ten weeks. Parathyroid function was assessed by inducing hypo- and hypercalcemia with low calcium (1.0 mEq/liter) and high calcium (4.0 mEq/liter) dialyses before and after ten weeks of intravenous calcitriol therapy. To avoid hypercalcemia during calcitriol administration, the dialysate calcium was reduced to 2.5 mEq/liter. Parathyroid hormone (PTH) values (pg/ml) from dialysis-induced hypo- and hypercalcemia were plotted against serum ionized calcium, and the sigmoidal relationship between PTH and calcium was evaluated. Basal PTH levels ...
TY - JOUR. T1 - Sequential versus combined treatment of human breast cancer cells with antiestrogens and the vitamin D analogue EB1089 and evaluation of predictive markers for vitamin D treatment. AU - Christensen, G L. AU - Jepsen, J S. AU - Fog, C K. AU - Christensen, I J. AU - Lykkesfeldt, A E. PY - 2004/5. Y1 - 2004/5. N2 - Development of resistance to antihormonal therapy is a major problem in the treatment of breast cancer patients. Metastatic tumors, which progress after a period of response to treatment, often respond to second line endocrine treatment, but eventually develop estrogen independent growth. Vitamin D analogues are promising new drugs, using alternative mechanisms to inhibit growth of breast cancer cells. The sensitivity to antiestrogens and vitamin D analogues has been proposed to be inverse, indicating that the sensitivity to vitamin D analogues might increase after development of antiestrogen resistance and vice versa. In this study, the inverse sensitivity between ...
Hostutler, R. A., DiBartola, S. P., Chew, D. J., Nagode, L. A., Schenck, P. A., Rajala-Schultz, P. J. and Drost, W. T. (2006), Comparison of the Effects of Daily and Intermittent-Dose Calcitriol on Serum Parathyroid Hormone and Ionized Calcium Concentrations in Normal Cats and Cats with Chronic Renal Failure. Journal of Veterinary Internal Medicine, 20: 1307-1313. doi: 10.1111/j.1939-1676.2006.tb00743.x ...
1,25 Dihydroxyvitamin D circulating levels, calcitriol administration, and incidence of acute rejection, CMV infection, and polyoma virus infection in renal transplant recipients ...
To clarify the effects of active vitamin D3 on pressor and vascular responses to vasoconstrictor substances, we studied pressor responses to the intravenous injection of norepinephrine or angiotensin II (Ang II) and vasoconstrictor responses to norepinephrine. Sprague-Dawley rats were given 1,25-dihydroxyvitamin D3 subcutaneously (200 ng/kg per day) for 14 days. The administration of 1,25-dihydroxyvitamin D3 augmented the pressor responses to norepinephrine and Ang II in conscious rats and was associated with a significant increase in serum calcium concentration (11.0 +/- 0.2 mg/dl). To further clarify whether the increased pressor response to vasoconstrictors may be due to the calcemic or direct action of active vitamin D3, we studied the effect of its noncalcemic analogue, 22-oxacalcitriol, and its inactive analogue, 24,25-dihydroxyvitamin D3, on the pressor response to vasoconstrictors in rats. The pressor responses to norepinephrine and Ang II were apparently augmented in ...
OUTLINE: This is a dose-escalation study of calcitriol.. In the first stage of the study, cohorts of 3-6 patients receive escalating doses of oral calcitriol on days 1-3. Dose escalation continues until the maximum tolerated dose (MTD) is determined.. In the second stage, patients receive escalating doses of oral calcitriol on days 1-3 and a fixed dose of oral dexamethasone on days 0-4. Treatment continues weekly in the absence of disease progression or unacceptable toxicity. Dose escalation continues until the MTD is determined.. Six additional patients may receive calcitriol and dexamethasone at one dose level below the MTD determined in the second stage, to confirm the MTD.. The MTD is defined as the dose preceding that at which 2 of 3 or 2 of 6 patients experience dose-limiting toxicity.. PROJECTED ACCRUAL: Approximately 40 patients will be accrued for this study. ...
To elucidate the biosynthesis of 25-hydroxyvitamin D3-26,23-lactone, two known metabolites of 25-hydroxyvitamin D3--23,25-dihydroxyvitamin D3 and 25,26-dihydroxyvitamin D3--were incubated individually with kidney homogenate prepared from vitamin D-supplemented chickens, a preparation known to produce the lactone from 25-hydroxyvitamin D3. The 25-hydroxyvitamin D3-26,23-lactone produced in vitro was then separated, purified, identified, and quantitated by consecutive straight-phase and reverse-phase high-performance liquid chromatography. 23,25-Dihydroxyvitamin D3 is a far better substrate for production of 25-hydroxyvitamin D3-26,23-lactone than is 25,26-dihydroxyvitamin D3. Production of lactone is highly selective for the natural 23(S)-hydroxy-23,25-dihydroxyvitamin D3 while both epimers of 25,26-dihydroxyvitamin D3 resulted in small amounts of product comigrating with natural lactone. It appears that 23(S),25-dihydroxyvitamin D3, but not 25,26-dihydroxyvitamin D3, is a natural precursor in ...
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DN-101 is an investigational drug that has not been approved by the U.S. Food and Drug Administration (FDA). It is a newly formulated pill that contains high amounts of calcitriol, a naturally occurring hormone and the biologically active form of vitamin D. Administration of DN-101 results in much higher blood levels of calcitriol than the body can produce from dietary vitamin D or vitamin D supplements. These higher levels of calcitriol are associated with anti-cancer effects in laboratory models of human cancer. Laboratory models also indicate that calcitriol has synergy with many commonly used chemotherapeutic agents used to treat cancer.. Calcitriol, at very low doses, is currently approved for use in patients with chronic kidney failure. DN-101 was specifically designed for cancer and contains 30 times the amount of calcitriol found in the calcitriol pill commercially available today. In order to take an amount of calcitriol equivalent to 1 DN-101 pill, cancer patients would need to swallow ...
The mechanism of action of calcitriol in the treatment of psoriasis is accounted for by their antiproliferative activity for keratinocytes and their stimulation of epidermal cell differentiation. The anticarcinogenic activity of the active form of Calcitriol appears to be correlated with cellular vitamin D receptor (VDR) levels. Vitamin D receptors belong to the superfamily of steroid-hormone zinc-finger receptors. VDRs selectively bind 1,25-(OH)2-D3 and retinoic acid X receptor (RXR) to form a heterodimeric complex that interacts with specific DNA sequences known as vitamin D-responsive elements. VDRs are ligand-activated transcription factors. The receptors activate or repress the transcription of target genes upon binding their respective ligands. It is thought that the anticarcinogenic effect of Calcitriol is mediated via VDRs in cancer cells. The immunomodulatory activity of calcitriol is thought to be mediated by vitamin D receptors (VDRs) which are expressed constitutively in monocytes ...
Calcitriol ,Calcitriol manufacturer,Calcitriol CAS No 32222-06-3,Calcitriol Molecular Formula C27H44O3,Calcitriol Synonyms (1R,3S)-5-[2-[(1R,3aR,7aS)-1-[(2R)-6-hydroxy-6-methyl-heptan-2-yl]-7a-methyl-2,3,3a,5,6,7-hexahydro-1H- inden-4-ylidene]ethylidene]-4-methylidene-cyclohexane-1,3-diol,Calcitriol Molecular weight 416.64 g/mol,Calcitriol manufacturing by A.S.Joshi & Company
Ongoing studies are attempting to determine the optimal combination of calcimimetics and calcitriol analogs for the treatment of SHPT. The ACHIEVE study recently compared the effects of Cinacalcet plus fixed low-dose calcitriol analogs with flexible doses of calcitriol analogs on PTH, Ca, and P levels (25). In this study, we used samples from ACHIEVE to perform a per-protocol analysis of the effects of treatment on FGF23, a factor associated with poor outcomes in ESRD (15). We found that the treatment regimen using Cinacalcet plus fixed low-dose calcitriol analogs results in a relative decrease in FGF23 levels compared with an approach using escalating doses of calcitriol analogs alone. This study is the first report of the disparate effects of different treatment strategies on FGF23 levels in HD patients.. The existence of complex interactions between treatment agents and mineral metabolic parameters make it difficult to ascribe the observed differences in FGF23 to a specific therapeutic ...
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TY - JOUR. T1 - The in vitro evaluation of 25-hydroxyvitamin D3 and 19-nor-1α,25- dihydroxyvitamin D2 as therapeutic agents for prostate cancer. AU - Chen, Tai C.. AU - Schwartz, Gary G.. AU - Burnstein, Kerry L.. AU - Lokeshwar, Bal L.. AU - Holick, Michael F.. PY - 2000/3/1. Y1 - 2000/3/1. N2 - Prostate cancer cells contain specific receptors [vitamin D receptors (VDRs)] for 1α,25-dihydroxyvitamin D3 (1α,25(OH)2D3), which is known to inhibit the proliferation and invasiveness of these cells. These findings support the use of 1α,25(OH)2D3 for prostate cancer therapy. However, because 1α,25(OH)2D3 can cause hypercalcemia, analogues of 1α,25(OH)2D3 that are less calcemic but that exhibit potent antiproliferative activity would be attractive as therapeutic agents. We investigated the effects of two different types of less calcemic vitamin D compounds, 25-hydroxyvitamin D3 [25(OH)D3] and 19-nor-1α,25-dihydroxyvitamin D2 [19-nor-1,25(OH)2D2], and compared their activity to 1α,25(OH)2D3 on ...
We observed an association of oral calcitriol with lower mortality among adults with stages 3 to 4 CKD and hyperparathyroidism, independent of measured comorbidity, kidney function, and serum PTH levels. Associations were statistically similar according to baseline PTH level, eGFR, and diabetes status, although stratified analyses were limited by sample size. These are among the first data to describe clinical outcomes associated with oral activated vitamin D agents in nondialysis patients with CKD.. There is biologic plausibility for an association of calcitriol use with lower mortality. Vitamin D is a pleiotropic steroid hormone that binds to its intracellular receptor to elicit a diverse genetic response.12 Experimental and epidemiologic studies have connected lower 25-hydroxyvitamin D and 1,25-dihydroxyvitamin D levels with cardiovascular risk factors, including increased renin activity, hypertension, inflammation, insulin resistance, diabetes, and albuminuria.14,22-24 Calcitriol blocks ...
AbstractAfter the Second World War, infatuation with modern products has exponentially widened the spectrum of chemicals used. Some of them are capable of hijacking the endocrine system by blocking or imitating a hormone and are referred to as hormonally active chemicals or endocrine disruptors. These are chemicals that the body was not designed for evolutionarily and they are present in every matrix of the environment. We are living in a chemical world where the exposures are ubiquitous and take place in combinations that can interact with the endocrine system and some other metabolic activities in unexpected ways. The complexity of interaction of these compounds can be understood by the fact that they interfere with gene expression at extremely low levels, consequently harming an individual life form, its offspring or population. As the endocrine system plays a critical role in many biological or physiological functions, by interfering bodys endocrine system, endocrine disrupting compounds (EDCs)
At the same time medications pain pills discount 0.25mcg calcitriol otc, neurosciences are providing the first compelling evidence that neuropsychiatric and neurodevelopmental disorders reflect fundamental differences in brain structure and function medications with weight loss side effect buy calcitriol 0.25 mcg online. Discrepancies affect the capacity to medications nursing cheap calcitriol 0.25mcg with visa learn 86 treatment ideas practical strategies calcitriol 0.25mcg without a prescription, to judge and to respond to behavioral and pharmacological treatments They impinge upon the capacity to solve cognitive conflicts implicated in impulsivity (behavioral disinhibiting) and to make decisions. While diversities are genetically based or determined by the onset of pathologies, socio-cultural interactions are fundamental in shaping the scale of brain diversity one may carry. In 2001 the National Research Council released a report demonstrating that individuals with neurodevelopmental ...
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There is a close correlation between treatment with calcitriol and the development of hypercalcemia.. All other vitamin D compounds and their derivative, including proprietary compounds or foodstuffs which may be fortified with vitamin D, should be withheld during treatment with calcitriol.. An abrupt increase in calcium intake as a result of changes in diet (e.g. increased consumption of dairy products) or uncontrolled intake of calcium preparations may trigger hypercalcaemia. Patients and their families should be advised that strict adherence to the prescribed diet is mandatory and they should be instructed on how to recognise the symptoms of hypercalcaemia.. As soon as the serum calcium levels rise to 1 mg/100 ml (250 pmol/l) above normal (9-11 mg/100 ml, or 2250-2750 pmol/l), or serum creatinine rises to , 120 pmol/l, treatment with calcitriol should be stopped immediately until normocalcemia ensues.(see section 4.2). Immobilized patients, e.g. those who have undergone surgery, are ...
