Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020437 (hypercalcemia)
 10,293 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

When the canine thyroid gland was stained by immunofluorescence and immunoperoxidase methods using undiluted thyroglobulin antiserum, a considerably stronger immunoreactivity was revealed in the parafollicular cells than in the colloid droplets and follicular cells. After induced hypercalcemia and antithyroid drug treatment, the immunoreactivity of the parafollicular cells coinciding with the movement of secretory granules containing calcitonin was conspicuously decreased. An application of diluted serum (above 1:10) produced a strong reaction in the colloid.
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PMID:Occurrence of immunoreactive thyroglobulin in the parafollicular cells of dogs. 40 40

The importance of calcitonin in the homeostatic response to the chronic hypercalcemia of primary hyperparathyroidism is uncertain. To clarify this issue, we have used a new, sensitive radioimmunoassay for human calcitonin to measure basal plasma calcitonin concentrations in 50 patients with primary hyperparathyroidism (32 female, 18 male). We assayed calcium-stimulated calcitonin concentrations preoperatively in 22 of the patients (16 female, 6 male) and postoperatively in 6. Finally, we assayed pentagastrin-stimulated calcitonin concentrations preoperatively in eight of the patients (three female, five male). Plasma calcitonin values after an overnight fast were indistinguishable from those in normal subjects (mean+/-SE, males, 48+/-3 normal and 46+/-5 pg/ml hyperparathyroid, females, 31+/-2 normal and 37+/-3 pg/ml hyperparathyroid.) Among hyperparathyroid patients of both sexes, increases of calcitonin during Ca infusion (15 mg Ca/kg in 4 h) were within normal limits. However, the mean maximal increase of calcitonin was significantly lower in hyperparathyroid than in normal subjects (P < 0.05). In six patients normocalcemic 5-15 mo after parathyroid surgery, fasting plasma calcitonin values were not significantly different, but responses to Ca infusion were greater than preoperatively (Delta calcitonin +/-SE: 13+/-4 preoperatively and 53+/-35 pg/ml postoperatively). The mean maximal increase of calcitonin after pentagastrin (0.5 mug/kg i.v.) was slightly lower than normal in the patients (mean+/-SE, males, 45+/-8 normal and 38+/-10 pg/ml hyperparathyroid, females, 6+/-2 normal and 0 pg/ml hyperparathyroid). Thus, primary hyperparathyroidism is accompanied by normal steady-state concentrations of circulating calcitonin, and normal-to-blunted C-cell responses to pentagastrin or induced hypercalcemia, the response to calcium generally increasing after successful parathyroid surgery. These results clearly show that primary hyperparathyroidism is not characterized by hypercalcitoninemia. The seemingly paradoxical absence of elevated steady-state calcitonin concentrations may be accounted for partly by decreased secretory reserve. However, primary hyperparathyroidism may also be accompanied by an increase in the threshold of sensitivity for calcium stimulation of calcitonin secretion.
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PMID:Pre- and postoperative studies of plasma calcitonin in primary hyperparathyroidism. 43 24

A 17-year-old woman manifested fever, abdominal pain, headache, and hypertension caused by a solitary, benign pheochromocytoma. She also had hypercalcemia and elevated plasma immunoreactive calcitonin levels. After removal of the pheochromocytoma, calcium and calcitonin levels returned to normal. Studies of peripheral and tumor venous blood showed no excess or ectopic parathyroid hormone secretion, but the tumor contained and secreted calcitonin. Sporadic pheochromocytoma may secrete calcitonin and cause hypercalcemia by non-parathyroid hormone-mediated mechanisms. The potential is clearly present for confusion with multiple endocrine neoplasia, type 2 (medullary thyroid carcinoma, pheochromocytoma, and primary hyperparathyroidism).
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PMID:Pheochromocytoma associated with hypercalcemia and ectopic secretion of calcitonin. 46 64

A blind prospective study was undertaken to determine the use of calcitonin (CT) as a tumor marker. After final diagnosis, results revealed elevated plasma CT (greater than 150 pg/ml) in common cancers as follows: lung, 38%; colon, 24%; breast, 38%; pancreas, 42%; and gastric, 30%. Fifty-eight percent of oat cell carcinomas were associated with elevated plasma CT. CT immunoreactivity was detected in 14% of tumor extracts and was not detectable in normal tissue other than thyroid. Hypercalcemia was not the cause of hypercalcitonemia. Incubation studies of [125I]human CT in cancer plasma and tumor extracts demonstrated that measurements were not an artifact of label degradation. In a survey of control patients with nonneoplastic disease, elevated CT was noted in renal failure, acute gastrointestinal bleeding, and in some patients with chronic obstructive lung disease. In conclusion, plasma CT is elevated in a substantial proportion of common neoplasms and is useful as a tumor marker.
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PMID:Calcitonin in nonthyroidal cancer. 46 77

