What is the clinical significance of calcitonin?

As we all know, when people enter the aging stage, their bones become very fragile. Perhaps a small impact or a fall may cause a fracture in the elderly. Although fractures can be treated with surgery in most cases, postoperative recovery is still quite difficult for the elderly. So, what is the clinical significance of calcitonin?

Calcitonin is a polypeptide hormone involved in calcium bone metabolism and was discovered by Copp et al. in 1961. In 1961, Kumar, Foster and others further proved that calcitonin in mammals comes from the thyroid gland, but calcitonin in fish is produced in the posterior parotid gland. All calcitonins are structurally similar, consisting of a single chain of 32 amino acids arranged in different orders, which depend on the species, but their effects are essentially similar. Fish calcitonin binds to the mammalian calcitonin receptor more strongly than mammalian calcitonin. For this reason, fish calcitonin is currently used in clinical practice.

Calcitonin has an acute inhibitory effect on osteoclasts and can reduce the amount of calcium in the body migrating from bones to blood. In patients or experimental animals with increased bone turnover rate, plasma calcium decreases significantly after injection of calcitonin, but adults with normal bone turnover rate do not have the above reaction. Fish calcitonin increases the excretion of sodium, calcium, and phosphorus in the urine, but the above effects of human calcitonin are mild. The main effect of calcitonin is during the "calcium stress period", such as children's growth period, women's pregnancy and lactation period, etc. During this period, serum calcitonin increases significantly, which promotes bone development and protects bones. Bone loss increases in postmenopausal women, an associated phenomenon is a decrease in blood calcium and calcitonin levels. Calcitonin treatment can reduce this continued bone loss. In addition to inhibiting bone resorption, calcitonin also has a good therapeutic effect on bone pain symptoms caused by many bone metabolic diseases, but its mechanism of action is not yet fully understood.

The main function of calcitonin is to lower blood calcium by regulating bones, kidneys and gastrointestinal tract.

(1) Effect on bone marrow In vitro bone culture has shown that calcitonin inhibits bone absorption and bone autolysis, reducing calcium release from the bone marrow. At the same time, bones continuously absorb calcium from plasma, leading to low blood calcium. Calcitonin can also inhibit the dissolution and transfer of bone salts, inhibit the decomposition of bone matrix, increase bone turnover rate, increase urinary calcium and urinary phosphorus excretion, and cause hypocalcemia or hypophosphatemia. The calcium-lowering effect in vivo is short-lived; calcitonin counteracts the effect of parathyroid hormone on the bone marrow.

(2) Its effect on the kidneys can inhibit the reabsorption of calcium, phosphorus, and sodium by the renal tubules, thereby increasing their excretion in urine, but it has little effect on potassium and hydrogen.

(3) Its effects on the gastrointestinal tract can inhibit intestinal calcium transport and the secretion of gastric acid, gastrin and insulin.

After oral administration, calcitonin is rapidly degraded in gastric juice. The blood concentration reaches its peak about 0.5 to 1 hour after intramuscular or subcutaneous injection and disappears from the blood after 12 hours. The half-life is about 10 minutes, and the elimination rate is 8.4±1.1 per minute.

mg/Kg. The bioavailability of nasal spray is approximately 50% of that of injection.