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Query: UMLS:C0020437 (hypercalcemia)
 10,293 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of salmon calcitonin (0.25 MRC mU/g body wt) on the serum calcium and phosphate levels as well as on the activity of ultimobranchial body and parathyroid glands was investigated in the frog, Rana tigrina for 15 days. The hormone evokes hypocalcemia (on day 1 and day 3) which is followed by a significant hypercalcemia on day 10. Thereafter, the level of calcium decreases again on day 15. Calcitonin induces hypophosphatemia (on day 3 and day 5). Thereafter, hyperphosphatemia is recorded on day 10. By day 15 normal serum phosphate value is achieved. After treatment with calcitonin, the ultimobranchial body becomes inactive and the parathyroid glands get activated.
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PMID:Ultimobranchial body and parathyroid gland of the frog, Rana tigrina in response to calcitonin administration. 248 19

Vitamin D has complex effects in bone: it stimulates matrix formation and bone maturation but also enhances osteoclastic activity and may influence differentiation of bone cell precursors. Calcitonin inhibits the function of osteoclasts, reducing bone resorption, thus, the combination of vitamin D and calcitonin could result in a positive bone balance. We tested the hypothesis that chronic treatment with high doses of vitamin D (150,000 U/week), moderate doses of salmon calcitonin (120 MRC U/week), and adequate Ca supplementation (1 g/day) could be beneficial in osteoporosis. Thirteen women with postmenopausal osteoporosis received this treatment for 2-6 years (mean 3.5 years). No side effects, hypercalcemia, or hypercalciuria occurred. There was marked reduction in bone pain. The fracture rate in 11 patients with vertebral compression fracture was 240/1,000 patient years, threefold lower than the reported 834 fractures for untreated patients of similar age. Single photon bone densitometry of the radius did not change. Iliac crest bone biopsies obtained at the initiation and conclusion of the study showed a 43% increment in trabecular bone volume (P = 0.0003), without changes of the normal osteoid thickness, surface, and volume. Because single photon densitometry reflects mostly cortical bone, the data suggest that the combination of vitamin D and calcitonin increases trabecular bone mass and prevents the fall of cortical bone mass in osteoporosis. Previous reports suggest that calcitonin alone or with small doses of vitamin D increased bone mass for about 2 years. The present study suggests a prolonged beneficial effect of the combination of high doses of vitamin D with rather moderate (less than 150 MRC U/week) doses of calcitonin in postmenopausal osteoporosis.
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PMID:Effect of calcitonin and vitamin D in osteoporosis. 250 3

The effect of salmon calcitonin (0.25 MRC mU/g body wt) was investigated on the serum calcium and inorganic phosphate levels of the frog. Rana tigrina. The hormone evokes hypocalcemia (on Day 1 and Day 3) which is followed by a significant hypercalcemia on Day 10. Thereafter, the level of calcium decreases again on Day 15. Calcitonin induces hypophosphatemia (on Day 3 and Day 5). Thereafter, hyperphosphatemia is recorded on Day 10. Normal serum phosphate value is achieved by Day 15. The results obtained in R. tigrina have been discussed in relation to the increased calcium deposits in the paravertebral lime sacs and to the possible enhanced secretion of the parathyroid glands.
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PMID:Influence of calcitonin administration of serum calcium and inorganic phosphate level of the frog, Rana tigrina. 273 50

Therapy should be individualized on the basis of patient symptoms, severity of hypercalcemia, and prospects for inducing a remission in the underlying malignancy. We have found the most effective approach to be vigorous hydration of the patient, usually intravenously with normal saline at a rate of 300 to 500 mL/h. Intravenous furosemide is given as needed to prevent fluid overload. If the patient is volume replete and if hypercalcemia persists after 24 to 48 hours of intravenous hydration, calcitonin, 200 MRC units subcutaneously every 12 hours plus prednisone, 20 mg orally four times daily, are added. In most cases, a response is seen shortly after institution of this therapy. Meanwhile, attempts to treat the malignancy are initiated, including palliative radiation therapy for bony metastases. If the patient is still hypercalcemic and symptomatic after seven days of this therapy, treatment with plicamycin is given unless the patient's condition is clearly terminal. At present, use of prostaglandin synthetase inhibitors is not recommended, and bisphosphonates are available only for investigational use.
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PMID:Hypercalcemia of malignancy: diagnosis and therapy. 294 51

