Indication |
Used for the prevention and treatment of rickets or osteomalacia,
and to manage hypocalcemia associated with hypoparathyroidism or
pseudohypoparathyroidism. Also used for the treatment of vitamin D
dependent rickets, rickets or osteomalacia secondary to long-term high
dose anticonvulsant therapy, early renal osteodystrophy, osteoporosis
(in conjunction with calcium), and hypophosphatemia associated with
Fanconi syndrome (with treatment of acidosis). |
Pharmacodynamics |
Dihydrotachysterol is hydroxylated in the liver to
25-hydroxydihydrotachysterol, which is the major circulating active form
of the drug. It does not undergo further hydroxylation by the kidney
and therefore is the analogue of 1, 25-dihydroxyvitamin D.
Dihydrotachysterol is effective in the elevation of serum calcium by
stimulating intestinal calcium absorption and mobilizing bone calcium in
the absence of parathyroid hormone and of functioning renal tissue.
Dihydrotachysterol also increases renal phosphate excretion. |
Mechanism of action |
Once hydroxylated to 25-hydroxydihydrotachysterol, the modified
drug binds to the vitamin D receptor. The bound form of the vitamin D
receptor serves as a transcriptional regulator of bone matrix proteins,
inducing the expression of osteocalcin and suppressing synthesis of type
I collagen. Vitamin D (when bound to the vitamin D receptor)stimulates
the expression of a number of proteins involved in transporting calcium
from the lumen of the intestine, across the epithelial cells and into
blood. This stimulates intestinal calcium absorption and increases renal
phosphate excretion. These are functions that are normally carried out
by the parathyroid hormone. |
Absorption |
Not Available |
Volume of distribution |
Not Available |
Protein binding |
>99% |
Metabolism |
Not Available |
Route of elimination |
Not Available |
Half life |
Not Available |
Clearance |
Not Available |
Toxicity |
Toxicity associated with dihydrotachysterol is similar to that seen with large doses of vitamin D. |