Calcijex Injection (Calcitrol) Drug Information: Clinical Pharmacology

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May 25, 2012

Calcijex

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Osteoporosis facts

Osteoporosis is a condition of increased susceptibility to fracture due to fragile bone.
Osteoporosis weakens bone and increases risk of bone fracture.
Bone mass (bone density) decreases after 35 years of age and decreases more rapidly in women after menopause.
Key risk factors for osteoporosis include genetics, lack of exercise, lack of calcium and vitamin D, personal history of fracture as an adult, cigarette smoking, excessive alcohol consumption, history of rheumatoid arthritis, low body weight, and family history of osteoporosis.
Patients with osteoporosis have no symptoms until bone fractures occur.
The diagnosis of osteoporosis can be suggested by X-rays and confirmed by tests to measure bone density.
Treatments for osteoporosis, in addition to prescription osteoporosis medications, include stopping use of alcohol and cigarettes, and assur...

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Calcijex Injection

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CLINICAL PHARMACOLOGY

Calcitriol is the active form of vitamin D₃ (cholecalciferol). The natural or endogenous supply of vitamin D in man mainly depends on ultraviolet light for conversion of 7-dehydrocholesterol to vitamin D₃ in the skin. Vitamin D₃ must be metabolically activated in the liver and the kidney before it is fully active on its target tissues. The initial transformation is catalyzed by a vitamin D₃-25-hydroxylase enzyme present in the liver, and the product of this reaction is 25-(OH)D₃ (calcifediol). The latter undergoes hydroxylation in the mitochondria of kidney tissue, and this reaction is activated by the renal 25-hydroxyvitamin D₃-l-α-hydroxylase to produce 1,25-(OH)₂D₃ (calcitriol), the active form of vitamin D₃.

The known sites of action of calcitriol are intestine, bone, kidney and parathyroid gland. Calcitriol is the most active known form of vitamin D₃ in stimulating intestinal calcium transport. In acutely uremic rats, calcitriol has been shown to stimulate intestinal calcium absorption. In bone, calcitriol, in conjunction with parathyroid hormone, stimulates resorption of calcium; and in the kidney, calcitriol increases the tubular reabsorption of calcium. In vitro and in vivo studies have shown that calcitriol directly suppresses secretion and synthesis of PTH. A vitamin D-resistant state may exist in uremic patients because of the failure of the kidney to adequately convert precursors to the active compound, calcitriol.

Calcitriol when administered by bolus injection is rapidly available in the blood stream. Vitamin D metabolites are known to be transported in blood, bound to specific plasma proteins. The pharmacologic activity of an administered dose of calcitriol is about 3 to 5 days. Two metabolic pathways for calcitriol have been identified, conversion to 1,24,25-(OH)₃D₃ and to calcitroic acid.

Last reviewed on RxList: 3/26/2012
This monograph has been modified to include the generic and brand name in many instances.