Although calcitonin is a natural, nontoxic, and rapid inhibitor of bone resorption, its use in the treatment of hypercalcemia is limited because of its transient efficacy and the need for repeated parenteral administration. In normal subjects, suppositories of calcitonin have been shown to be biologically active. Peak plasma concentrations of salmon calcitonin after rectal administration in six normal subjects were similar to those measured after parenteral administration. To evaluate the efficacy of calcitonin suppositories in disease states, 10 patients with moderate hypercalcemia due to malignancy were treated with salmon calcitonin, administered as suppositories containing 300 MRC units, three times a day for seven days. The mean plasma calcium level decreased significantly from 2.96 +/- 0.09 mmol/liter to 2.57 +/- 0.09 after one week (p less than 0.005) and rose again after discontinuation of treatment to 2.86 +/- 0.09 mmol/liter one week later. Urinary calcium and hydroxyproline values decreased during treatment and rose after discontinuation of treatment. The plasma calcium level decreased rapidly in six patients, becoming normal in five; three patients showed only a partial response, and one patient had no response at all. No side effects were observed, and clinical improvement was noted in nine of the 10 patients. Little or no response was observed in patients with extremely high urinary calcium or, to a lesser extent, high hydroxyproline excretion. There was a significant negative correlation between the maximal decrease in plasma calcium concentration and initial urinary calcium excretion (r -0.78, p less than 0.01). Thus, salmon calcitonin administered by the rectal route appears to be an easy, safe, and effective treatment of moderate hypercalcemia without apparent side effects.
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PMID:Effectiveness of salmon calcitonin administered as suppositories in tumor-induced hypercalcemia. 356 31

Hypercalcemia is one of the most critical complications in patients with malignancy. We have used salmon calcitonin for treatment of hypercalcemia in these patients. The subjects were 49 hypercalcemic patients with various malignancies. Synthetic salmon calcitonin (SCT) was provided by Teikoku Hormone Mfg. Co. Ltd., Japan and 40 MRC units was administered twice daily i.m. or i.v. In 21 of 33 cases treated i.m. and in 8 of 16 cases treated i.v., a serum Ca decrease of more than 2 mg/dl was observed. The hypercalcemia was managed in 59% of patients within 6 days after initiation of the treatment and effective duration was 14 days. On the other hand, ineffective cases treated with a combination of SCT and glucocorticoid or SCT and mithramycin were managed in 57% and 86%. The 50% survival time was 69 days in the effective cases and 23 days in the uncontrolled cases (P less than 0.01). The main causes of death in the ineffective cases were renal insufficiency. On the other hand, in the effective cases, improvements of renal function were observed. The side effects were slight, and nausea and flushing were observed in 24% of cases. These data indicate that SCT is effective for lowering the serum Ca level in hypercalcemic patients with malignancies.
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PMID:[Synthetic salmon calcitonin as an antihypercalcemic agent for hypercalcemia in malignancy]. 374 Aug 62

The authors describe histologically confirmed medullary carcinoma of the thyroid gland in a living patient. The tumor produces excessive amounts of calcitonin and releases it into the blood stream. In healthy subjects, the plasma concentration of calcitonin is 0.2-1.0 mU MRC/ml plasma; in medullary carcinoma it is 5.66 mU/ml. The tumor responds to artificially induced hypercalcemia by a further increase of plasma calcitonin. 60-120 minutes after a hypercalcemic stimulus, the calcitonin level declines well below the initial value but remains elevated. The patient has a permanently normal blood calcium level. This is probably due to secondary hyperparathyroidism, a compensatory phenomenon. (Author's modified)
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PMID:[Medullary carcinoma of the thyroid gland producing calcitonin]. 501 38

