D-Cure Mechanism of Action

Pharmacotherapeutic Group: Vitamin D, cholecalciferol. ATC Code: A11CC05.
Pharmacology: Pharmacodynamics: In its biologically active form Vitamin D stimulates intestinal calcium absorption, incorporation of calcium into the osteoid, and release of calcium from bone tissue. In the small intestine it promotes rapid and delayed calcium uptake. The passive and active transport of phosphate is also stimulated. In the kidney, it inhibits the excretion of calcium and phosphate by promoting tubular resorption. The production of parathyroid hormone (PTH) in the parathyroids is inhibited directly by the biologically active form of vitamin D3. PTH secretion is inhibited additionally by the increased calcium uptake in the small intestine under the influence of biologically active vitamin D.
Pharmacokinetics: The pharmacokinetics of vitamin D is well known.
Absorption: Vitamin D is well absorbed from the gastro-intestinal tract in the presence of bile, so the administration with the major meal of the day might therefore facilitate the absorption of Vitamin D.
Distribution and biotransformation: It is hydroxylated in the liver to form 25-hydroxy-cholecalciferol and then undergoes further hydroxylation in the kidney to form the active metabolite 1, 25-dihydroxycholecalciferol (calcitriol).
Elimination: The metabolites circulate in the blood bound to a specific α - globin, vitamin D and its metabolites are excreted mainly in the bile and faeces.
Characteristics in Specific Groups of Subjects or Patients: A 57% lower metabolic clearance rate is reported in subjects with renal impairment as compared with that of healthy volunteers.
Decreased absorption and increased elimination of vitamin D occurs in subjects with malabsorption.
Obese subjects are less able to maintain vitamin D levels with sun exposure, and are likely to require larger oral doses of vitamin D to replace deficits.
Toxicology: Preclinical safety data: Pre-clinical studies conducted in various animal species have demonstrated that toxic effects occur in animals at doses much higher than those required for therapeutic use in humans.
In toxicity studies at repeated doses, the effects most commonly reported were increased calciuria and decreased phosphaturia and proteinuria.
Hypercalcaemia has been reported in high doses. In a state of prolonged hypercalcaemia, histological alterations (calcification) were more frequently borne by the kidneys, heart, aorta, testes, thymus and intestinal mucosa.
Colecalciferol has been shown to be teratogenic at high doses in animals.
At doses equivalent to those used therapeutically, cholecalciferol has no teratogenic activity.
Cholecalciferol has no potential mutagenic or carcinogenic activity.