Its been proposed that cellular Ca2+ signals activate hormone secretion. polypeptide with two EF-calcium-binding sites that are usually expressed in the mammalian intestine, uterus, and pituitary gland. The major role of this protein is buffering of Ca2+ ions [1]. The discovery of a high affinity receptor in the pancreas for the hormonally active form of vitamin D, 1,25-dihydroxyvitamin D3 (1,25(OH)2D3), in 1979 was the first demonstration of a nonclassical target tissue to contain vitamin D receptors (VDR) [2]. Impaired insulin secretory capacity in pancreatic cells was also observed in mice lacking a functional VDR [3]. 1,25(OH)2D3 and its cognitive VDR regulate many target genes, including CaBP-9k. The expression of CaBP-9k has been shown to be mediated by vitamin D response element (VDRE) on its promoter. CaBP-9k regulates the amount of intracellular calcium to prevent cell death from reaching the toxicity of free calcium [4]. Calcium signaling in all secretory cells (nerve cell, endocrine ...
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Calcitriol or 1,25-dihydroxycholecalciferol (abbreviated 1,25-(OH)2-D3) is the active form of vitamin D found in the body (vitamin D3). Calcitriol is marketed under various trade names including Rocaltrol (Roche), Calcijex (Abbott) and Decostriol (Mibe, Jesalis). It is produced in the kidneys via 25-hydroxyvitamin D-1 α-hydroxylase by conversion from 25-hydroxycholecalciferol (calcidiol). This is stimulated by a decrease in serum calcium, phosphate (PO43−) and parathyroid hormone (PTH) levels. It regulates calcium levels by increasing the absorption of calcium and phosphate from the gastrointestinal tract, increasing calcium and phosphate reabsorption in the kidneys and inhibiting the release of PTH. Calcitriol is also commonly used as a medication in the treatment of hypocalcemia and osteoporosis.
Calcitriol Receptors: Proteins, usually found in the cytoplasm, that specifically bind calcitriol, migrate to the nucleus, and regulate transcription of specific segments of DNA with the participation of D receptor interacting proteins (called DRIP). Vitamin D is converted in the liver and kidney to calcitriol and ultimately acts through these receptors.
Calcitriol will work only if you get the right amount of calcium from the foods you eat. If you get too much calcium from foods, you may experience serious side effects of calcitriol, and if you do not get enough calcium from foods, calcitriol will not control your condition. Your doctor will tell you which foods are good sources of these nutrients and how many servings you need each day. If you find it difficult to eat enough of these foods, tell your doctor. In that case, your doctor can prescribe or recommend a supplement.. If you are being treated with dialysis (process of cleaning the blood by passing it through a machine), your doctor may also prescribe a low-phosphate diet. Follow these directions carefully.. If you do not have kidney disease, you should drink plenty of fluids while taking calcitriol. If you have kidney disease, talk to your doctor about how much fluid you should drink each day.. ...
Calcitriol will work only if you get the right amount of calcium from the foods you eat. If you get too much calcium from foods, you may experience serious side effects of calcitriol, and if you do not get enough calcium from foods, calcitriol will not control your condition. Your doctor will tell you which foods are good sources of these nutrients and how many servings you need each day. If you find it difficult to eat enough of these foods, tell your doctor. In that case, your doctor can prescribe or recommend a supplement.. If you are being treated with dialysis (process of cleaning the blood by passing it through a machine), your doctor may also prescribe a low-phosphate diet. Follow these directions carefully.. If you do not have kidney disease, you should drink plenty of fluids while taking calcitriol. If you have kidney disease, talk to your doctor about how much fluid you should drink each day.. ...
Before Its News). Market Research Store has been recently published a fresh research report- Global Calcitriol (CAS 32222-06-3) Market by Manufacturers, Countries, Type and Application, Forecast to 2022 . This added to the companys collection of research reports. This report offers a deep examination of the Calcitriol market for the period 2013-2023. As per the report, the Calcitriol market is estimated to grow at elevated CAGR recorded in 2017. The towering competitive Calcitriol market has been observing huge and whooping investments in development and research from government as well as private firms.. This report divides the market on the basis of regions, manufacturers, application, and type. It also showcases the growing factors, reasons for decline in the market, segmentations, and openings and breaks expected to power the market expansion during this time span. The primary factors such as revenues, supply chain management, product valuation and other crucial factors are also examined ...
TY - JOUR. T1 - [63] A Sensitive Radioreceptor Assay for 1α,25-Dihydroxyvitamin D in Biological Fluid. AU - Chandler, John S.. AU - Wesley Pike, J.. AU - Hagan, Laura A.. AU - Haussler, Mark R.. PY - 1980/1/1. Y1 - 1980/1/1. N2 - This chapter discusses a sensitive radioreceptor assay for lα,25-dihydroxyvitamin D in biological fluids. Vitamin D has been recognized as a principal regulator of calcium and phosphate homeostasis in a variety of animal species, including humans. Some studies describe 1α,25-dihydroxyvitamin D [lα,25-(OH)2D] as the hormonal metabolite responsible for mediating intestinal transport of these minerals and hence necessitate development of a precise method for quantitating this sterol in biological fluids, particularly serum. It has been demonstrated that chick intestinal mucosa contained a cytosolic protein that rapidly and specifically bound lα,25-(OH)2D3 both in vivo and in vitro with high affinity. Furthermore, the sterol-protein complex was rapidly translocated to ...
TY - JOUR. T1 - Electromechanical effects of 1,25-dihydroxyvitamin D with antiatrial fibrillation activities. AU - Hanafy, Dicky A.. AU - Chang, Shih Lin. AU - Lu, Yen Yu. AU - Chen, Yao Chang. AU - Kao, Yu Hsun. AU - Huang, Jen Hung. AU - Chen, Shih Ann. AU - Chen, Yi Jen. PY - 2014. Y1 - 2014. N2 - Electromechanical Effects of 1,25-Dihydroxyvitamin D on the LA Introduction Treatment with 1,25-dihydroxyvitamin D (1,25[OH]2D) has several cardiovascular benefits. 1,25[OH]2D has direct cellular effects, but its effects on the atrium are not clear. We evaluated the effects of 1,25[OH]2D on the atrial electrophysiology and atrial fibrillation (AF). Methods Conventional microelectrodes were used to record action potentials (APs) and contractility in isolated rabbit left atrium (LA) tissue preparations before and after the administration of 0.01, 0.1, and 1 nM 1,25[OH] 2D with and without rapid atrial pacing (RAP) and acetylcholine (5 mM)-induced AF. Surface ECG and intracardiac electrograms were ...
Herein, we describe a versatile and efficient total synthesis of 1α,25-dihydroxyvitamin D3 (calcitriol). The synthetic strategy relies on an unprecedented Si-assisted SN2′-syn displacement of carbamates by cuprates to set the challenging pivotal quaternary methyl group at the fused-ring junction of the CD-tr
Breast cancer is the second leading cause of cancer deaths among females and a leading cause of death of all middle age women in the United States. Epidemiologic evidence suggests a role for vitamin D deficiency in the development of breast cancer. Moreover, vitamin D receptors have been found in most breast cancers, and their presence appears to be a favorable prognostic sign. While much clinical focus has been given to the vitamin A related retinoids, little is known about the role for vitamin D in the development of breast cancer although vitamin D and its active metabolites and analogs represent a class of compounds which at the molecular and cellular level have strong similarities to the vitamin A metabolites and analogs. With the development of potent but non hypercalcemic analogs of vitamin D, the potential role of vitamin D in the etiology and treatment of breast cancer can now be tested both in vitro and in vivo. In the past decade, a number of tissues have been found to contain receptors for
Calcitriol (ergocalciferol, 1,25-dihydroxycholecalciferol, 1,25-dihydroxyvitamin D3) is a synthetic form of vitamin D[1]. Calcitriol causes increased calcium absorption from the gut. This product is used for treatment of hypocalcemia associated with rickets and hypoparathyroidism[2]. Regular monitoring of blood calcium is important to avoid development of hypercalcemia. Recommended dose in dogs is 25,000 - 50,000 U/day given orally[3]. ...
We have examined the effects of the seco-steroid hormone 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] on membrane phosphoinositide metabolism, protein kinase C (PKC) activation and influx of extracellular Ca2+ in chick-embryo muscle-cell (myoblast) cultures. At physiological concentrations, the hormone induces a rapid (15 s) and transient release of inositol triphosphate (InsP3) and diacylglycerol (DAG). InsP3 release is maximal at 60 s (80% above controls) and then declines. The effects of 1,25(OH)2D3 on InsP3 production exhibited specificity, as 25-hydroxy-vitamin D3 and 24,25-dihydroxy-vitamin D3 did not alter myoblast InsP3 levels. The stimulation of DAG is biphasic, with peaks at 60 s (+105%) and 5 min (+700%). The second phase of DAG release is not associated with changes in InsP3. 1,25(OH)2D3 induces a rapid (within 60 s) accumulation of InsP2, and its effect on InsP is delayed (120 s). The hormone rapidly activates myoblast PKC, with maximal translocation of activity from the cytosol to the ...
Biological activity of 1 alpha, 25-dihydroxyvitamin D derivatives--24-epi-1 alpha, 25-dihydroxyvitamin D-2 and 1 alpha,25-dihydroxyvitamin D-7. Biochim Biophys Acta. 1991 Jan 31; 1091(2):188-92 ...
TY - JOUR. T1 - Phase I study of weekly DN-101, a new formulation of calcitriol, in patients with cancer. AU - Beer, Tomasz (Tom). AU - Javle, Milind M.. AU - Ryan, Christopher. AU - Garzotto, Mark. AU - Lam, Gilbert N.. AU - Wong, Alvin. AU - Henner, W. David. AU - Johnson, Candace S.. AU - Trump, Donald L.. PY - 2007/4. Y1 - 2007/4. N2 - Background: DN-101 is a new, high-dose, oral formulation of calcitriol under investigation for the treatment of cancer. We sought to evaluate the tolerability and pharmacokinetics (PK) of weekly doses of DN-101 in patients with advanced cancer. Methods: Patients who completed a previously reported single dose escalation study of DN-101 [Beer et al. (2005) Clin Cancer Res 11:7794-7799] were eligible for this continuation weekly dosing study. Cohorts of 3-10 patients were treated at doses of 15, 30, 45, 60, and 75 μg calcitriol. Once 45 μg was established as the maximum tolerated dose (MTD), this cohort was expanded to include 18 patients. Dose limiting ...
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Because there are currently no effective drugs for liver fibrosis, we believe our findings would open a new door for treatment, says senior author Ronald M. Evans, a professor in Salks Gene Expression Laboratory and lead researcher in the Institutes new Helmsley Center for Genomic Medicine. The Salk study focused on a star-shaped stellate cell in the liver that serves as a beacon for damage. When called into action, stellate cells produce fibrotic proteins in an attempt to heal an injury. Under chronic stress, however, localized fibrosis expands, eventually leading to cirrhosis, increased risk of liver cancer, and the need for a liver transplant in advanced cases. The Evans lab discovered a genetic switch through which vitamin D-related ligands such as calcitriol, a hormonally active form of the vitamin, can put the brakes on fibrosis. Preclinical results suggest the vitamin D brake is highly efficacious and led us to believe that the time is right to consider a trial in the context of ...
TY - JOUR. T1 - 1,25-Dihydroxyvitamin D3-induced alterations of lipid metabolism in human monocyte-macrophages. AU - Roullet, J. B.. AU - Haluska, M.. AU - Morchoisne, O.. AU - McCarron, D. A.. PY - 1989/1/1. Y1 - 1989/1/1. N2 - An in vivo atherogenic role of dietary vitamin D has been postulated. To address this hypothesis we sought to determine the in vitro effects of its active circulating metabolite, 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] on lipid metabolism in human monocyte-derived macrophages. When cultured 6 days in the presence of 10-8 M 1,25(OH)2D3 monocyte-macrophage accumulated significantly more triglycerides than control cells: 987.6 ± 26.8 vs. 779.3 ± 24.1 μg/mg protein (P , 0.001). Triglyceride accumulation was associated with a hormone-induced stimulation of triglyceride synthesis as determined by [3H]oleate incorporation into cellular triglycerides. The effect of the hormone was significant after 24 h and dose dependent [10-11 to 10-8 M 1,25(OH)2D3]. It was specific since ...
TY - JOUR. T1 - C-terminal proteolysis of the avian 1,25-dihydroxyvitamin D3 receptor. AU - Allegretto, Elizabeth A.. AU - Pike, J. Wesley. AU - Haussler, Mark R.. PY - 1987/8/31. Y1 - 1987/8/31. N2 - Exposure of the 60 kDa chick intestinal 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) receptor to carboxypeptidase A resulted in a time dependent decrease in receptor hormone-binding; after 2 h, there was no detectable macro-molecular-bound 1,25(OH)2[3H]D3. Upon DNA-cellulose chromatography of this preparation, a 56 kDa protein adsorbed to the column and eluted as a function of para-chloromercuribenzene sulfonate (a sulfhydryl blocking reagent). The 56 kDa fragment was detected by anti-receptor monoclonal antibodies via immunoblot technology. The 1,25(OH)2[3H]D3 eluted in the fall through fractions of the column. Thus, cleavage of up to 40 amino acids from the carboxy-terminus of the 1,25(OH)2D3 receptor results in a protein which no longer binds to hormone, but retains its capacity to interact with ...
