Calcitriol is the active hormonal form of Vitamin D3 (1,25-dihydroxycholecalciferol). It is a potent regulator of calcium and phosphate homeostasis, acting primarily on the intestines, bones, kidneys, and parathyroid glands. Unlike nutritional vitamin D, calcitriol does not require hepatic or renal hydroxylation for activation, making it the drug of choice in patients with impaired renal function, such as those with chronic kidney disease (CKD) and hypoparathyroidism.
Adult: Initial: 0.25 mcg/day orally. May increase by 0.25 mcg/day at 4-8 week intervals based on biochemical response. Typical maintenance: 0.25 to 1.0 mcg/day. For hypoparathyroidism: 0.5 to 2.0 mcg/day.
Note: Take orally, preferably with or after food to enhance absorption. Can be taken in the morning. Do not crush or chew capsules. Maintain adequate dietary calcium intake (800-1000 mg/day) unless contraindicated (e.g., hypercalciuria).
Calcitriol binds to the intracellular Vitamin D Receptor (VDR), which then heterodimerizes with the Retinoid X Receptor (RXR). This complex translocates to the nucleus, binds to Vitamin D Response Elements (VDREs) in target genes, and modulates transcription. Primary actions include: 1) Increased intestinal absorption of calcium and phosphate. 2) Promotion of bone mineralization by maintaining adequate calcium-phosphate product. 3) Suppression of Parathyroid Hormone (PTH) synthesis and secretion via direct action on parathyroid gland VDRs. 4) Regulation of cell differentiation and proliferation in various tissues.
Pregnancy: Category C. Animal studies show teratogenicity (skeletal abnormalities). Use only if potential benefit justifies potential fetal risk. Maternal hypercalcemia can suppress fetal parathyroid function, leading to neonatal hypocalcemia and tetany. Monitor serum calcium closely.
Driving: May cause dizziness, somnolence, or vertigo, especially with hypercalcemia. Patients should be cautioned about driving or operating machinery until their response is known.
| Thiazide Diuretics (e.g., Hydrochlorothiazide) | Increased risk of hypercalcemia due to reduced renal calcium excretion. | Major |
| Cardiac Glycosides (Digoxin) | Hypercalcemia may potentiate digitalis toxicity, leading to arrhythmias. | Major |
| Magnesium-containing Antacids/Laxatives | Increased risk of hypermagnesemia, especially in dialysis patients. | Moderate |
| Ketoconazole, Antifungals (CYP3A4 inhibitors) | May increase calcitriol levels by inhibiting its metabolism. | Moderate |
| Phenytoin, Phenobarbital (Enzyme Inducers) | May increase metabolism of calcitriol, reducing its efficacy. | Moderate |
| Calcium Supplements/Phosphate Binders (Calcium-based) | Additive hypercalcemic effect. Monitor serum calcium closely. | Moderate |
| Cholestyramine, Mineral Oil | May reduce intestinal absorption of calcitriol. | Moderate |