Four antisera raised in the goat have very different properties: all recognized the immunoreactive calcitonin (iCT) of medullary carcinoma of the thyroid (MCT), one the response of normal subjects to induced or endogenous hypercalcemia and 2 others a different molecular species which occurs in half the patients with cancer of breast and 3/4 of patients with cancer of the lung. The latter two antisera are most sensitive to the 22-32 sequence of human calcitonin. Depending on the antiserum used, 4 or 7 peaks of immunoreactivity are found in eluates by column chromatography or stimulated serum from MCT. Not all elevated levels of iCT in serum are diagnostic of MCT and ectopic production by lung and breast cancer must be considered. Presence of higher levels of iCT with greater amounts of cancer tissue and undetectable levels after surgery or radiotherapy when using antisera which require intact molecule of calcitonin for recognition suggest the possibility that sequential calcitonin levels with differentiating antisera may be helpful in assessing the extent of disease and response to therapy.
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PMID:Immuno-heterogeneity of the calcitonins of hypercalcemia, breast and lung cancers and medullary carcinoma of thyroid. 47 68

This paper contains the first demonstration of quantitative changes in the levels of calcitonin-like immunoreactivity in the pituitary. The concentration of calcitonin-like material in lean Zucker rats (?/+) was 0.42 +/- 0.09 ng/mg wet weight of pituitary. The pituitaries of obese rats (fa/fa) contained significantly greater levels (1.56 +/- 0.56 ng/mg wet weight). This 271% increase represents the first indication that pituitary calcitonin-like material may have a physiological role in genetically obese rats. Thyroidal calcitonin also elevated in the obese (111%). These large elevations in the calcitonin content of the glands of obese rats were not accompanied by significant elevations of calcitonin in the blood. This suggests that obese rats have problems with mechanisms for the release of calcitonin into the blood and might not be able to combat hypercalcemia as effectively as leans. However, this hypothesis remains to be tested.
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PMID:Elevation of calcitonin immunoreactivity in the pituitary and thyroid glands of genetically obese rats (fa/fa). 48 13

To examine the relative importance of calcium and gastrin in regulation of calcitonin secretion, we administered graded oral doses of calcium to 10 normal men, ages 23-29 yr. Each subject had previously shown an appropriate increase in calcitonin secretion in response to a pharmacologic (0.5 mug/kg) pentagastrin injection. On separate days and in random order, each man drank 250 ml of distilled water containing 0.0, 0.5, 1.5, and 3.0 g of elemental calcium as the gluconate salt. Blood samples were drawn before and at 30, 60, 90, 120, 180, and 240 min after the oral calcium dose. The samples were analyzed for calcium by atomic absorption spectroscopy, and for gastrin and calcitonin by radioimmunoassays of established sensitivity and specificity. Ingestion of water (control) caused no change in any of the three variables. Calcium ingestion resulted in dose-related increases, within the normal range, of all three variables. Immunoreactive gastrin rose promptly, peaking at 30 min, and returning to basal levels or below by 120 min. In contrast, calcium and immunoreactive calcitonin levels rose slowly and in parallel, peaking at 120-240 min. Changes in calcitonin and changes in calcium were strongly and positively correlated, r = 0.73, when all data were pooled. Furthermore, individual linear regressions for changes in calcitonin and calcium levels (calculated separately for the three oral calcium doses in each subject) had positive slopes in 28 out of 30 sets (P < 0.01). The changes in calcitonin concentrations were much more poorly correlated with the corresponding changes in serum gastrin levels; in fact, the regression coefficient was weakly negative, r = -0.20. These results show that, at least in young adult men, changes of ambient calcium concentration within the normal range may be of major importance in physiologic regulation of calcitonin secretion. The findings are consistent with the hypothesis that calcitonin functions to prevent excessive postprandial hypercalcemia.
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PMID:Regulation of calcitonin secretion in normal man by changes of serum calcium within the physiologic range. 50 Aug 34

1. Hypercalcemia was induced in S. murinus by alternate day intramuscular injections of vitamin D (25 000 IU) and by providing them 1% CaCl2 solution (prepared in tap water) for drinking. 2. After such a treatment the serum calcium values recorded a rise as compared to those of the control specimens. 3. The histological picture of the thyroid of the treated specimens reveals increased number of calcitonin cells. This observation is supported by the occurrence of mitotic figures among them. 4. Perpetual calcium challenge results in degranulation of the secretory material (calcitonin) among these cells (at 26th and 30th day of treatment). 5. It also results in degenerative changes in certain number of C cells. 6. The blood capillaries around these cells get dilated and secretory granules of C cells tend to gather at the periphery of cytoplasm and towards vascular pole. 7. The parathyroid shows atrophic changes.
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PMID:Studies of calcitonin cells and parathyroid gland of house shrew, Suncus murinus in response to experimental hypercalcemia. 53 67

Two thyrotoxic patients with significant hypercalcaemia are described. The hypercalcaemia failed to suppress with hydrocortisone, propranolol and calcitonin but serum calcium fell rapidly to normal with carbimazole treatment. Both patients were subsequently treated surgically and at operation no evidence of parathyroid disease was found. Thyroid disease must be controlled before co-existing parathyroid disease is diagnosed in hypercalcaemic thyrotoxic patients.
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PMID:