Some authors have reported that vitamin D treatment worsens renal function. We studied 10 patients with stable renal function, who were given calcitriol (0.5 micrograms/day) for a 4-month period. Creatinine and inulin clearance were performed at the beginning and at the end of the treatment. Althoug …
Calcitriol is vitamin D3. Vitamin D is important for the absorption of calcium from the stomach and for the functioning of calcium in the body. Calcitriol is used to treat hyperparathyroidism (overactive parathyroid glands) and metabolic bone disease in people who have chronic kidney failure and are not receiving...
Calcitriol-a treatment for chronic kidney failure in your cat or dog. Calcitriol as the active form of Vitamin D is actually a hormone over 1,000 times as potent ...
Avet Pharmaceuticals Inc. announced the immediate availability of Calcitriol soft gel capsules in 0.25 and 0.5 mcg strengths. This product is the AB rated generic equivalent to the synthetic Vitamin D drug Rocaltrol®* and adds to Avets robust portfolio of generic oral soft gel products. According to IMS data for the twelve-months ended April 2013, the U.S. market for Calcitriol approximated $60 million. *Rocaltrol is a registered trademark of Hoff-mann LaRoche-Validus.. Download Press Release. ...
Calcitriol (1,25-dihydroxyvitamin D3), the hormonally dynamic type of vitamin D, inhibits the development of several malignant cells including breasts tumor (BCa) cells. estrogens. Therefore the inhibition of estrogen synthesis and signaling by calcitriol and its own 162011-90-7 manufacture anti-inflammatory activities will play a significant part in inhibiting ER+ BCa. We hypothesize that diet supplement D would display very similar anticancer activity because of the presence from the enzyme 25-hydroxyvitamin D-1-hydroxylase (CYP27B1) in breasts cells ensuring transformation of circulating 25-hydroxyvitamin D to calcitriol locally inside the breasts micro-environment where it could act within a paracrine way to inhibit BCa development. Cell lifestyle and in vivo data in mice highly claim that calcitriol and eating supplement D would play an advantageous function in the avoidance and/or treatment of ER+ BCa in females. category of genes [7,27] and in various other BCa cells potentiates the ...
The active hormonal form of vitamin D, 1,25-dihydroxyvitamin D (1,25D) is an important modulator of the immune system, inhibiting cellular proliferation and regulating transcription of immune response genes. In order to characterize the genetic basis of variation in the immunomodulatory effects of 1,25D, we mapped quantitative traits of 1,25D response at both the cellular and the transcriptional level. We carried out a genome-wide association scan of percent inhibition of cell proliferation (Imax) induced by 1,25D treatment of peripheral blood mononuclear cells from 88 healthy African-American individuals. Two genome-wide significant variants were identified: rs1893662 in a gene desert on chromosome 18 (p = 2.32 x 10−8) and rs6451692 on chromosome 5 (p = 2.55 x 10−8), which may influence the anti-proliferative activity of 1,25D by regulating the expression of nearby genes such as the chemokine gene, CCL28, and the translation initiation gene, PAIP1. We also identified 8 expression ...
Calcitriol: Calcitriol stimulates intestinal absorption of calcium and accounts for supplementing calcium levels in management of postmenopausal osteoporosis.
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TY - JOUR. T1 - Effect of calcitriol on bone loss after cardiac or lung transplantation. AU - Sambrook, Philip. AU - Henderson, N. Kathy. AU - Keogh, Anne. AU - MacDonald, Peter. AU - Glanville, Allan. AU - Spratt, Phillip. AU - Bergin, Peter. AU - Ebeling, Peter. AU - Eisman, John. PY - 2000/1/1. Y1 - 2000/1/1. N2 - Rapid bone loss after cardiac and lung transplantation results in an increased risk of osteoporotic fracture. This study examined the efficacy of treatment with calcitriol (1,25-dihydroxyvitamin D3) in preventing bone loss in patients undergoing cardiac or lung transplantation. In this 2-year double-blind, stratified study, 65 patients undergoing cardiac or single lung transplantation were randomly allocated to receive either placebo or calcitriol (0.5-0.75 μg/day), the latter for either 12 months or 24 months. All patients received 600 mg calcium/day. Bone mineral density (BMD) was measured every 6 months for 2 years by dual-energy X-ray absorptiometry. There was no significant ...
Chronic renal failure is almost always associated with secondary uraemic hyperparathyroidism. Action should be taken as early as possible to avoid it or reduce its severity in patients with chronic kidney disease (CKD). Over the last decade, the most effective way of achieving this has been defined as therapy with active vitamin D derivatives. However, the so‐called non‐hypercalcaemic vitamin D derivatives, which are said to be superior, have not met our expectations so far. In contrast, calcimimetic agents, the new class of compounds that act specifically on the calcium‐sensing receptor, are very promising for the treatment and prevention of hyperparathyroidism. CKD is associated with disturbances in calcium, phosphate, and vitamin D metabolism that occur early in the course of renal disease. In most patients, these disturbances lead to secondary hyperparathyroidism and osteitis fibrosa or associated, more complex, skeletal lesions. Here, we focus on recent advances in the prevention ...
In a retrospective study, we have assessed the efficacy of oral calcitriol on the evolution of hyperparathyroid bone disease in patients on hemodialysis. 33 patients who had received calcitriol for at least one year and up to 7 years were carefully matched with controls for gender, years on
We have investigated how Wnt and vitamin D receptor signals regulate epidermal differentiation. Many epidermal genes induced by β-catenin, including the stem cell marker keratin 15, contain vitamin D response elements (VDREs) and several are induced independently of TCF/Lef. The VDR is required for β-catenin induced hair follicle formation in adult epidermis, and the vitamin D analog EB1089 synergises with β-catenin to stimulate hair differentiation. Human trichofolliculomas (hair follicle tumours) are characterized by high nuclear β-catenin and VDR, whereas infiltrative basal cell carcinomas (BCCs) have high β-catenin and low VDR levels. In mice, EB1089 prevents β-catenin induced trichofolliculomas, while in the absence of VDR β-catenin induces tumours resembling BCCs. We conclude that VDR is a TCF/Lef-independent transcriptional effector of the Wnt pathway and that vitamin D analogues have therapeutic potential in tumors with inappropriate activation of Wnt signalling.. ...
Antibodies to 1 alpha, 25-dihydroxy vitamin D3 25-hemisuccinate linked to albumin were produced and an immunoassay for 1,25-dihydroxy vitamin D developed. Plasma 1,25-dihydroxy vitamin D concentrations were compared using an immunoassay and cytosol radioreceptor assay. Both assays gave comparable results but the immunoassay was more reproducible, slightly more sensitive and had a lower detection limit. Using the immunoassay the plasma 1,25-dihydroxy vitamin D was 110.5 pmol/l (S.D. 29.4) in normal subjects; there was no difference between males and premenopausal females. It was negatively related to plasma phosphate. In renal failure and primary hyperparathyroidism plasma 1,25(OH)2D was positively related to radiocalcium absorption. Following 1 and 2 microgram of 1,25-dihydroxy vitamin D3 given orally the peak plasma concentration occurs within 12 h.
To the Editor:. We read with interest the paper by Hsia and colleagues1 in which the authors demonstrated that a daily vitamin D supplement of 400 IU (10 μg) in combination with 1000 mg calcium has no beneficial effects on cardiovascular risk. In our opinion, the data interpretation is complicated by the lack of 25-hydroxyvitamin D and 1,25-dihydroxyvitamin D (calcitriol) measurements. It may be that the vitamin D dose was too low to influence circulating calcitriol concentrations. It may also be that baseline 25-hydroxyvitamin D concentrations were already sufficient enough to produce adequate amounts of calcitriol. Calcitriol is the only vitamin D metabolite with known physiological actions. Experimental data demonstrate that calcitriol has important protective vascular effects such as suppression of renin activity, inhibition of vascular calcification, and reduction of thrombogenicity.2 Several retrospective studies already indicate that calcitriol and other active vitamin D analogs reduce ...
Vitamin D is a generic designation for a group of fat-soluble, structurally similar sterols including ergocalciferol D2 from plants and cholecalciferol D3 from animals. Vitamin D in the body is derived from 2 sources: exogenous (dietary: D2 and D3) and endogenous (biosynthesis: D3). Endogenous D3 is produced in the skin from 7-dehydrocholesterol, under the influence of ultraviolet light. Both forms of vitamin D are of similar biologic activity.. Vitamin D is rapidly metabolized in the liver to form 25-hydroxy (OH) vitamin D. Additional hydroxylation of 25-OH vitamin D takes place in the kidney by 1-alpha hydroxylase, under the control of parathyroid hormone, to yield 1,25-dihydroxy vitamin D.. 1,25-Dihydroxy vitamin D is the most potent vitamin D metabolite. It stimulates calcium absorption in the intestine and its production is tightly regulated through concentrations of serum calcium, phosphorus, and parathyroid hormone.. 1,25-Dihydroxy vitamin D levels may be high in primary ...
1 alpha,25-Dihydroxyvitamin D (1,25 D; also know as calcitriol), the hormonal form of vitamin D, can inhibit the proliferation and promote the differentiation of human prostate adenocarcinoma cells. However, little is known about the effects of 1,25 D on the invasive ability of prostate cancer cells. We used an in vitro bioassay of cell invasion (Amgel assay) to examine the effects of 1,25 D and a noncalcemic vitamin D analogue, 1,25-dihydroxy-16-ene-23-yne-cholecalciferol (16-23-D3), on the invasiveness of three well-characterized human prostate carcinoma cell lines: DU 145, PC-3, and LNCaP. PC-3 and LNCaP cells were poorly invasive in Amgel and were hardly affected by treatment with 1,25 D or 16-23-D3 (, 3%). Conversely, DU 145 cells were highly invasive in Amgel, and their invasion was markedly inhibited by 1,25 D and 16-23-D3 (maximally 66 and 59.4% respectively). This effect was both dose-dependent, with maximal inhibition at 1 x 10(-7) M and 72 h. Significant inhibition of invasion was ...
Absorption 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 Rocaltrol. 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. Following multiple-dose administration, serum calcitriol levels reached steady-state within 7 days. Distribution 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). Metabolism In vivo and in vitro studies indicate the presence of two pathways ...
The Wnt-β-catenin pathway is aberrantly activated in most colon cancers. DICKKOPF-1 (DKK-1) gene encodes an extracellular Wnt inhibitor that blocks the formation of signalling receptor complexes at the plasma membrane. We report that 1α,25-dihydroxyvitamin D3 [1,25(OH)2D3], the most active vitamin D metabolite, increases the level of DKK-1 RNA and protein in human SW480-ADH colon cancer cells. This effect is dose dependent, slow and depends on the presence of a transcription-competent nuclear vitamin D receptor (VDR). Accordingly, 1,25(OH)2D3 activates a 2300 bp fragment of the human DKK-1 gene promoter. Chromatin immunoprecipitation assays revealed that 1,25(OH)2D3 treatment induced a pattern of histone modifications which is compatible with transcriptionally active chromatin. DKK-1 is expressed at high level in colon cancer cell lines with a differentiated phenotype such as Caco-2 or HT-29. Exogenous expression of E-cadherin into SW480-ADH cells results in a strong adhesive phenotype and a ...
TY - JOUR. T1 - The dichotomy in the effects of 1,25 dihydroxyvitamin D3 and 24,25-dihydroxyvitamin D3 on bone γ-carboxyglutamic acid-containing protein in serum and bone in vitamin D-deficient rats. AU - Wientroub, Shlomo. AU - Price, Paul A.. AU - Reddi, A Hari. PY - 1987/5. Y1 - 1987/5. N2 - Vitamin D-deficient, second generation, rachitic rats showed significant decrease in bone Gla protein (BGP) levels in circulation and in the skeleton. 1,25 dehydroxyvitamin D3 (1,25 (OH)2D3) exhibited the most potent influence on serum BGP levels in a dose-dependent manner. At a dose 25 ng/100 g body weight 1,25 (OH)2D3 showed a cumulative effect, i.e., the longer the treatment, the more circulating BGP was detected 24,25 dehydroxyvitamin D3 (24,25(OH)2D3) at the same doses did not show similar effect on the serum BGP levels, regardless of the serum calcium levels. Bone BGP levels assayed at various sites representing endochondral and intramenbranous ossification demonstrated an opposite pattern. ...
