It is produced in the kidneys via 25-Hydroxyvitamin D3 1-alpha-Hydroxylase by conversion from 25-hydroxycholecalciferol (calcidiol).
This is stimulated by a decrease in serum calcium and/or phosphate (PO43−), and an increase in parathyroid hormone (PTH) levels. It increases blood 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 sometimes used topically in the treatment of psoriasis, however the evidence to support its efficacy is inconclusive. The vitamin D analogue calcipotriol is more commonly used for psoriasis.
The main adverse drug reaction associated with calcitriol therapy is hypercalcaemia – early symptoms include: nausea, vomiting, constipation, anorexia, apathy, headache, thirst, sweating, and/or polyuria). Compared to other vitamin D compounds in clinical use (cholecalciferol, ergocalciferol), calcitriol has a higher risk of inducing hypercalcaemia. However, such episodes may be shorter and easier to treat due to its relatively short half-life.