Calcix-D
Calcix-D Uses, Dosage, Side Effects, Food Interaction and all others data.
Calcium is used to prevent or treat negative calcium balance. It also helps facilitate nerve and muscle performance as well as normal cardiac function. Bone mineral component; cofoactor in enzymatic reactions, essential for neurotransmission, muscle contraction, and many signal transduction pathways.
Both components of calcium lactate, calcium ion and lactic acid, play essential roles in the human body as a skeletal element an energy source, respectively .
Vitamin D ultimately comprises a group of lipid-soluble secosteroids responsible for a variety of biological effects, some of which include increasing the intestinal absorption of calcium, magnesium, and phosphate. With reference to human use, there are 2 main forms of vitamin D - vitamin D3 (cholecalciferol) and vitamin D2 (ergocalciferol). When non-specific references are made about 'vitamin d', the references are usually about the use of vitamin D3 and/or D2.
Vitamin D3 and D2 require hydroxylation in order to become biologically active in the human body. Since vitamin D can be endogenously synthesized in adequate amounts by most mammals exposed to sufficient quantities of sunlight, vitamin D functions like a hormone on vitamin D receptors to regulate calcium in opposition to parathyroid hormone. Vitamin D plays an essential physiological role in maintaining calcium homeostasis and metabolism. There are several different vitamin D supplements that are given to treat or to prevent osteomalacia and rickets, or to meet the daily criteria of vitamin D consumption.
The in vivo synthesis of the predominant two biologically active metabolites of vitamin D occurs in two steps. The first hydroxylation of vitamin D3 or D2 occurs in the liver to yield 25-hydroxyvitamin D while the second hydroxylation happens in the kidneys to give 1, 25-dihydroxyvitamin D . These vitamin D metabolites subsequently facilitate the active absorption of calcium and phosphorus in the small intestine, serving to increase serum calcium and phosphate levels sufficiently to allow bone mineralization . Conversely, these vitamin D metabolites also assist in mobilizing calcium and phosphate from bone and likely increase the reabsorption of calcium and perhaps also of phosphate via the renal tubules . There exists a period of 10 to 24 hours between the administration of vitamin D and the initiation of its action in the body due to the necessity of synthesis of the active vitamin D metabolites in the liver and kidneys . It is parathyroid hormone that is responsible for the regulation of such metabolism at the level of the kidneys .
| Trade Name | Calcix-D |
| Generic | Calcium Lactate + Vitamin D |
| Weight | 200mg, 3160iu |
| Type | Caplet |
| Therapeutic Class | |
| Manufacturer | Sampharindo Perdana |
| Available Country | Indonesia |
| Last Updated: | September 19, 2023 at 7:00 am |
Uses
Calcium Lactate is used for heartburn, calcium supplement, calcium deficiencies.
Vitamin D is an ingredient found in a variety of supplements and vitamins.
Vitamin D is indicated for use in the treatment of hypoparathyroidism, refractory rickets (also known as vitamin D resistant rickets), and familial hypophosphatemia .
Calcix-D is also used to associated treatment for these conditions: Calcium DeficiencyDeficiency, Vitamin D
How Calcix-D works
In aqueous environments such as the gastrointestinal (GI) tract, calcium lactate will dissociate into calcium cation and lactic acid anions, the conjugate base of lactic acid. Lactic acid is a naturally-occurring compound that serves as fuel or energy in mammals by acting as an ubiquitous intermediate in the metabolic pathways . Lactic acid diffuses through the muscles and is transported to the liver by the bloodstream to participate in gluconeogenesis .
Most individuals naturally generate adequate amounts of vitamin D through ordinary dietary intake of vitamin D (in some foods like eggs, fish, and cheese) and natural photochemical conversion of the vitamin D3 precursor 7-dehydrocholesterol in the skin via exposure to sunlight.