1,25-Dihydroxyvitamin D(3) (1,25(OH)(2)D(3)), the biologically active metabolite of Vitamin D(3), not only regulates bone and calcium metabolism but also exerts other biological activities, including immunomodulation via the nuclear Vitamin D receptor expressed in antigen-presenting cells and activated T cells. This regulation is mediated through interference with nuclear transcription factors such as NF-AT and NF-kappaB or by direct interaction with Vitamin D responsive elements in the promoter regions of cytokine genes. Dendritic cells (DCs) are primary targets for the immunomodulatory activity of 1,25(OH)(2)D(3), as indicated by inhibited DC differentiation and maturation, leading to down-regulated expression of MHC-II, costimulatory molecules and IL-12. Moreover, 1,25(OH)(2)D(3) enhances IL-10 production and promotes DC apoptosis. Together, these effects of 1,25(OH)(2)D(3) inhibit DC-dependent T cell activation. Immunomodulation by 1,25(OH)(2)D(3) and its analogs in vivo has been ...
In the first pilot trial with calcitriol, Walter et al. (5) reported no differences in fasting C-peptide, AUC C-peptide, and peak C-peptide after a mixed meal between treated and placebo groups at 9 and 18 months. A1C and insulin requirement were also similar between the groups. In the aforementioned study, no threshold of C-peptide level at study entry was defined. We designed a trial in which patients were younger at diagnosis, including also children, and should have had basal C-peptide levels at entry ,0.25 nmol/l so that a possible effect of calcitriol on disease progression could have been detected. We have shown that calcitriol does not affect residual β-cell function in such patients, even those of younger age. Similar to the German trial describing a mean C-peptide decrease of ∼40% at 18 months, in our study, decline of C-peptide after 24 months was 44.4% in the calcitriol group and 42.5% in the placebo group. These findings substantially confirm the data from combined studies ...
Genome- and transcriptome-wide data has significantly increased the amount of available information about primary 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) target genes in cancer cell models, such as human THP-1 myelomonocytic leukemia cells. In this study, we investigated the genes G0S2, CDKN1A and MYC as master examples of primary vitamin D receptor (VDR) targets being involved in the control of cellular proliferation. The chromosomal domains of G0S2 and CDKN1A are 140-170 kb in size and contain one and three VDR binding sites, respectively. This is rather compact compared to the MYC locus that is 15 times larger and accommodates four VDR binding sites. All eight VDR binding sites were studied by chromatin immunoprecipitation in THP-1 cells. Interestingly, the site closest to the transcription start site of the down-regulated MYC gene showed 1,25(OH)2D3-dependent reduction of VDR binding and is not associated with open chromatin. Four of the other seven VDR binding regions contain a typical DR3-type VDR
A new study published this month finds that the hormonally active form of vitamin D, Calcitriol 1,25-dihydroxyvitamin D(3), inhibits the growth of many kinds of cancerous cells, including breast cancer, indicating that vitamin D3 can be useful in treating and even preventing a variety of cancers. Authors of the study said that caner cell growth is inhibited by anticancer actions including cell cycle arrest, promotion of apoptosis and inhibition of invasion, metastasis, and angiogenesis. Vitamin Ds anti-inflammatory properties and interference with estrogen synthesis further explains its anti-tumor properties. Two studies from 2007 used meta-analysis, which combines data from multiple reports, to find that therapeutic doses of vitamin D could prevent up to half of all cases of breast cancer, and two-thirds of all cases of colorectal cancer in the United States. The studies showed a direct correlation between blood levels of vitamin D and cancer. Those with the highest blood levels were found ...
en] Metastatic breast cancer cells are characterized by their high propensity to colonize the skeleton and form bone metastases, causing major morbidity and mortality. Identifying key proteins involved in the osteotropic phenotype would represent a major step toward the development of both new prognostic markers and new effective therapies. Cell surface proteins differentially expressed in cancer cells are preferred potential targets for antibody-based targeted therapies. In this study, using cell surface biotinylation and a mass spectrometric approach, we have compared the profile of accessible cell surface proteins between the human breast cancer cell line MDA-MB-231 and its highly osteotropic B02 subclone. This strategy allowed the identification of several proteins either up- or downregulated in the osteotropic cell line, and differential protein expressions were validated using antibody-based techniques. Class I HLAs were down-regulated in the bone metastatic variant, whereas ...
Some scientists believe that a low blood level of Vitamin D (calcifediol) is not necessarily linked to a low level of active vitamin D (calcitriol). On the contrary, for a minority with chronic illness, the body may try to downregulate the production of calcifediol when calcitriol is already in excess, following a disregulation of the VDR. Therefore, routine vitamin D3 supplementation of all patients based on their calcifediol blood test may be counterproductive for a minority of individuals. Their blood levels should be tested for calcitriol rather than calcifediol although this alternative test is not a standardized blood test. More to come in next episode. Resources :. [1] Ulrike Lehmann, Frank Hirche, Gabriele I. Stangl, Katja Hinz, Sabine Westphal, Jutta Dierkes. Bioavailability of Vitamin D2 and D3 in Healthy Volunteers, a randomised placebo-controlled trial. JCEM jc.2012-4287.. [2] Anne Marie Uwitonze, BDT, MS; Mohammed S. Razzaque, MBBS, PhD (2018) Review : Role of Magnesium in Vitamin D ...
Hypercalciuria due to combined growth hormone and calcitriol therapy in uremia: effects of growth hormone on mineral homeostasis in 75% nephrectomized weanling rats.
0006] In the research leading to the present invention, it was surprisingly found that certain three-component surfactant-solvent mixtures of a type which self-emulsifies in the presence of an excess of water to form microemulsions are suitable for inclusion in topical compositions for application on skin. The mixtures also exhibit a good solubilization capacity in dissolving sparingly water-soluble active ingredients such as vitamin D derivatives and analogues. The compositions are easily spreadable, and therefore likely to improve patient compliance, and exhibit an adequate physical and chemical stability. Compositions according to the invention comprising a vitamin D derivative or analogue have surprisingly been found to lead to a very high activation of the target gene cathelicidin in the biological assay described in Example 7 below, suggesting that the active ingredient is internalized by the keratinocytes on which the compositions are applied and activates the vitamin D receptor to a ...
Protein which interacts with any form of the fat-soluble vitamin D or protein whose transcription is regulated by the biologically active form of vitamin D, i.e. 1,25-dihydroxy vitamin D3 (1,25 dihydroxycholecalciferol) also termed calcitriol. Active calcitriol is derived from ergosterol (produced in plants) and 7-dehydrocholesterol (produced in the skin). Ergocalciferol (vitamin D2) and cholecalciferol (vitamin D3) are formed by UV irradiation of ergosterol and 7-dehydrocholesterol, respectively, and processed by the same enzymatic pathway in the body to D2-calcitriol and D3-calcitriol. Deficiency in vitamin D leads to the disease rickets, in children, and osteomalacia, in adults ...
and Thomasset M. (1990) Endocrinology 127:580-587). The bone-oriented assays include: 1) assessment of bone resorption as determined via the release of Ca2+ from bone in vivo (in animals fed a zero Ca2+diet) (Hibberd K.A. and Norman A.W. (1969) Biochem. Pharmacol 18:2347-2355; Hurwitz S. etal (1967)7. Nutr. 91:319-323), or from bone explants in vitro (Bouillon R. et al (1992) J. Biol Chem. 267:3044-3051), 2) measurement of serum osteocalcin levels [osteocalcin is an osteoblast-specific protein that after its synthesis is largely incorporated into the bone matrix, but partially released into the circulation (or tissue culture medium) and thus represents a good market of bone formation or turnover] (Bouillon R. et al (1992) Clin. Chem. 38:2055-2060), or 3) bone ash content (Norman A.W. and Wong R.G. (1972) J. Nutr. 102:1709-1718). Only one kidney-oriented assay has been employed. In this assay, urinary Ca2+ excretion is determined (Hartenbower D.L. et al (1977) Walter de Gruyter, Berlin pp ...
PBMC VDR expression is inversely associated with disease activity and inflammation in SLE patients, and VDR downregulation is likely driven by inflammation.
Hostutler RA, DiBartola SP, Chew DJ, Nagode LA, Schenck PA, Rajala-Schultz PJ, Drost WT: Comparison of the effects of daily and intermittent-dose calcitriol on serum parathyroid hormone and ionized calcium concentrations in normal cats and cats with chronic renal failure. J Vet Intern Med 20(6): 1307-1313, 2006 ...
The influence of vitamin D3 and its metabolites calcifediol (25(OH)D) and calcitriol on immune regulation and inflammation is well described, and raises the question of potential benefit against bacterial infections. In the current study, 25(OH)D was encapsulated in liposomes to enable aerosolisation, and tested for the ability to prevent pulmonary infection by Pseudomonas aeruginosa. Prepared 25(OH)D-loaded liposomes were nanosized and monodisperse, with a negative surface charge and a 25(OH)D entrapment efficiency of approximately 23%. Jet nebulisation of liposomes was seen to yield an aerosol suitable for tracheo-bronchial deposition. Interestingly, 25(OH)D in either liposomes or ethanolic solution had no effect on the release of the proinflammatory cytokine KC from Pseudomonas-infected murine epithelial cells (LA-4); treatment of infected, human bronchial 16-HBE cells with 25(OH)D liposomes however resulted in a significant reduction in bacterial survival. Together with the importance of ...
The metabolite of vitamin D, 1α,25-dihydroxyvitamin D3 (also known as calcitriol), is a biologically active molecule required to maintain the physiological functions of several target tissues in the human body from conception to adulthood. Its molecular mode of action ranges from immediate nongenomic responses to longer term mechanisms that exert persistent genomic effects. The genomic mechanisms of vitamin D action rely on cross talk between 1α,25-dihydroxyvitamin D3 signaling pathways and that of other growth factors or hormones that collectively regulate cell proliferation, differentiation and cell survival. In vitro and in vivo studies demonstrate a role for vitamin D (calcitriol) in modulating cellular growth and development. Vitamin D (calcitriol) acts as an antiproliferative agent in many tissues and significantly slows malignant cellular growth. Moreover, epidemiological studies have suggested that ultraviolet-B exposure can help reduce cancer risk and prevalence, indicating a potential role
OP appears to have similar efficacy and safety compared with oral calcitriol (OC) in dialysis patients with secondary hyperparathyroidism (SHPT).
TY - JOUR. T1 - Maturation state determines the response of osteogenic cells to surface roughness and 1,25-dihydroxyvitamin D3. AU - Lohmann, C. H.. AU - Bonewald, L. F.. AU - Sisk, M. A.. AU - Sylvia, V. L.. AU - Cochran, D. L.. AU - Dean, D. D.. AU - Boyan, Barbara D.. AU - Schwartz, Z.. PY - 2000/1/1. Y1 - 2000/1/1. N2 - In this study we assessed whether osteogenic cells respond in a differential manner to changes in surface roughness depending on their maturation state. Previous studies using MG63 osteoblast-like cells, hypothesized to be at a relatively immature maturation state, showed that proliferation was inhibited and differentiation (osteocalcin production) was stimulated by culture on titanium (Ti) surfaces of increasing roughness. This effect was further enhanced by 1,25-dihydroxyvitamin D3 [1,25(OH)2D3]. In the present study, we examined the response of three additional cell lines at three different maturation states: fetal rat calvarial (FRC) cells (a mixture of multipotent ...
5 µCi quantities of 1 a, 25-[26, 27-3H]-Dihydroxyvitamin D3, are available for your research. Application of [3H] Dihydroxyvitamin D3 can be found in: appearance of the rat testicular receptor during development in steroid biochemistry, in determination as a major intermediate in 25-hydroxyvitamin D3-26,23-lactone formation, receptors in the choroid plexus and ependyma in cellular neuroscience, etc.. ...
Maxacalcitol 22-Oxacalcitriol is a Vitamin D3 analog which is Non-calcemic as well as a VDR ligand. 22-Oxacalcitriol has been shown to decrease parathyroid hormone (PTH) mRNA expression in vitro. Additionally has been noted to exhibit similar effects to calcitriol in. ...
To the editor: We read with interest the recent report by Breslau and associates (1). We have recently studied the case of a patient with Hodgkins disease with hypercalcemia and increased calcitriol levels.. A 51-year-old white man was admitted to St. Josephs Hospital and Medical Center with polyuria, polydyspia, and constipation. The only abnormal findings on physical examination were hard 1- to 2-cm left inguinal lymphadenopathy and a spleen tip palpable on deep inspiration. Laboratory data included serum calcium, 11.7 mg/dL; inorganic phosphorus, 2.1 mg/dL; creatinine, 2.9 mg/dL; albumin, 4.3 mg/dL; magnesium, 2.1 mg/dL; and alkaline phosphatase, 0.52 IU/L. Thyroid ...
Depression has been linked to (lack of) sunlight exposure and raised intracellular calcium levels. In this pathway, the role of the vitamin D pathway in calcium signaling in depression is shown. Active 1,25-dihydroxy-vitamin D3 is formed from 7-dehydrocholesterol by multiple conversion steps. It associates with RXR and VDR in the nucleus, which stimulates transcription of VDR target genes, resulting in lower intracellular calcium levels. Less sunlight exposure results in lower 1,25-dihydroxyvitamin D3 levels and therefore higher calcium levels ...
