Calcitonin (human)
Calcitonin (human) Uses, Dosage, Side Effects, Food Interaction and all others data.
Calcitonin was first discovered in isolated parathyroid tissue as a substance with a serum-calcium-lowering effect. It is constituted as a 32-amino acid single chain polypeptide structure that gets secreted as a regulatory agent in calcium-phosphorus metabolism. It is used as an alternative for people developing antibodies against salmon calcitonin.
Administration of human calcitonin has shown to increase bone calcium content and reduce the levels of serum calcium and serum phosphorus. This calcium inhibition leads to decreases in urinary calcium, magnesium and urine hydroxyproline. Some reports indicate a calcitonin-driven reduction of phosphate plasma concentration which is thought to be related to increased excretion of phosphate. Calcitonin can increase excretion of calcium, phosphate, and sodium. It also is proven to induce the appearance of normal lamellar bone against the diseased trabeculae and a striking decrease in the number of osteoclasts. Bone pain tends to be relieved within a few weeks, and it does not present an important effect on normal bone. It is important to point out that human calcitonin is less active than the salmon calcitonin. This characteristic happens because of a high tendency to aggregate, and thus, human calcitonin is used just in cases where the usage of salmon calcitonin generated the formation of antibodies. For this reason, the use of human calcitonin is only indicated when there is the appearance of a high-titer of antibodies anti-salmon calcitonin because these antibodies are suggested to cause a relapse.
Trade Name | Calcitonin (human) |
Generic | Human calcitonin |
Human calcitonin Other Names | Calcitonin (human synthetic), Calcitonin (human), Calcitonin human, Calcitonin, human, Calcitonin, human synthetic |
Type | |
Formula | C151H226N40O45S3 |
Weight | 3417.9 Da |
Groups | Approved, Investigational |
Therapeutic Class | |
Manufacturer | |
Available Country | |
Last Updated: | September 19, 2023 at 7:00 am |
Uses
Calcitonin (human) is indicated for the treatment of Paget's disease in the cases where the use of salmon calcitonin may provoke the generation of high-titer of antibodies. Paget's disease is a metabolic bone disorder characterized by focal areas of increased and disorganized bone turnover coupled with an increased bone formation. The majority of the cases are asymptomatic but some clinical manifestations include pain, bone deformity and some complications such as pathological fractures and deafness. The increased activity in bone is associated with a rise in serum level of alkaline phosphatase and the increased urinary excretion of hydroxyproline which is a product of bone breakdown.
How Calcitonin (human) works
Calcitonin inhibits osteoclast-mediated bone resorption through the regulation of the number and activity of osteoclasts. The action of human calcitonin on osteoclasts is due to a disruption of cytoskeletal organization, by the distraction of actin rings, and due to a disappearance of the cellular polarity of osteoclasts. At the subcellular level, calcitonin is suggested to perform its activity by the modulation of the cAMP-PKA signaling pathway.
Elimination Route
The human calcitonin tends to aggregate irreversibly forming amyloid fibrils. This property compromises the bioavailability and therapeutic activity of exogenous human calcitonin. When human calcitonin reaches the intestine, by intracolonic administration, it is absorbed within minutes and it is distributed intact in plasma. The level of absorption is low and the bioavailability can range from 0.01-2.7%.
Half Life
Intravenous administration of human calcitonin presents a half-life in the range of 10.2-37.8 min.
Clearance
The metabolic secretion rate is in the range of 6-9 ml/min.kg while the secretion rate is 59 ng/dl.kg for men and 22 ng/dl.kg for women. The total renal clearance of human calcitonin is 1.96 ml/min. The renal clearance exceeds the glomerular filtration rate which indicates a filtration-independent removal.
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