Calcitonin phosphate levels

Calcitonin is a polypeptide hormone that (along with PTH and the vitamin D derivative, 1,25-dihydroxycholecalciferol) plays a central role in regulating serum ionized calcium (Ca2+) and inorganic phosphate (Pi) levels. The adult human body contains up to 2 kg of calcium, of which 98 per cent is present in the skeleton (i.e. bone). Up to 85 per cent of the 1 kg of phosphorus present in the body is also found in the skeleton (the so-called mineral fraction of bone is largely composed of Ca3(P04)2, which acts as a body reservoir for both calcium and phosphorus). Calcium concentrations in human serum approximate to 0.1 mg ml-1 and are regulated very tightly (serum phosphate levels are more variable). 

With the exception of the possible development of a hypervitaminosis associated with high-dose administration of vitamin D2 or D3, the compounds discussed in this chapter are relatively safe. Allergic reactions to the injection of calcitonin and PTH have occurred and chronic use of some bisphosphonates has been associated with the development of osteomalacia. The principal side effects of intravenous bisphosphonates are mild and include low-grade fever and transient increases in serum creatinine and phosphate levels. Oral bisphosphonates are poorly absorbed and can cause esophageal and gastric ulceration. They should be taken on an empty stomach the individual must remain upright for 30 minutes after ingestion. 

Calcitonin is a peptide hormone produced in the thyroid gland that serves to lower serum calcium and phosphate levels by inhibiting bone resorption. Calcitonin has been used in the treatment of a variety of diseases, such as primary hyperparathyroidism, Paget s disease, and postmenopausal osteoporosis [99,100]. Salmon calcitonin has a longer half-life than human calcitonin. Salmon calcitonin, 3.6 kDa, is available as a nasal formulation that contains only benzalkonium chloride as a preservative, without an absorption enhancer, and as a parenteral product for injection. The direct effect of benzalkonium chloride on the nasal mucosa is under... 

Giving intravenous phosphate is probably the fastest and surest way to reduce serum calcium, but it is a hazardous procedure if not done properly. Intravenous phosphate should be used only after other methods of treatment (pamidronate, calcitonin, saline diuresis with furosemide, and plicamycin) have failed to control symptomatic hypercalcemia. Phosphate must be given slowly (50 mmol or 1.5 g elemental phosphorus over 6-8 hours) and the patient switched to oral phosphate (1-2 g/d elemental phosphorus, as one of the salts indicated below) as soon as symptoms of hypercalcemia have cleared. The risks of intravenous phosphate therapy include sudden hypocalcemia, ectopic calcification, acute renal failure, and hypotension. Oral phosphate can also lead to ectopic calcification and renal failure if serum calcium and phosphate levels are not carefully monitored, but the risk is less and the time of onset much longer. Phosphate is available in oral and intravenous forms as the sodium or potassium salt. Amounts required to provide 1 g of elemental phosphorus are as follows ... 

Calcitonin is a 32-amino-acid polypeptide hormone that was hrst purihed in 1962 by Copp and Cheney (121). It was originally thought as a product from parathyroid glands, but later it was discovered to be made by the C cells of the thyroid gland. Calcitonin participates in calcium and phosphorus metabolism, lowers plasma calcium and phosphate levels, and it has been used as a drug for bone and mineral disorders for a long time. 

One method of treatment is to inject calcitonin, which decreases blood Ca " concentration and increases bone calcification (33). Another is to increase the release of calcitonin into the blood by increasing the blood level of Ca " ( 4). This latter treatment is accompHshed by increasing Ca " absorption from the intestine requiring dietary calcium supplements and avoidance of high phosphate diets. The latter decrease Ca " absorption by precipitation of the insoluble calcium phosphate. 

Calcitonin. This hormone, which is also secreted from the thyroid gland, is synthesized by the parafollicular cells (C cells) located between the follicles. The primary effect of calcitonin is to decrease the blood levels of calcium and phosphate. The mechanism of action involves the direct inhibition of osteoclast activity, which decreases bone resorption. This results in less demineralization of the bone and therefore a decrease in the release of calcium and phosphate from the bone into the blood. Calcitonin has no direct effect on bone formation by osteoblasts. 