Administration of Rocaltrol (calcitriol) to patients in excess of their daily requirements can cause hypercalcemia, hypercalciuria, and hyperphosphatemia. Since calcitriol is a derivative of vitamin D, the signs and symptoms of overdose are the same as for an overdose of vitamin D (see ADVERSE REACTIONS).
It may be more important than ever for older people to get enough vitamin D in their systems, either from the sun or through nutritional supplements. According to a new study, their lives may depend on it.... Full Story ...
TY - JOUR. T1 - 1.25 dihydroxyvitamin D3 receptor exist of osteoclast precursors. AU - Kamioka, Hiroshi. PY - 1991. Y1 - 1991. M3 - Article. VL - 28. SP - 185. EP - 189. JO - Dentitry in Japan. JF - Dentitry in Japan. ER - ...
Calcitriol Inhibits the Th1 and Promotes the Th2 Profile in Mice with TNBS Colitis. Th1 lymphocyte differentiation is known to be based on a sequence of cell-intrinsic and exogenous, DC-derived factors, including augmentation of the transcription factor T-bet following activation by DC-derived IL-12. The observed reduction of the Th1 mediators, especially after treatment with the combination of dexamethasone and calcitriol, was further confirmed by immunoblot analysis of the T-bet. The combined administration of calcitriol and dexamethasone led to a significant reduction of T-bet protein expression compared with dexamethasone monotherapy (P , 0.001 versus dexamethasone, Fig. 3, A and B). As a next step to assess a possible role of calcitriol and dexamethasone in promoting the Th2 subset, we analyzed IL-4 production as well as the relevant Th2 lineage commitment factor GATA3. Calcitriol significantly up-regulated IL-4, whereas dexamethasone alone did not cause any significant change in IL-4 ...
The active form of 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] regulates calcium homeostasis, immunity, and other physiological processes while its effect in T-helper lymphocyte type 2 models is not very clear. The prevention effect of 1,25(OH)2D3 for allergic asthma in a rat asthma model was investigated. Healthy Wistar rats were randomly divided into four groups: control group, asthma group, drug prevention group, and treatment group. Asthma was induced in rats by sensitization and challenges with ovalbumin (OVA). The drug prevention group and treatment group were given 1,25(OH)2D3 or vitamin D3 on different schedules. The effects of 1,25(OH)2D3 on the development of asthma were analyzed. The airway hyperresponsiveness, the inflammatory cell infiltration in bronchoalveolar lavage (BAL) fluid, and histological changes of lung cells were examined. Nitric oxide production and the expression and activity of induced nitric oxide synthase (iNOS) in the lungs were examined also. Our study showed that ...
The aim of this study was to assess the impact of 1α,25-dihydroxyvitamin D3 (vitamin D3) on osteogenic and inflammatory properties of human periodontal ligament (PDL) cells and investigate underlying mechanisms ...
Semantic Scholar extracted view of [clinical Significance of the New Vitamin B 12 and Intrinsic Factor Research]. by Konrad-Felix Krentz
1 Answer - Posted in: calcitriol, cholecalciferol - Answer: No - the doses are not the same. One IU of Vitamin D (Cholecalciferol) ...
Hayes CE, Cantorna MT, DeLuca HF. Department of Biochemistry, University of Wisconsin-Madison 53706, USA.. Recently, it has been clearly demonstrated that exogenous 1,25-dihydroxyvitamin D3, the hormonal form of vitamin D3, can completely prevent experimental autoimmune encephalomyelitis (EAE), a widely accepted mouse model of human multiple sclerosis (MS). This finding has focused attention on the possible relationship of this disease to vitamin D. Although genetic traits certainly contribute to MS susceptibility, an environmental factor is also clearly involved. It is our hypothesis that one crucial environmental factor is the degree of sunlight exposure catalyzing the production of vitamin D3 in skin, and, further, that the hormonal form of vitamin D3 is a selective immune system regulator inhibiting this autoimmune disease. Thus, under low-sunlight conditions, insufficient vitamin D3 is produced, limiting production of 1,25-dihydroxyvitamin D3, providing a risk for MS. Although the evidence ...
The invention provides a new vitamin D2 compound, 1α-hydroxy-24-epi-vitamin D2 and certain hydroxy-protected derivatives thereof. The new compound exhibits a distinctive activity pattern comprising high potency in stimulating intestinal calcium transport and little or no activity in inducing bone calcium mobilization or the differentiation of undifferentiated cells in culture, thereby evincing utility in the treatment of diseases characterized by loss of bone mass.
Carrillo-López N, Fernández-Martín JL, Cannata-Andía JB (2009-04-01). "[The role of calcium, calcitriol and their receptors in ... calcitriol), which is released into the circulation. This latter form of vitamin D is the active hormone which stimulates ... Calcitriol Increase in serum phosphate. Fibroblast growth factor-23 (FGF23) is produced in osteoblasts (from bone) in response ...
Rocaltrol (calcitriol), for osteoporosis and hypocalcaemia. Rocephin (ceftriaxone), a broad-spectrum cephalosporin antibiotic. ...
... is a form of vitamin D. Calcitriol (Vitamin D3) analogues have been proposed for use as antitumor agents. Studies on ... The motive to develop 1α-Hydroxyvitamin D5 stemmed from the tendency of calcitriol, or 1,25 dihydroxy vitamin D3, a natural ... Thus, the therapeutic effects of 1α-Hydroxyvitamin D5 as a potential antitumor agent without the side effects of calcitriol ... Beer, Tomasz M.; Myrthue, Anne (March 2004). "Calcitriol in cancer treatment: from the lab to the clinic". Molecular Cancer ...
... (INN) is an analog of calcitriol. It has a higher potency both in vivo and in vitro systems, and longer duration ...
Caniggia A, Nuti R, Lore F, Martini G, Turchetti V, Righi G (April 1990). "Long-term treatment with calcitriol in ...
"Long-term treatment with calcitriol in postmenopausal osteoporosis". Metabolism. 39 (4 Suppl 1): 43-9. doi:10.1136/bmj.1.223. ...
See also: Vitamin D receptor and Calcitriol. Calcitriol enters the target cell and binds to the vitamin D receptor in the ... Calcifediol is then converted by the kidneys to calcitriol, the biologically active form of vitamin D. Calcitriol circulates as ... to form calcitriol (1,25-dihydroxycholecalciferol, 1,25(OH)2D). The conversion of calcifediol to calcitriol is catalyzed by the ... Calcitriol itself is auto-regulated in a negative feedback cycle, and is also affected by parathyroid hormone, fibroblast ...
... inhibition of production of calcitriol, stimulation of breakdown of calcitriol, and inhibition of production/secretion of ... FGF23 is secreted by osteocytes in response to increased calcitriol. FGF23 acts on the kidneys, where it decreases the ...
Calcitriol (1,25-dihydroxycholecalciferol) is the active form of vitamin D3. It has numerous functions involved in blood ... Recent research indicates that calcitriol leads to a reduction in osteoclast formation, and bone resorption. It follows that an ... the precursor to calcitriol. Calcitonin is a hormone secreted by the thyroid in humans. Calcitonin decreases osteoclast ...
Calcitriol (Rocaltrol) and cinacalcet (a calcimimetic) are used as pharmacologic treatments. Age and gender have an effect on ...
Oral phosphate and calcitriol may be given for treatment of hypophosphatemia. For growth hormone excess, treatment with ...
La forma anàloga activa de la vitamina D (calcitriol),[13] que ajuda a mantenir el calci per als ossos i l'equilibri químic ... Lung, BE; Mowery, ML; Komatsu, DEE «Calcitriol» (en anglès). StatPearls [Internet]. StatPearls Publishing LLC, 2020 Jun 3; ...
Calcitriol (vitamin D) significantly inhibits the expression of the COX-2 gene. Caution should be exercised in combining low ...
Synthesis of osteopontin is stimulated by calcitriol (1,25-dihydroxy-vitamin D3). Regulation of the osteopontin gene is ... Hypocalcemia and hypophosphatemia (instances that stimulate kidney proximal tubule cells to produce calcitriol (1α,25- ...
Calcitriol, the activated form of vitamin D, promotes intestinal absorption of calcium and the renal reabsorption of phosphate ... For example, they convert a precursor of vitamin D to its active form, calcitriol; and synthesize the hormones erythropoietin ... The kidneys secrete a variety of hormones, including erythropoietin, calcitriol, and renin. Erythropoietin is released in ...
Calcitriol, the activated form of vitamin D, promotes intestinal absorption of calcium and the renal reabsorption of phosphate ... The kidneys secrete a variety of hormones, including erythropoietin, calcitriol, and renin. Erythropoietin is released in ...
... calcidiol into calcitriol. Only after binding to calcitriol can T-cells perform their intended function. Other immune system ... the steroid hormone calcitriol. T-cells have a symbiotic relationship with vitamin D. Not only does the T-cell extend a vitamin ... D receptor, in essence asking to bind to the steroid hormone version of vitamin D, calcitriol, but the T-cell expresses the ...
PTH is parathyroid hormone, 1,25 OH VIT D3 is calcitriol or 1,25 dihydroxyvitamin D3, and CALCITONIN is a hormone secreted by ... calcitriol), which is released into the circulation. This latter form of vitamin D is the active hormone which stimulates ...
"Activated vitamin D (calcitriol) is a pluripotent pleiotropic secosteroid hormone. As a steroid hormone, which regulates more ... Recent research indicates that intracellular calcitriol levels in numerous human tissues, including nerve and muscle tissue, ... and calcitriol do not appear to be effective.[4] ... than 1000 vitamin D-responsive human genes, calcitriol may ...
... such as calcitriol, doxercalciferol, paricalcitol; and phosphate binders, which are either calcium-based and non-calcium based ...
... calcitriol, performs its function through interactions with the calcitriol receptor. This nuclear hormone receptor is ... This greater affinity is 2.7-fold that of the active vitamin D form of calcitriol. Eldecalcitol is readily absorbed into the ... The chemistry of eldecalcitol allows for its binding 2.7-fold more potently than calcitriol. In addition, some vitamin D ... The eldecalcitol analog of calcitriol, contains a hydroxypropyl group in the lower cyclohexane ring. The synthesis of ...
Hence the activation of naive T cells is crucially dependent on adequate calcitriol levels. In summary, activation of T cells ... However, activated TCR signaling through p38 upregulates VDR expression and calcitriol activated VDR, in turn, upregulates PLC- ... the expression of PLC-γ1 is dependent on VDR activated by calcitriol. Naive T cells have very low expression of VDR and PLC-γ1 ...
It is also treated with medications including human growth hormone, calcitriol, and phosphate. The prevalence of the disease is ... Biochemically in blood, XLH is recognized by hypophosphatemia and an inappropriately low level of calcitriol (1,25-(OH)2 ... while calcitriol levels are low or within the lower reference range. Most importantly, urinary loss of phosphate is above the ... calcitriol; in the event of severe bowing, an osteotomy may be performed to correct the leg shape. The monoclonal antibody ...
Calcitriol (1,25-dihydroxyvitamin D3), the active metabolite of vitamin D3, after being synthesized from calcifediol in the ... About ten days are needed for the body to process vitamin D3 into calcitriol. S-adenosylmethionine (SAMe), a cosubstrate ...
It stimulates the manufacture and release, by the kidneys, of calcitriol into the blood. This steroid hormone acts on the ...
The action of calcitriol is mediated by the vitamin D receptor, a nuclear receptor which regulates the synthesis of hundreds of ... It is converted in the liver to calcifediol (25-hydroxyvitamin D) which is then converted in the kidney to calcitriol (1,25- ... Hydroxylation in the kidneys of calcifediol to calcitriol by 1-alpha-hydroxylase is tightly regulated: it is stimulated by ... 25-Hydroxyvitamin D3 1-alpha-Hydroxylase, a kidney enzyme that converts calcifediol to calcitriol. Coulston AM, Boushey C, ...
These plants contain calcitriol or similar substances that cause rises in calcium ion levels. Hypercalcemia is most common in ... see calcitriol under Vitamin D) levels (e.g. sarcoidosis and other granulomatous diseases such as tuberculosis, berylliosis, ...
It has been suggested, based on animal research, that calcitriol, the active metabolite of vitamin D, can provide significant ... Cass WA, Smith MP, Peters LE (2006). "Calcitriol protects against the dopamine- and serotonin-depleting effects of neurotoxic ...
The levels of the active form of vitamin D, calcitriol, are inversely correlated with coronary calcification.[23] Moreover, the ... Intake of vitamin D raises the concentration of vitamin D metabolites which exceed DBP binding capacity and free calcitriol ... Intake of vitamin D raises calcitriol concentrations in the plasma and cell ...
Expression could be induced by treating these animals with vitamin D metabolites such as calcitriol. They were found to exist ... Expression of S100G, like that of calbindin 1, is stimulated by the active vitamin D metabolite, calcitriol although the ...
