Calcitonin Treatment Research Articles

The acute response to calcitonin in Paget's disease: its relationship to the serum alkaline phosphatase level and the effect of phosphate treatment.

The 4- to 8-hour response to 100 MRC Units of salmon calcitonin was measured in 10 patients with Paget's disease. The fall in blood calcium was directly related to the initial serum alkaline phosphatase level, and not to the initial serum calcium or phosphate levels. The fall in blood phosphate was not related to the serum alkaline phosphatase level but was directly related to the fall in serum calcium. Administration of phosphate supplements for 6 days decreased the blood calcium acutely in 4 patients. When calcitonin was given during phosphate treatment the effect was additive and the hypocalcemic response increased in 6 of 8 patients. These results indicate that in Paget's disease, the hypocalcemic response to calcitonin depends on the prevailing rate of bone turnover. The data suggest that phosphate supplements might be beneficial in some patients during calcitonin treatment.

Calcitonin treatment in Ekman-Lobstein disease.

Calcitonin treatment in Ekman-Lobstein disease.

The Effect of Porcine Calcitonin on Osteoporosis Induced by Adrenal Cortical Steroids

Effects of porcine calcitonin (five MRC units per kilogram per day) on development of osteoporosis induced by cortisone (fifteen milligrams per kilogram per day) have been investigated in adult rabbits. Measurements of surface undergoing resorption and formation were determined from cross sections of femoral mid-diaphyses, femoral metaphyses, ribs, and vertebral bodies using the quantitative microradiographic method of Jowsey. Intact femora and vertebral bodies were evaluated for gross rarefaction by high resolution macnoradiography. Bone mass per unit area was determined and mineral content of femora, ribs, and vertebrae was esimated by ashing. Cortisone treatment alone: (1) decreased bone formation and increased bone resorption at all skeletal sites evaluated, (2) decreased the amount of bone mass per unit area in both cortical and cancellous specimens, (3) caused gross macroradiographic rarefaction of femora and vertebral bodies, and (4) reduced the ash weight of ribs and vertebrae. Calcitonin treatment alone: (1) increased bone formation in cortical specimens and reduced bone resorption in vertebral bodies, (2) caused increased density of metaphyseal zones of vertebral bodies as shown by macroradiognaphy, and (3) increased the ash content of femora, ribs, and vertebrae. When compared with specimens removed from animals receiving only cortisone, specimens removed from animals receiving both hormones exhibited: (1) reduction in bone resorption rates in the cancellous specimens, (2) increased rates of bone formation in femoral diaphyses, (3) increased mass per unit area in both cortical and cancellous bone, (4) less macroradiographic rarefaction of femora and ventebral bodies, and (5) increased ash content of vertebral bodies. These results support the possibility that exogenous calcitonin may be capable of retarding some of the detrimental effects of the adrenal cortical steroids on osseous tissue, especially cancellous bone.

Secondary hyperparathyroidism in young rats given prolonged treatment with calcitonin.

ABSTRACT Bone resorption, intestinal absorption of calcium, and urinary calcium excretion were studied in young rats given prolonged calcitonin treatment. The animals soon developed a resistance to the hypocalcaemic effect of calcitonin, probably due to a secondary hyperparathyroidism. In one of the experiments the rats were given 45Ca 2 weeks before the start of the calcitonin treatment in order to label the deep parts of bone. The release of isotope from bone was inhibited after the first injections of the hormone, but even after a few days of calcitonin treatment no differences could be detected between the treated animals and their corresponding controls. An increased release of isotope from bone was registered as soon as the treatment was interrupted, indicating the presence of a secondary hyperparathyroidism. No conclusive changes could be detected in the intestinal absorption of calcium. A transitory reduction in the excretion of calcium in the urine was followed by a considerable loss of calcium.

Effect of calcitonin on the regeneration of a circumscribed bone defect (bored hole in the rat tibia).