Conversely, vitamin D deficiency can often occur from a combination of insufficient exposure to sunlight, inadequate dietary intake of vitamin D, genetic defects with endogenous vitamin D receptor, or even severe liver or kidney disease . Such deficiency is known for resulting in conditions like rickets or osteomalacia, all of which reflect inadequate mineralization of bone, enhanced compensatory skeletal demineralization, resultant decreased calcium ion blood concentrations, and increases in the production and secretion of parathyroid hormone . Increases in parathyroid hormone stimulates the mobilization of skeletal calcium and the renal excretion of phosphorus . This enhanced mobilization of skeletal calcium leads towards porotic bone conditions .
Ordinarily, while vitamin D3 is made naturally via photochemical processes in the skin, both itself and vitamin D2 can be found in various food and pharmaceutical sources as dietary supplements. The principal biological function of vitamin D is the maintenance of normal levels of serum calcium and phosphorus in the bloodstream by enhancing the efficacy of the small intestine to absorb these minerals from the diet . At the liver, vitamin D3 or D2 is hydroxylated to 25-hydroxyvitamin D and then finally to the primary active metabolite 1,25-dihydroxyvitamin D in the kidney via further hydroxylation . This final metabolite binds to endogenous vitamin d receptors, which results in a variety of regulatory roles - including maintaining calcium balance, the regulation of parathyroid hormone, the promotion of the renal reabsorption of calcium, increased intestinal absorption of calcium and phosphorus, and increased calcium and phosphorus mobilization of calcium and phosphorus from bone to plasma to maintain balanced levels of each in bone and the plasma .
Dosage
Calcix-D dosage
19-50 year: 1,000 mg elemental Calcium Lactate per day.
>50 year: 1,200 mg elemental Calcium Lactate per day.
Side Effects
Gl discomfort e.g. nausea, vomiting, constipation; bradycardia, arrhythmias. Dry mouth, increased thirst or increased urination. Mental confusion, milk-alkali syndrome.
Toxicity
The LDLo of calcium lactate pentahydrate following intravenous administration in mouse is 140 mg/kg .
The use of pharmacological or nutraceutical vitamin d and/or even excessive dietary intake of vitamin d is contraindicated in patients with hypercalcemia, malabsorption syndrome, abnormal sensitivity to the toxic effects of vitamin d, and hypervitaminosis D .
Hypersensitivity to vitamin d is one plausible etiologic factor in infants with idiopathic hypercalcemia - a case in which vitamin d use must be strictly restricted .
As vitamin d intake is available via fortified foods, dietary supplements, and clinical drug sources, serum concentrations and therapeutic dosages should be reviewed regularly and readjusted as soon as there is clinical improvement . Dosage levels are required to be individualized on an individual patient by patient basis as caution must be exercised to prevent the presence of too much vitamin d in the body and the various potentially serious toxic effects associated with such circumstances .
In particular, the range between therapeutic and toxic doses is quite narrow in vitamin d resistant rickets . When high therapeutic doses are used, progress should be followed with frequent blood calcium determinations .
When treating hypoparathyroidism, intravenous calcium, parathyroid hormone, and/or dihydrotachysterol may be required .
Maintenance of normal serum phosphorus levels by dietary phosphate restriction and/or administration of aluminum gels as intestinal phosphate binders in those patients with hyperphosphatemia as frequently seen in renal osteodystrophy is essential to prevent metastatic calcification .
Mineral oil interferes with the absorption of lipid-soluble vitamins, including vitamin d preparations .
The administration of thiazide diuretics to hypoparathyroid patients who are concurrently being treated with vitamin d can result in hypercalcemia .
At this time, no long term animal studies have been performed to evaluate vitamin potential for carcinogens, mutagenesis, or fertility .
As various animal reproduction studies have demonstrated fetal abnormalities in several species associated with hypervitaminosis D, the use of vitamin d in excess of the recommended dietary allowance during normal pregnancy should be avoided . The safety in excess of 400 USP units of vitamin d daily during pregnancy has not been established . The abnormalities observed are similar to the supravalvular aortic stenosis syndrome described in infants that is characterized by supravalvular aortic stenosis, elfin facies, and mental retardation .