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Calcitriol: learn about side effects, dosage, special precautions, and more on MedlinePlus ... If you become pregnant while taking calcitriol, call your doctor. You should not breastfeed while you are taking calcitriol. ... Calcitriol comes as a capsule and a solution (liquid) to take by mouth. It usually is taken once a day or once every other day ... Calcitriol will work only if you get the right amount of calcium from the foods you eat. If you get too much calcium from foods ...
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Calcitriol (Rocaltrol) is prescribed to treat and prevent low levels of calcium in people with kidney disease or parathyroid ... How should I keep calcitriol stored?. Calcitriol should be stored at room temperature, between 15 C and 30 C (59 F and 86 F). ... calcitriol (Rocaltrol). *What is calcitriol, and how does it work (mechanism of action)? ... Higher doses of calcitriol may be necessary if these drugs are used together with calcitriol. ...
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  • Calcitriol (Rocaltrol, Calcijex is a discontinued brand) is a medication prescribed to treat low levels of calcium in people with kidney disease, rickets, and familial hypophosphatemia. (
  • Does Rocaltrol (calcitriol) cause side effects? (
  • Rocaltrol ( calcitriol ) is a synthetic active form of vitamin D3 ( cholecalciferol ) used to treat and prevent low levels of calcium in the blood of patients who have kidney disease or problems with their parathyroid gland, the gland that controls the amount of calcium in blood through its secretion of parathyroid hormone. (
  • Calcitriol is marketed under various trade names including Rocaltrol (Roche), Calcijex (Abbott) and Decostriol (Mibe, Jesalis). (
  • What is calcitriol (Rocaltrol)? (
  • What is the most important information I should know about calcitriol (Rocaltrol)? (
  • What should I discuss with my healthcare provider before taking calcitriol (Rocaltrol)? (
  • Calcitriol yw cynhwysyn actif Rocaltrol a Vectical. (
  • Calcitriol (Brand names: Vectical, Rocaltrol) is prescribed for the treatment of low calcium and psoriasis. (
  • Calcitriol(Rocaltrol) generic Alfa D3 (1 mcg) is a synthetic vitamin D analog, prescribed for hypocalcemia in patients undergoing chronic renal dialysis. (
  • Rocaltrol, also known as Calcitriol, is a medication used to treat conditions that are caused as a result of high or low parathyroid hormone levels. (
  • Rocaltrol (Calcitriol) is a form of vitamin D, necessary for normal bone development. (
  • The beneficial effect of calcitriol in renal osteodystrophy appears to result from correction of hypocalcemia and secondary hyperparathyroidism. (
  • In this study, we selected this approach to test several hypotheses about the effect of calcitriol (1,25-dihydroxycholecalciferol), the active form of vitamin D, on early-stage human prostate cancer. (
  • Secondary objective was to evaluate the effect of calcitriol on migration and invasion of OS cell lines, and the role of matrix metalloproteins (MMPs) in migration/invasion. (
  • We examined the effect of calcitriol versus cholecalciferol supplementation on vascular endothelial function in patients with CKD. (
  • It is the active form of vitamin D 3 , produced fom calciol via hydoxylation in the liver to form calcidiol, which is subsequently oxidised in the kidney to give calcitriol. (
  • Calcitriol is a synthetic (man-made) active form of vitamin D3 ( cholecalciferol ). (
  • Calcitriol is the most active known form of vitamin D 3 in stimulating intestinal calcium transport. (
  • Calcitriol is the active form of vitamin D, normally made in the kidney. (
  • Calcitriol was identified as the active form of vitamin D in 1971 and the drug was approved for medical use in the United States in 1978. (
  • Calcitriol or 1,25-dihydroxycholecalciferol (abbreviated 1,25-(OH) 2 -D3) is the active form of vitamin D found in the body (vitamin D3). (
  • Researchers from Canada, United States and Europe are registering men with advanced prostate cancer for a study involving a treatment that combines chemotherapy with high-dose of Calcitriol, a naturally occurring active form of vitamin D. (
  • Calcitriol is a form of vitamin D that is active in the body. (
  • CALCITRIOL (kal si TRYE ole) is a man-made form of vitamin D. It is used to treat patients with low levels of calcium who are on chronic renal dialysis. (
  • We show that calcitriol, the hormonally active form of vitamin D, regulates the expression of aromatase in a tissue-selective manner. (
  • OBJECTIVE We investigated whether supplementation of the active form of vitamin D (calcitriol) in recent-onset type 1 diabetes can protect β-cell function evaluated by C-peptide and improve glycemic control assessed by A1C and insulin requirement. (
  • The aim of this pilot trial was to investigate whether the supplementation of the active form of vitamin D (calcitriol) in subjects with recent-onset type 1 diabetes is able to protect residual β-cell function (C-peptide) and to improve metabolic control. (
  • A double-blind trial was designed with patients randomized to 0.25 μg/daily calcitriol (the active form of vitamin D, 1.25-dihydroxyvitamin D3) or placebo and followed-up for 2 years. (
  • CALCITRIOL (kal si TRYE ole) is a man made form of vitamin D. It is used on the skin to treat plaque psoriasis. (
  • CALCITRIOL (kal si TRYE ole) is a man made form of vitamin D. It helps your body keep the proper levels of calcium and phosphorus and maintain healthy bones and teeth. (
  • A team led by Michel Vallée, MD, PhD, of Maisonneuve-Rosemont Hospital, University of Montreal, studied a retrospective cohort of 45 chronic HD patients with SHPT who were switched from oral alfacaclidol-which requires 25-hydoxylation in the liver to be effective-to oral calcitriol -the fully hydoxylated active form of vitamin D3. (
  • also know as calcitriol), the hormonal form of vitamin D, can inhibit the proliferation and promote the differentiation of human prostate adenocarcinoma cells. (
  • Due to the hypercalcemic side effects of vitamin D and its derivatives in higher plasma concentrations, the anti-cancer benefits of calcitriol (the active form of vitamin D) have not been fully realized in prostate cancer (PCa) chemoprevention and/or treatment. (
  • COX-2 is naturally inhibited by calcitriol (the active form of Vitamin D). Both the peroxidase and PTGS activities are inactivated during catalysis by mechanism-based, first-order processes, which means that PGHS-2 peroxidase or PTGS activities fall to zero within 1-2 minutes, even in the presence of sufficient substrates. (
  • If you get too much calcium from foods, you may experience serious side effects of calcitriol, and if you do not get enough calcium from foods, calcitriol will not control your condition. (
  • What are the side effects of calcitriol? (
  • The effects of Calcitriol Ointment on calcium metabolism following treatment durations greater than 52 weeks have not been evaluated. (
  • Many of the effects of calcitriol are mediated by its interaction with the calcitriol receptor, also called the vitamin D receptor or VDR. (
  • This study will explore the potential anti-proteinuric and anti-inflammatory effects of Calcitriol in the treatment of IgA nephropathy, which has no specific treatment at present. (
  • Hypercalcemia and hypercalciuria, the most common side effects of calcitriol therapy, were not documented in the trials reviewed, and might have been the result of the low dosages used. (
  • 1 yr) effects of calcitriol replacement treatment have not been reported. (
  • Objective: Our primary objective is to investigate effects of calcitriol in combination with cisplatin on the osteosarcoma cell apoptosis, invasion and migration. (
  • Calcitriol comes as an ointment to apply to the skin. (
  • Apply calcitriol ointment at around the same times every day. (
  • Apply calcitriol ointment exactly as directed. (
  • In children 2 to 6 years of age, do not use more than one tube (100 gm) of calcitriol ointment per week. (
  • In adults and children 7 years of age and older, do not use more than two tubes (200 gm) of calcitriol ointment per week. (
  • Apply calcitriol ointment to the areas of skin affected by plaque psoriasis. (
  • Do not apply calcitriol ointment to healthy skin or anywhere on your face, eyes, lips, or vagina. (
  • Do not cover the skin where you applied calcitriol ointment with a bandage or dressing unless your doctor tells you that you should. (
  • Wash your hands well with soap and water after you apply calcitriol ointment. (
  • Do not freeze or refrigerate calcitriol ointment. (
  • These highlights do not include all the information needed to use Calcitriol Ointment safely and effectively. (
  • See full prescribing information for Calcitriol Ointment. (
  • The safety and effectiveness of Calcitriol Ointment in patients with known or suspected disorders of calcium metabolism have not been evaluated. (
  • Apply Calcitriol Ointment to affected areas of the body twice daily ( 2 ). (
  • If aberrations in parameters of calcium metabolism are noted discontinue Calcitriol Ointment until these normalize. (
  • Apply Calcitriol Ointment to affected areas twice daily, morning and evening. (
  • Calcitriol Ointment should not be applied to the eyes, lips, or facial skin. (
  • Calcitriol Ointment is not for oral, ophthalmic or intravaginal use. (
  • Each gram of Calcitriol Ointment contains 3 micrograms (mcg/g) of calcitriol. (
  • In controlled clinical trials hypercalcemia was observed in subjects exposed to Calcitriol Ointment. (
  • Calcitriol is prescribed for: Treatment of hypocalcaemia - hypoparathyroidism, osteomalacia (adults), rickets (infants, children), renal osteodystrophy, chronic kidney disease Treatment of osteoporosis Prevention of corticosteroid-induced osteoporosis Calcitriol has been used in an ointment for the treatment of psoriasis, although the vitamin D analogue calcipotriol (calcipotriene) is more commonly used. (
  • Calcitriol Ointment is a vitamin D analog. (
  • Some medical conditions may interact with Calcitriol Ointment. (
  • Ask your health care provider if Calcitriol Ointment may interact with other medicines that you take. (
  • Use Calcitriol Ointment as directed by your doctor. (
  • Apply a thin layer of Calcitriol Ointment and gently rub it into the skin until it is absorbed. (
  • Wash your hands immediately after using Calcitriol Ointment unless your hands are part of the treated area. (
  • Calcitriol Ointment is for use on the skin only. (
  • If you miss a dose of Calcitriol Ointment, use it as soon as possible. (
  • Ask your health care provider any questions you may have about how to use Calcitriol Ointment. (
  • Calcitriol Ointment may cause you to become sunburned more easily. (
  • Avoid the sun, sunlamps, or tanning booths while using Calcitriol Ointment. (
  • You will need to discuss the benefits and risks of using Calcitriol Ointment while you are pregnant. (
  • It is not known if Calcitriol Ointment is found in breast milk. (
  • If you are or will be breast-feeding while you use Calcitriol Ointment, check with your doctor. (
  • Calcitriol is used to treat and prevent low levels of calcium and bone disease in patients whose kidneys or parathyroid glands (glands in the neck that release natural substances to control the amount of calcium in the blood) are not working normally. (
  • Calcitriol is also sometimes used to increase the amount of calcium in the blood of premature babies. (
  • Calcitriol will work only if you get the right amount of calcium from the foods you eat. (
  • Calcitriol increases blood levels of calcium by increasing the absorption of calcium in the kidneys, increasing the absorption of calcium and phosphorus from the intestine, and increasing the release of calcium and phosphorus from the bones. (
  • Calcitriol helps the body to use calcium found in foods and supplements . (
  • Since calcitriol also increases calcium levels, taking these two types of medications together may cause hypercalcemia (abnormally highly levels of calcium). (
  • Because of the short biological half-life of calcitriol, pharmacokinetic investigations have shown normalization of elevated serum calcium within a few days of treatment withdrawal, i.e., much faster than in treatment with vitamin D 3 preparations. (
  • 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. (
  • In acutely uremic rats calcitriol has been shown to stimulate intestinal calcium absorption. (
  • Calcitriol increases blood calcium (Ca2+) mainly by increasing the uptake of calcium from the intestines. (
  • mycobacterium avium, leprosy, lipoid pneumonia, cat scratch fever, berylliosis Calcitriol increases blood calcium levels ([Ca2+ ]) by: Promoting absorption of dietary calcium from the gastrointestinal tract. (
  • When calcitriol binds to the receptor, the ligand-receptor complex translocates to the cell nucleus, where it acts as a transcription factor promoting the expression of a gene encoding a calcium binding protein. (
  • You should not use this medication if you have high levels of calcium or vitamin D in your blood, or if you have ever had an allergic reaction to calcitriol or other forms of vitamin D. (
  • Calcitriol is also used to treat calcium deficiency (hypocalcemia) and metabolic bone disease in people who are receiving dialysis. (
  • Calcitriol is also used to treat calcium deficiency in people with hypoparathyroidism (underactive parathyroid glands) caused by surgery, disease, or other conditions. (
  • Do not take vitamins, calcium supplements, or other forms of vitamin D while you are taking calcitriol. (
  • Calcitriol is used to help increase the amount of calcium in the blood and help with proper bone formation for people with chronic kidney failure that are undergoing dialysis. (
  • We studied whether corticosteroid-induced osteoporosis could be prevented by treatment with calcium, calcitriol (1,25-dihydroxyvitamin D3), and calcitonin. (