ABSTRACT In 20 intact and 20 parathyroidectomized female Sprague-Dawley rats, holes with a diameter of 1.8 mm were bored into the proximal third of the tibia. Half the animals served as controls and received the vehicle, the remainder received daily subcutaneous injections of 100 MRCmU calcitonin in 5 % gelatin. Tetracycline labelling was performed weekly. 5 animals from each group were sacrificed after 3 weeks, the other 5 after 6 weeks. Nondecalcified ground sections through the center of the holes were evaluated with an integration ocular; the surface of the newly formed bone was compared with the original size of the defect. The course of the regeneration for the control animals was in agreement with previous data in the literature. Calcitonin treatment produced a distinct acceleration of the healing process. Presumably, the hormone does not only act via inhibition of bone resorption, but also by stimulating the activity of osteoblasts and by increasing the mineralization of the osteoid seams.

Effects of calcitonin in metastatic bone carcinoma, osteoporosis, polyostotic fibrous dysplasia and hypercalcemia.

Porcine calcitonin was administered intramuscularly at doses of 4.5-10MRC u. per day to patients with metastatic bone carcinoma, osteoporosis and polyostotic fibrous dysplasia during 22-50 days period. Transient effects of calcitonin were also investigated in hypercalcemia of primary hyperparathyroidism, multiple myeloma and vitamin D intoxication.Serum calcium and/or magnesium showed gradual decrease during the period of administration in metastatic bone carcinoma, senile osteoporosis and polyostotic fibrous dysplasia. Urinary calcium and/or magnesium also decreased in metastatic bone carcinoma and osteoporosis. Alkaline phosphatase did not change during the period of calcitonin treatment but was lowered in the posttreatment period in polyostotic fibrous dysplasia. Serum hydroxyproline showed a transient decrease in metastatic bone carcinoma.Hypercalcemia of multiple myeloma and vitamin D intoxication was improved temporarily by calcitonin. These results suggest a beneficial effect of calcitonin in the treatment of some of the bone diseases and hypercalcemia.

The effect of calcitonin on disuse atrophy of bone in the rat

In thirty female Sprague-Dawley rats the left hind leg was immobilized with plaster casts. According to treatment they were divided into the following groups: A) Control, no casts. B) No treatment. C) 50 MRC mU calcitonin (own preparation) in 5% gelatin subcutaneously per day. D) Vehicle alone subcutaneously. E) 50 MRC mU calcitonin (Ciba) in 5% gelatin subcutaneously per day. In addition, untreated rats without casts served as control (group A). After 6 weeks the femora and tibiae were X-rayed, weighed and examined histologically. The bones of the left and right legs did not differ in control group A. In groups B, C, D, and E a disuse osteoporosis had developed in the left legs (rarefication of trabecular bone volume of femur neck) which could not be seen in X-rays. Calcitonin treatment did not prevent the development of the bone atrophy. However, the pressure of the plaster casts had induced a periosteal apposition in some tibiae, and under calcitonin treatment the extent of this new formation in all femora and tibiae was markedly increased. The vehicle alone was ineffective. It can be concluded that whereas calcitonin is without effect on disuse osteoporosis, it probably favours new bone formation which is induced by other mechanisms.

Effects of porcine calcitonin on some urine electrolytes in the rat.

ABSTRACT Bidaily (b. i. d.) subcutaneous administration of porcine calcitonin (CT) to intact rats resulted in dose-related increases in urinary excretion of water, calcium, phosphorus and magnesium. The effects required several days of treatment to reach maximum levels and persisted for several days after treatment ceased. Although hypocalcaemia occurred immediately following CT injections in chronically treated rats, animals treated for 8 days were significantly hypercalcaemic 18 hours later. Bidaily administration of CT (9 a. m. and 3 p. m.) induced a distinct 24 hour periodicity in urinary excretion patterns of calcium, magnesium and urine volume, with maximal excretion at night. In the case of magnesium, this represented a direct reversal of the diurnal excretion pattern seen in control rats. Urine volume and urine calcium were increased in parathyroidectomized (PTX) and thyroparathyroidectomized (TPTX) rats treated daily with CT. Surprisingly, the initial low blood calcium levels of these rats were elevated toward normal with daily CT treatment and returned to pretreatment levels following cessation of CT injections. PTX rats treated with parathyroid extract (PTE) exhibited hypercalcaemia and hypercalciuria. Hypercalcaemia was only partially prevented by simultaneous treatment with high doses of CT and hypercalciuria was essentially unaltered.

Calcitonin treatment for root resorption.

Calcitonin treatment for root resorption.