(Asu) E-CT is a deaminodicarba-analog of the synthetic eel-calcitonin (E-CT) that shows specific activity and the potency reasonably high in comparison with that of the most potent natural hormone. The structure of its molecule indicates that the disulphide bond in calcitonins is not essential for the biological activity but only for the maintenance of the specific conformation by forming an intramolecular bridge. The instability of calcitonins should mainly be attributed to the presence of the disulfide bond and (Asu)E-CT proved to be more stable "in vitro" than native calcitonins. The more prolonged hypocalcemic effect of E-CT and its aminosuberic analog (Asu)E-CT has been accounted for to a greater stability of and persistence at the receptor site. (Asu) E-CT has been largely studied in Japan on experimental animals and successfully used in the treatment of hypercalcemia in man. On the contrary investigations on human administration of this analog are very scarce. The present paper reports studies carried out in normal subjects and Paget's disease patients to investigate the effects of (Asu)E-CT in man in comparison with the effects of synthetic human calcitonin (H-CT) and synthetic salmon calcitonin (S-CT). Two different experimental procedures have been used: 1) rapid intravenous injection of (Asu)E-CT (80 MRC. U.) or respectively of H-CT and S-CT (100 MRC. U.) in 15 subjects (7 normals and 8 with Paget's disease); 2) slow 7 days continuous subcutaneous infusion of similar daily amounts of (Asu)E-CT, H-CT and S-CT administered by a microjet pump device in 21 subjects (7 normals and 14 with Paget's disease). The intravenous administration of (Asu)E-CT induced a rapid and persistent decrease in total plasma calcium, ionized calcium and plasma phosphate that was more evident in Paget's disease patients than in normal subjects. No clearly cut differences have been observed with the hypocalcemic and hypophosphatemic effect of H-CT and S-CT administered intravenously; nevertheless the hypocalcemic effect proved to be more persistent in Paget's disease patients treated with (Asu)E-CT. After intravenous infusion of (Asu)E-CT the plasma level of cAMP rose more evidently in pagetic than in normal subjects but the rise was lower than in H-CT and S-CT treated subjects.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Asu(1,7)E-CT, an analog of eel calcitonin. A comparative study in man with reference to other synthetic calcitonins]. 608 15

(Asu1,7) E-CT (carbocalcitonin-elcatonin) is the aminoasuberic analogue of eel calcitonin differing from the natural hormone in that an ethylene bridge replaces the disulphide bridge in position 1-7. This modification preserves the conformation of natural calcitonin but enhances the physical, chemical and biological stability of the molecule. This in its turn facilitates maximum purification of the product as well as enhancing its resistance to degradation both in vitro and in vivo. The specific activity of carbocalcitonin is equivalent to 5000 U.MRC/mg and it possesses all the pharmacological and clinical properties of natural calcitonins. It has the same hypocalcemic potency of eel or salmon calcitonin, superior to the human and porcine types. Carbocalcitonin has the typical pharmacological effects of the natural hormone on the kidneys, bone and gastrointestinal tract, the target organs of calcitonins. When injected into the cerebral ventricle of laboratory animals it was found to have an analgesic effect. In clinical terms (Asu1,7) E-CT gave good results when used in the treatment of hypercalcaemia and senile osteoporosis. Carbocalcitonin was also employed in conditions characterised by a high bone metabolism turnover such as Paget's disease, Sudeck's atrophy and immobilisation osteoporosis. Experiments to date have shown carbocalcitonin to be extremely interesting in terms of tolerability with very few side effects being noted. This may well be attributable to the greater stability conferred by the absence of the S-S bridge.
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PMID:[Profile of a new calcitonin: carbocalcitonin-(Asu1,7) E-CT]. 620 66

Experimental studies have suggested that in primary hyperparathyroidism (HPT) the cells of the hyperfunctioning parathyroid tissue retain some capacity for stimulation and that an increase in secretion of parathyroid hormone (PTH) can occur when the extracellular calcium concentration is lowered within the hypercalcaemic range. We have tested this hypothesis in 23 patients with HPT, 10 patients with hypercalcaemia of other origin (7 of whom had disseminated malignant disease) and 17 normal subjects. In all three groups a single injection of 100 MRC units of salmon calcitonin caused a reduction in serum calcium of approximately 3 to 5%. In the hypercalcaemic patients this reduction was correlated to the basal calcium level (r = -0.57, P less than 0.01). In the patients with HPT, although they all remained hypercalcaemic, the decrease in serum calcium was associated with a mean increase in serum PTH of 10%. Only in 2 patients did such an increase fail to occur despite an adequate decrease in serum calcium. These 2 patients had high basal PTH levels and the lack of response might have been due to a high degree of autonomous parathyroid function. Calcitonin also reduced serum calcium and increased serum PTH in normal subjects. None of the patients with hypercalcaemia of other origin than primary HPT displayed a secretory PTH response to serum calcium reduction. Thus, this test could be of practical clinical value, particularly in patients with borderline PTH values. A calcitonin-induced rise in PTH while serum calcium is lowered within the hypercalcaemic range strongly suggests primary HPT.
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PMID:A stimulation test with calcitonin for differential diagnosis of hypercalcaemia. 649 90


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