  • One hundred three patients starting long-term corticosteroid therapy were randomly assigned to receive 1000 mg of calcium per day orally and either calcitriol (0.5 to 1.0 microgram per day orally) plus salmon calcitonin (400 IU per day intranasally), calcitriol plus a placebo nasal spray, or double placebo for one year. (
  • Calcitriol (mean dose, 0.6 microgram per day), with or without calcitonin, prevented more bone loss from the lumbar spine (mean rates of change, -0.2 and -1.3 percent per year, respectively) than calcium alone (-4.3 percent per year, P = 0.0035). (
  • In the second year, lumbar bone loss did not occur in the group previously treated with calcitonin plus calcitriol (+0.7 percent per year), but it did occur in the group given calcium alone (-2.3 percent per year). (
  • Calcitriol and calcium, used prophylactically with or without calcitonin, prevent corticosteroid-induced bone loss in the lumbar spine. (
  • Calcitriol increases intestinal absorption of calcium and phosphorus, and in concert with parathyroid hormone increases bone resorption. (
  • Bypassing hepatic 25-hydroxylation appears to be associated with greater efficacy of calcitriol at increasing serum calcium and inhibiting PTH secretion, the investigators concluded. (
  • The decreases in vascular calcium content were associated with an increase in vascular Mg. Calcitriol treatment alone significantly decreased TRPM7 protein whereas the combination treatment increased both the mRNA and protein expression. (
  • Calcitriol, a calcitrophic hormone that can be suppressed by high dietary calcium, favors fatty acid synthesis and inhibits lipolysis via non-genomic modulation of Ca 2 + influx. (
  • 1.5 were randomly allocated to an E group (each cycle = oral etidronate 400 mg daily for 14 days followed by calcium 500 mg daily for 76 days) or an E+C group (as for E plus oral calcitriol 0.5 μg daily). (
  • There is also some evidence that calcitriol (1,25-dihydroxyvitamin D 3 ), a vitamin D analogue, may reduce vertebral fracture rates, 4 and a combination of vitamin D 3 and calcium supplements can reduce the risk of hip fractures and increase hip BMD in elderly women. (
  • Phosphate includes about one% of total Calcitriol entire body body weight, about eighty five% resides in bone, fourteen% in cells, and one% in serum and ECFs.12-14,86 Calcitriol Upkeep of serum phosphate inside of usual boundaries lets an optimum calcium-phosphate item for bone mineralization devoid of deposition in smooth tissues. (
  • Renal production of calcitriol is stimulated by PTH, low calcium and low phosphate and it is reduced by high phosphate and FGF23. (
  • In CKD stage, 3-4 moderate doses of calcitriol are effective to control secondary hyperparathyroidism and observational studies suggest that calcitriol therapy increases survival and slows the progression of renal disease as long as phosphate and calcium levels are controlled. (
  • Calcium and calcitriol therapy in osteoporotic postmenopausal women with impaired calcium absorption. (
  • The effects of oral calcitriol (0.25 and 0.50 micrograms/d), together with calcium (1 g/d), on calcium absorption and bone resorption were measured in postmenopausal osteoporotic women with calcium malabsorption. (
  • Hypercalcemia has been reported in patients treated with calcitriol. (
  • Compared to other vitamin D compounds in clinical use (cholecalciferol, ergocalciferol), calcitriol has a higher risk of inducing hypercalcemia. (
  • We have recently studied the case of a patient with Hodgkin's disease with hypercalcemia and increased calcitriol levels. (
  • Antineoplastic activity of calcitriol in preclinical systems is seen at concentrations significantly above the physiologic range, typically above 1 nmol/L. Such concentrations cannot be reached with conventional daily dosing of calcitriol due to predictable hypercalcemia and hypercalcuria ( 15 ). (
  • Incident calcitriol users and nonusers were selected on the basis of stages 3 to 4 CKD, hyperparathyroidism, and the absence of hypercalcemia before calcitriol use and then were matched by age and estimated kidney function. (
  • Calcitriol use was associated with a greater risk for hypercalcemia. (
  • In dialysis patients, the administration of calcitriol reduces serum PTH levels but it is also known that high doses of calcitriol are associated with hypercalcemia and worse control of hyperphosphatemia. (
  • Calcitriol comes as a capsule and a solution (liquid) to take by mouth. (
  • Each orange, opaque, oval, soft gelatin capsule with "O25" printed in black contains 0.25 µg of calcitriol. (
  • Each orangeish-to-red, opaque, oval, soft gelatin capsule with "O50" printed in black contains 0.50 µg of calcitriol. (
  • Cholestyramine ( Questran ), colestipol ( Colestid ), mineral oil, and orlistat ( Alli , Xenical ) may decrease the intestinal absorption of calcitriol. (
  • Classically, there are four principal acknowledged regulators of phosphate metabolism: (one) nutritional phosphate ingestion and absorption, (two) calcitriol, which can boost phosphorus resorption from bone and absorption from intestine, (three) PTH, which straight leads to phosphorus resorption from bone, and indirectly activates intestinal absorption by way of stimulation of calcitriol output, and (4) renal tubular reabsorption of phosphorus that is stimulated by tubular filtered load of phosphorus and inhibited by PTH. (
  • OUTLINE: This is a dose-limiting toxicity study of calcitriol. (
  • OUTLINE: This is a dose-escalation study of calcitriol. (
  • Methodology/Principal Findings: We conducted a post-hoc analysis of a double-blind, placebo-controlled study of calcitriol supplementation to preserve β-cell function. (
  • Higher doses of calcitriol may be necessary if these drugs are used together with calcitriol. (
  • Cohorts of 3-6 patients receive escalating doses of calcitriol until the maximum tolerated dose (MTD) is determined. (
  • Our testing protocol left one week between pulse doses of Calcitriol while taking VitD daily. (
  • PTH also stimulates the production of calcitriol (see below). (
  • We have studied whether or not the development of rachitic lesions in piglets with PVDRI is due to altered binding properties of the intestinal calcitriol receptor in addition to the defective renal production of calcitriol. (
  • Determine the effect of administration of calcitriol on the pharmacokinetics of paclitaxel in these patients. (
  • CONCLUSIONS: Parathyroid adenoma injection is an alternative method of treatment for some patients resistant to treatment by means of vitamin D3 pulses or intravenous administration of calcitriol. (
  • In kidney transplant patients, the administration of calcitriol, 0.5 µg/48h prevents bone mass loss during the first few months after transplantation. (
  • The two known sites of action of calcitriol are intestine and bone. (
  • The kidneys of uremic patients cannot adequately synthesize calcitriol, 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. (
  • Calcitriol is used to treat hyperparathyroidism (overactive parathyroid glands) and metabolic bone disease in people who have chronic kidney failure and are not receiving dialysis. (
  • Calcitriol may also be used to treat vitamin D-resistant rickets, a bone disease caused by too little vitamin D. (
  • Evidence from these trials shows that calcitriol monotherapy can improve bone mineral density in elderly osteoporotic Chinese patients but may be insufficient for long-term treatment. (
  • Calcitriol can also decrease bone turnover markers and bring about significant improvements in muscle strength. (
  • Further, calcitriol in combination with other therapeutic bone agents was shown to be well tolerated and capable of additional bone-preserving effects compared with use of calcitriol alone in areas including bone mineral density, bone turnover markers, bone pain improvement, and fracture incidence. (
  • Calcitriol significantly decreased aromatase expression in human BCa cells and adipocytes and caused substantial increases in human osteosarcoma cells (a bone cell model exhibiting osteoblast phenotype in culture) and modest increases in ovarian cancer cells. (
  • In addition to augmenting the ability of AIs to inhibit BCa growth, calcitriol acting as a selective aromatase modulator that increases aromatase expression in bone would reduce the estrogen deprivation in bone caused by the AIs, thus ameliorating the AI-induced side effect of osteoporosis. (
  • The calcitriol group also lost lumbar bone (-3.6 percent per year) but received more corticosteroid in the second year than the other two groups. (
  • The mRNA expressions of alkaline phosphatase (ALP), bone sialoprotein (BSP), core-binding factor alpha-1 (CBFA1), collagen-1 (Col-1), osteocalcin (OCN), and vitamin D 3 receptor (VDR) were assessed after incubation with calcitriol for 2 weeks. (
  • Treatment with calcitriol resulted in the normalization of biochemical parameters and mean lumbar spine areal bone mineral density z-scores within 3 months, whereas height z-scores increased more gradually. (
  • We investigated the effect of supplementation with calcitriol on bone turnover in recent-onset type 1 diabetes (T1D). (
  • Changes in bone formation (osteoclacin) and resorption (beta-CrossLaps) markers, and differences between placebo and calcitriol-treated group were evaluated. (
  • The aim of this study was to compare the effects of intermittent cyclical etidronate (E) therapy alone with a combination of cyclical etidronate and calcitriol (E+C) on spine and femoral neck bone mineral density (BMD) at one year. (
  • In a retrospective study, we have assessed the efficacy of oral calcitriol on the evolution of hyperparathyroid bone disease in patients on hemodialysis. (
  • At the bone level calcitriol suppresses pre-osteoblasts and activates mature osteoblasts. (
  • High calcitriol levels may also be seen in human disease states in patients not on supplementation. (
  • In this report, we present a girl with severe AD who under adequate supplementation with cholecalciferol was treated with calcitriol and subsequently with paricalcitol. (
  • We aimed to investigate effects of vitamin D supplementation on IGF-1 (primary outcome) and calcitriol (1,25(OH) 2 D) concentrations (secondary outcome). (
  • To assess the impact of calcitriol and phosphate supplementation on growth we analysed from a cohort of 18 patients treated at the Dept. of Paediatrics at O.-v.-Guericke-University Magdeburg. (
  • Conclusions: High-dose calcitriol down-regulates VDR expression in human prostate cancer. (
  • Are any trials upcoming for high dose calcitriol? (
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  • Magnesium containing medications (for example, antacids) should be avoided in patients undergoing chronic renal dialysis who are taking calcitriol. (
  • Local calcitriol injections as a suppressive treatment of secondary hyperparathyroidism in chronic dialysis patients. (
  • AIM: A prospective study was made of the effectiveness of repeatable local calcitriol injections therapy to suppress secondary hyperparathyroidism resistant to conventional therapy in chronic dialysis patients. (
  • DENVER-Oral paricalcitol (OP) appears to have similar efficacy and safety compared with oral calcitriol (OC) in dialysis patients with secondary hyperparathyroidism (SHPT) , according to results from a randomized, controlled trial. (
  • We evaluated associations of oral calcitriol use with mortality and dialysis dependence in 1418 nondialysis patients with CKD and hyperparathyroidism in the Veterans' Affairs Consumer Health Information and Performance Sets database. (
  • 18 - 21 Given biologic plausibility for an effect of oral calcitriol on survival and lack of clinical outcome data pertaining to this commonly prescribed CKD medication, we evaluated associations of oral calcitriol use with mortality and dialysis dependence in 1418 patients with stages 3 to 4 CKD and hyperparathyroidism. (
  • During follow-up, 75 calcitriol users and 142 nonusers initiated long-term dialysis (10.4 events per 100 person-years and 10.1 events per 100 person years among calcitriol users and nonusers, respectively). (
  • Cumulative incidence rates of mortality and mortality plus dialysis dependence remained lower among calcitriol users compared with nonusers throughout follow-up ( Figure 1 ). (
  • 5. It was concluded that in addition to 1,25-dihydroxyvitamin D 3 deficiency, secondary hyperparathyroidism may participate in the abnormal lipid metabolism, glucose tolerance and insulin secretion seen in dialysis patients and these abnormalities could be, at least in part, improved by intravenous calcitriol treatment. (
  • Determine the maximum tolerated dose of calcitriol administered with zoledronate in patients with progressive prostate cancer. (
  • Determine the toxic effects and maximum tolerated dose of calcitriol when combined with paclitaxel in patients with advanced solid tumors. (
  • Calcitriol is also commonly used as a medication in the treatment of hypocalcemia and osteoporosis. (
  • APO-Calcitriol is indicated for the:,- treatment of established osteoporosis diagnosed by objective measuring techniques, such as densitometry, or by radiographic evidence of a traumatic fracture . (
  • In a double-blind, randomized, placebo-controlled 2-year clinical trial reported in a recent issue, Ott and Chesnut (1) concluded that "calcitriol treatment is not effective in postmenopausal osteoporosis. (
  • Gallagher J, Riggs B. Calcitriol for Postmenopausal Osteoporosis. (
  • One study showed that treatment with calcitriol can improve quality of life in patients with osteoporosis, although not to the same extent as bisphosphonates. (
  • Conversion of oral alfacalcidol to oral calcitriol in the treatment of secondary hyperparathyroidism in chronic hemodialysis patients. (
  • Calcitriol may also be used for purposes not listed in this medication guide. (
  • 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. (
  • This study will aim to describe objective tumor responses to the combination of oral calcitriol and ketoconazole and hydrocortisone-among patients with measurable disease using modified RECIST 1.1 criteria. (
