Calcitonin hypocalcemia with

Other Calcium Disorders. In addition to hypocalcemia, tremors, osteoporosis, and muscle spasms (tetary), calcium deficiency can lead to rickets, osteomalacia, and possibly heart disease. These, as well as Paget s disease, can also result from faulty utilization of calcium. Calcium excess can lead to excess secretion of calcitonin, possible calcification of soft tissues, and kidney stones when combined with magnesium deficiency. 

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 ... 

In hypocalcemia, the parathyroid increases its secretion of parathormone, resulting in enhanced liberation of Ca2+. Calcitonin transfers active osteoclasts into a resting state. Calcitonin given therapeutically relieves pain associated with neoplastic bone metastases and vertebral body collapse. Estrogens diminish bone resorption by (a) inhibiting activation of osteoclasts by osteoblasts and (b) promoting apoptosis of osteoclasts. 

The infusion of calcitonin to rats induces increased calcium deposition in the bone and hypocalcemia. Thus, the hormone has properties antagonistic to those of parathormone. Fluorescent antibody techniques have demonstrated that the hormone is secreted by the C cells of the thyroid gland. A light cell hyperplasia outside the follicular walls of the thyroid has been observed in mice with hereditary hypocalcemia. 

Calcitonin is active in nephrectomized and parathy-roidectomized animals, indicating that the hormone does not act through the kidney or the parathyroid. Thyrocalcitonin causes hypocalcemia even in rats fed a low-calcium diet. Consequently, the hormone does riot seem to influence intestinal absorption of calcium. Calcitonin facilitates calcium retention in bone cultures. It is likely that the hormone acts by interfering with calcium resorption in bone, but the exact mechanism by which the interference takes place is not known. 

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