Calcitonin, a peptide produced in the C cells of the thyroid gland, inhibits the resorption of both calcium and phosphate ions. The result is an overall reduction in the plasma level of both ions. Calcitonin is thus a parathyrin antagonist relative to Ca ". ... 

The major location of calcium in the body is in the skeleton, which contains more than 90% of the body calcium as phosphate and carbonate. Bone resorption and formation keeps this calcium in dynamic equilibrium with ionized and complexed calcium in blood, cellular fluids and membranes. Homeostasis is mainly regulated by the parathyroid hormone and vitamin D which lead to increased blood calcium levels, and by a thyroid hormone, calcitonin, which controls the plasma calcium concentration J5 Increasing the concentration of calcitonin decreases the blood calcium level, hence injections of calcitonin are used to treat severe hyperalcaemia arising from hyperparathyroidism, vitamin D intoxication or the injection of too high a level of parathyroid extract. High levels of calcitonin also decrease resorption of calcium from bone. Hypocalcaemia stimulates parathyroid activity, leading to increased release of calcium from bone, reduction in urinary excretion of calcium and increased absorption of calcium from the intestine. Urinary excretion of phosphate is enhanced. 

Calcitonin causes the deposition of calicum phosphate in the skeleton by stimulation of the bone-forming cells, and hence reduces the levels of calcium and phosphate in the blood (hypocalcemia). Completely synthetic calcitonin products such as Salmcalci-tonin (Sandoz Ltd., Switzerland) 208), Elcitonin (Toyo Jozo Co., Japan) z09), and... 

Know the effects of parathyroid hormone, calcitonin, and vitamin D in controlling calcium and phosphate metabolism. Know what controls the levels of such hormones in the bloodstream. 

Calcium is essential for the normal growth and development of the body, especially (in the form of calcium phosphate) of the bones and teeth. Its level in the blood is regulated by the opposing actions of the thyroid hormone calcitonin, and the parathyroid hormone parathormone. Its uptake from food is enhanced by vitamin D (calciferol). Forms of calcium used therapeutically include the folinic acid supplement calcium foiinate, and the mineral supplements calcium bicarbonate, calcium carbonate, calcium gluconate and calcium lactate. 

The principal target organ for calcitonin is bone, but renal excretion of calcium and phosphate is also directly affected. In bone and kidney, calcitonin activates adenylate cyclase by binding to a distinct class of G-protein-coupled receptors. Calcitonin may also exert effects on cytosolic Ca + and IP3 levels by activation of the phospholipase... 

B. Hyperparathyroidism is the likely cause of all of the patient s symptoms. Increased parathyroid hormone leads to bone demineralization, increased calcium uptake from the intestine, increased blood levels of calcium, decreased calcium ion excretion by the kidney, and increased phosphate excretion in the urine. Increased blood calcium levels caused renal stones, while bone demineralization progressed to osteopenia. The patient s intake of calcium and vitamin D are not excessive. Calcitonin acts to decrease bone demineralization. Muscle weakness and depression reflect the widespread role of calcium ion in many physiologic processes. 

Paget s disease (Table 35.6) is characterized by excessive bone resorption, followed by replacement of the normally mineralized bone with soft, poorly mineralized tissue (20). It has been determined that the osteoclasts have an abnormal structure, are hyperactive, and are present at elevated levels (20). Patients afflicted with this painful condition often suffer from multiple compression fractures. Administration of calcitonin and oral calcium and phosphate supplements had been the treatment of choice until the bisphosphonate risedronate was approved by the U.S. Food and Drug Administration (FDA). Daily administration of risedronate results in a decreased rate of bone turnover and a decrease in the levels of serum alkaline phosphatase and urinary hydroxyproline, two biochemical markers of bone turnover (4,20). A significant advantage to treatment with the bisphosphonates is long-term suppression of the disease (20). Calcium supplementation, which often is necessary in these patients, must be dosed separately from risedronate, because calcium- and aluminum- or... 

Low levels of plasma phosphate stimulate the conversion of the 25-hydroxyl derivative to the 1,25-hy-droxyl compound, while high levels of plasma phosphate enhance the formation of the 24,25-hydroxylated derivative. The mobilization of calcium from bone seems to require both parathormone and the 1,25-hydroxylated derivative. An effect of calcitonin on... 

---