In a nursing mother given large doses of vitamin D, 25-hydroxycholecalciferol appeared in the milk and caused hypercalcemia in her child. Caution is subsequently required when contemplating the use of vitamin d in a nursing woman, and the necessity of monitoring infants' serum calcium concentration if vitamin d is administered to a breastfeeding woman .
Adverse reactions associated with the use of vitamin d are primarily linked to having hypervitaminosis D occurring [FDA Lanel]. In particular, hypervitaminosis D is characterized by effects specific effects on specific organ systems. At the renal system, hypervitaminosis D can cause impairment of renal function with polyuria, nocturne, polydipsia, hypercalciuria, reversible asotemia, hypertension, nephrocalcinosis, generalized vascular calcification, or even irreversible renal insufficiency which may result in death . Elsewhere, hypervitaminosis D can also cause CNS mental retardation . At the level of soft tissues, it can widespread calcification of the soft tissues, including the heart, blood vessels, renal tubules, and lungs . In the skeletal system, bone demineralization (osteoporosis) in adults can occur while a decline in the average rate of linear growth and increased mineralization of bones, dwarfism, vague aches, stiffness, and weakness can occur in infants and children . Finally, hypervitaminosis D can also lead to nausea, anorexia, and constipation at the gastrointestinal level as well as mild acidosis, anemia, or weight loss via metabolic processes .
The LD(50) in animals is unknown .
Precaution
Sarcoidosis; history of nephrolithiasis. Avoid IV admin of calcium in patients on cardiac glycosides. Increased risk of hypercalcaemia and hypercalciuria in hypoparathyroid patients receiving high doses of vitamin D. Caution when used in patients with history of kidney stones. Patients should be advised to administer vitamin D concurrently to optimise calcium absorption. Pregnancy.
Interaction
May reduce the efficacy of calcium-channel blockers. Concurrent admin of IV calcium salt with cardiac glycosides may lead to serious adverse events. Increased risk of hypercalcaemia when used with thiazide diuretics. May reduce absorption of tetracycline, alendronate, atenolol, iron, quinolone antibiotics, sodium fluoride and zinc.
Volume of Distribution
The majority of calcium absorbed (99%) is stored in the skeleton and teeth for structural integrity .
Elimination Route
In order to be absorbed, calcium must be in its freely soluble form (Ca2+) or bound to a soluble organic molecule. Calcium absorption mainly occurs at the duodenum and proximal jejunum due to more acidic pH and the abundance of the calcium binding proteins . The mean calcium absorption is about 25% of calcium intake (range is 10 – 40%) in the small intestine, and is mediated by both passive diffusion and active transport .
Vitamin D3 and D2 are readily absorbed from the small intestine (proximal or distal) .
Half Life
No pharmacokinetic data available.
Although certain studies suggest the half-life of 1,25-hydroxyvitamin D3 may be approximately 15 hours, the half-life of 25-hydroxyvitamin D3 appears to have a half-life of about 15 days . Intriguingly however, the half-lives of any particular administration of vitamin d can vary and in general the half-lives of vitamin D2 metabolites have been demonstrated to be shorter overall than vitamin D3 half-lives with this being affected by vitamin d binding protein concentrations and genotype in particular individuals .
Clearance
No pharmacokinetic data available.
Some studies propose an estimated clearance rate for 1,25-dihydroxyvitamin D as 31 +/- 4 ml/min in healthy adults .
Elimination Route
Following oral administration to a human volunteer, 20 to 30% of a dose of lactic acid of up to 3000 mg was excreted via the urine during a period of 14 hours .
The primary excretion route of vitamin D is via the bile into the feces .
Pregnancy & Breastfeeding use
Pregnancy Category-C. Animal reproduction studies have shown an adverse effect on the fetus and there are no adequate and well-controlled studies in humans, but potential benefits may warrant use of the drug in pregnant women despite potential risks
Contraindication
Conditions associated with hypercalcaemia and hypercalciuria.
Innovators Monograph
You find simplified version here Calcix-D