  • Additionally, we will determine toxicities, and tolerability of oral calcitriol combination with daily oral ketoconazole, and hydrocortisone in this patient population. (
  • Patients receive oral calcitriol weekly for 3 consecutive days and zoledronate IV monthly. (
  • During course 1, patients receive oral calcitriol daily on days 1-3 of weeks 1-6 and paclitaxel IV over 1 hour on day 1 of week 1 and day 3 of weeks 2-6. (
  • 1 strength combination of Benazepril/Calcitriol/Famotidine Oral Oil Suspension is available. (
  • In conclusion, oral calcitriol use is associated with lower mortality in nondialysis patients with CKD. (
  • 2 , 7 , 8 In clinical trials of predialysis patients with CKD, oral calcitriol or its analogues lowered serum PTH levels. (
  • Participants were randomly assigned to oral cholecalciferol (2000 IU daily) or calcitriol (0.5 μ g) daily for 6 months. (
  • Calcitriol should be used cautiously in patients taking digoxin ( Lanoxin ). (
  • The current study is set up a clinical trial phase II of vitamin D (calcitriol) in combination with 5-fluorouracil, Mitomycin C and Leucovorin in an open label-non-randomized study to evaluate the tumor response in patients with advanced intrahepatic cholangiocarcinoma. (
  • However there is one patient who responses to calcitriol and 5-fluorouracil/mitomycin C/leucovorin, the new 14 patients will be accrued during the secondary phase of study. (
  • In this portion of the study, all patients will get the same dose of calcitriol along with the standard chemotherapy (5-fluorouracil-mitomycin C-leucovorin). (
  • To assess quality of life (QOL) of patients who are received calcitriol in combination with 5-fluorouracil/mitomycin C/leucovorin. (
  • To assess the response of calcitriol in combination with 5-fluorouracil/mitomycin C/leucovorin in patients with advanced intrahepatic cholangiocarcinoma. (
  • Patients receive calcitriol (10mcg QD X3 weekly) in addition to ketoconazole (400mg QD) and hydrocortisone (20mg AM, 10 mg PM). (
  • Calcitriol therapy may be considered as a safe and efficacious treatment option for patients with severe AD, particularly for those with refractory AD, under monitoring for possible side effects. (
  • The number of patients to be included in the trial was calculated from setting a difference in basal C-peptide of 0.12 nmol/l at 2 years after diagnosis between the calcitriol and placebo groups. (
  • Methods: After selection of surgical treatment for histologically confirmed adenocarcinoma of the prostate, patients were randomized to either calcitriol 0.5 μg/kg or placebo weekly for 4 weeks. (
  • Calcitriol may be the optimal active vitamin D3 therapy for hemodialysis (HD) patients with secondary hyperparathyroidism (SHPT) , according to researchers. (
  • In light of these results, calcitriol may be the treatment of choice for SHPT in chronic hemodialysis patients, especially for those with resistant hyperparathyroidism, which does not respond adequately to alfacalcidol. (
  • Short- and long-term outcome of patients with pseudo-vitamin D deficiency rickets treated with calcitriol. (
  • MATERIALS AND METHODS: Thirty-nine patients (20 females) with PDDR received calcitriol for periods of 2.0-26 yr. (
  • In 21 patients, data were available at diagnosis and during the first 2 yr of treatment with calcitriol. (
  • As to long-term effects, adult patients who had received calcitriol before the pubertal growth spurt (n = 11) had normal height, whereas patients who were treated with calcitriol only after puberty (n = 14) on average were short (height z-score -2.2). (
  • Chronic kidney disease (CKD) patients are commonly treated with vitamin D analogs, such as calcitriol. (
  • These findings suggest that modifying the adverse effect profile of calcitriol with Mg may be a plausible approach to benefiting CKD patients prescribed calcitriol. (
  • During the study period, 12 (3%) calcitriol users and 40 (4%) control patients were lost to follow-up. (
  • 2. The effect of the partial suppression of hyperparathyroidism by intravenous calcitriol on lipid levels and glucose tolerance was studied in 15 haemodialysis patients with secondary hyperparathyroidism. (
  • 3. Before calcitriol treatment, uraemic patients with secondary hyperparathyroidism displayed a significant higher triglyceride and a significant lower HDL-C and apoprotein A-I as well as marked glucose intolerance with an increment of the area below the glucose curve when compared with healthy control subjects. (
  • Conclusions Six months of therapy with calcitriol or cholecalciferol did not improve vascular endothelial function or improve inflammation in patients with CKD. (
  • 33 patients who had received calcitriol for at least one year and up to 7 years were carefully matched with controls for gender, years on hemodialysis and severity of radiological hyperparathyroidism both at the start of haemodialysis and at the start of the study. (
  • Calcitriol dose-normalized AUC versus creatinine clearance in individual patients following the administration of a single dose of DN-101. (
  • Calcitriol (0.5 µg calcitriol twice per week) has been effective in decreasing proteinuria in patients with IgA nephropathy. (
  • Calcitriol topical is used to treat mild to moderate plaque psoriasis (a skin disease in which red, scaly patches form on some areas of the body) in adults and children 2 years of age and older. (
  • tell your doctor and pharmacist if you are allergic to calcitriol, any other medications, or any of the ingredients in calcitriol topical. (
  • If you are breastfeeding while using calcitriol topical, do not apply it directly to the nipple and areola (the colored area around each nipple). (
  • Calcitriol topical may cause side effects. (
  • There are no evaluations for Calcitriol topical. (
  • but, i have not been able to find anything published linking topical application to serum calcitriol status. (
  • Combinations of calcitriol with three different aromatase inhibitors (AIs) caused enhanced inhibition of BCa cell growth. (
  • Inhibition of calcitriol-induced monocyte CD14 expression by uremic toxins: Role of purines. (
  • Inhibition of calcitriol-induced mono. (
  • Because of hypercalciuria as a side effect from calcitriol therapy, treatment was continued with paricalcitol, a vitamin D analogue used in secondary hyperparathyroidism in chronic kidney disease. (
  • Improved growth rate in XLR children occured by combined phosphate and calcitriol treatment before 18 months. (
  • The major conditions with hypercalcaemia due to elevated calcitriol levels are lymphoma, tuberculosis and sarcoidosis where excess production occurs due to ectopic 25(OH)D-1-hydroxylase (CYP27B1) expressed in macrophages. (
  • 1 alpha,25-Dihydroxyvitamin D (calcitriol) inhibits the invasiveness of human prostate cancer cells. (
  • Calcitriol sensitization inhibits the migration of 143B-P cells in matrigel whereas no significant difference was observed in control and calcitriol treated 143B-MM cells. (
  • FGF-23 inhibits one-α-hydroxylase in the kidney and stimulates 24-hydroxylase action, thereby reducing calcitriol synthesis and growing calcitriol metabolic process to the inactive one,24,25(OH)3-vitamin D.105 In addition, FGF-23 inhibits the secretion of PTH prior to uremia is superior, but this is a minor effect as the big regulator of PTH secretion is serum iCa. (
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  • A calcitriol receptor-binding protein appears to exist in the mucosa of human intestine. (
  • For instance, the unbound inactive form of the calcitriol receptor in intestinal epithelial cells resides in the cytoplasm. (
  • Proteins, usually found in the cytoplasm, that specifically bind calcitriol, migrate to the nucleus, and regulate transcription of specific segments of DNA with the participation of D receptor interacting proteins (called DRIP). (
  • 4. No differences between PVDRI and control piglets were also found for the relative molecular mass (47 500 and 47700, respectively) and the Stokes' radius (3.04 and 3.05 nm, respectively) of the calcitriol receptor. (
  • 5. It is concluded that the intestinal calcitriol receptor of this animal model functions normally and that changes in binding properties and concentration of the intestinal calcitriol receptor do not contribute to the development of rachitic lesions in PVDRI piglets. (
  • The kinetics of human amyloid-β (hAβ) 40 were examined in the rat pursuant to intravenous and intracerebroventricular administration after pretreatment with calcitriol, the active vitamin D receptor ligand (6.4 nmol·kg −1 in 0.3 ml corn oil every other day for four intraperitoneal doses) to induce P-glycoprotein (P-gp) and enhance hAβ 40 brain efflux. (
  • Calcitriol is in a class of medications called vitamin D analogs. (
  • Research on the noncalcemic actions of calcitriol and other VDR-ligand analogs and their possible therapeutic applications has been reviewed. (
  • The Potential Role of Calcitriol Analogs in the Management of Breast Cancer. (
  • Furthermore they suggest that early markers of inflammatory dendritic cell and Th17 differentiation qualify as new target molecules for both calcitriol and highly selective immune-modulating vitamin D analogs. (
  • Many other medications may also interact with calcitriol, so be sure to tell your doctor about all the medications you are taking, even those that do not appear on this list. (
  • Which drugs or supplements interact with calcitriol? (
  • The combination of calcitriol and an AI may have potential benefits for BCa therapy. (
  • If you do not have kidney disease, you should drink plenty of fluids while taking calcitriol. (
  • Additional evidence suggests that calcitriol may also act on the kidney and the parathyroid glands. (
  • Vitamin D is converted in the liver and kidney to calcitriol and ultimately acts through these receptors. (
  • Megalin is important in regulating the response of the NaPi-IIa transporter to PTH that results in phosphaturia and calcitriol upregulates megalin expression in the kidney.10 The effects of PTH are rapid and the outcomes of FGF-23 acquire a lot more time. (
  • A third important effect of PTH on the kidney is its stimulation of the conversion of 25-hydroxy vitamin D into 1,25-dihydroxy vitamin D (calcitriol), which is released into the circulation. (
  • 1,25-(OH) 2 D 3 (calcitriol) is an active vitamin D metabolite. (
  • Four children of 2 families had alopecia associated with severe rickets, resistant to treatment and caused by defective cytoplasmic and nuclear receptors for the active vitamin D metabolite calcitriol (1,25-dihydroxycholecalciferol). (
  • 1 - 4 The kidneys play an important role in converting 25-hydroxyvitamin D to calcitriol, the most biologically potent vitamin D metabolite, under regulation by parathyroid hormone (PTH) and phosphate. (
  • In someone with hypercalcaemia and high calcitriol levels, low intact parathyroid hormone levels are usually present. (
  • The association of calcitriol with improved survival was not statistically different across baseline parathyroid hormone levels. (
  • OVA323-339/calcitriol liposomes suppressed expansion, differentiation, and function of Teffs and induced Foxp3+ and IL-10+ peripheral Tregs in an antigen-specific manner, which was dependent on PD-L1. (
  • Liposomes encapsulating calcitriol and disease-associated peptides suppressed the severity of rheumatoid arthritis and Goodpasture's vasculitis models with suppression of antigen-specific memory T cell differentiation and function. (
  • Design: Previous findings in our lab suggests, calcitriol act as differentiation agent in human osteosarcoma cell lines 143B and SaOS-2. (
  • Separating the administration of these medications and calcitriol may prevent this interaction. (
  • Phenytoin ( Dilantin ) and phenobarbital (Luminal) may reduce blood concentrations of calcitriol, decreasing treatment effectiveness. (
  • 1. Calcitriol (1,25-dihydroxyvitamin D 3 ) concentrations in plasma of humans and pigs with pseudo-vitamin D deficiency rickets type I (PVDRI) have been reported to be significantly lower than in normal subjects and animals. (
  • Sometimes, however, calcitriol concentrations are relatively high in these subjects and animals (50-80 pmol/l) and nevertheless clinical symptoms of rickets develop. (
  • PVDRI piglets with clinical and biochemical symptoms of rickets (hypocalcaemia, increased activity of alkaline phosphatase) and with calcitriol concentrations in plasma of 83.7 ± 4.2 pmol/l ( n = 7) were used. (
  • They were compared with unaffected piglets with normal calcitriol concentrations (178.0 ± 17.7 pmol/l, n = 9). (
  • Calcitriol is also sometimes used to treat rickets (softening and weakening of bones in children caused by lack of vitamin D), osteomalacia (softening and weakening of bones in adults caused by lack of vitamin D), and familial hypophosphatemia (rickets or osteomalacia caused by decreased ability to break down vitamin D in the body). (
  • Calcitriol is available as capsules containing 0.25 mcg. (
  • Calcitriol Capsules contain butylated hydroxyanisole (BHA) and butylated hydroxytoluene (BHT) as antioxidants. (
  • Take calcitriol exactly as directed. (
  • Your doctor will probably tell you not to take calcitriol. (
  • To make sure you can safely take calcitriol, tell your doctor about all of your medical conditions. (
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  • 5 , 6 A decline in calcitriol levels and a rise in serum PTH levels are among the first detectable mineral metabolism disturbances in CKD. (
  • Compared with matched control subjects, calcitriol users had higher serum PTH levels, modestly lower eGFR, more nephrology clinic visits, and a slightly greater prevalence of comorbid conditions. (
  • Therefore, the investigators plan to conduct a randomized clinical study to evaluate the efficacy of Calcitriol in the treatment of IgA nephropathy. (
  • In a study, calcitriol showed superior efficacy compared with alfacalcidol with respect to inhibiting parathyroid hormone secretion. (