Regulate gene transcription via the vitamin D receptor.

↑ blood Ca⁺² levels by promoting absorption of Ca⁺² from the GI tract and ↑ renal reabsorption of Ca⁺² and phosphate. Stimulates release of Ca+2 from bone by its action on osteoblasts, causing them to release RANKL, which in turn activates osteoclasts.

↓PTH; promote innate immunity; inhibit adaptive immunity

Hypercalcemia, hypercalciuria

The vitamin D preparation have much longer half-life than the metabolites and analogs.

Type I rickets (vitamin D

deficiency), type II rickets (mutated vitamin D receptor), intestinal osteodystrophy, osteoporosis, osteomalacia, renal failure, malabsorption, symptomatic hypocalcemia, hypoparathyroidism

Suppress activity of osteoclasts in part via inhibition of farnesyl pyrophosphate synthase (enzyme that is critical for osteoclast survival).  Inhibit bone resorption and secondarily bone formation.

↓ Osteoclast activity

↓ Vitamin D production

↓ Intestinal Ca2+ export

Adynamic bone, possible renal failure, rare osteonecrosis of the jaw

Osteoporosis, bone metastases, hypercalcemia, Paget’s

Recombinant form of PTH

Stimulates normal bone formation and ↓ incidence of fractures.

Stimulates bone turnover

Hypercalcemia and hypercalciuria

Osteoporosis

↑bone mass and ↓spine fractures

Suppresses bone resorption

Osteoporosis, hypercalcemia

Paget’s

Interacts selectively with estrogen receptors; Inhibits bone resorption without stimulating breast or uterus

↑risk of thrombophlebitis

Rx: osteoporosis (spine but not hip

fractures), prophylaxis of breast cancer in high risk women

Activates Ca⁺² sensing receptor in the parathyroid gland →

↓PTH secretion

nausea

Secondary hyperparathyroidism in chronic kidney disease, parathyroid carcinoma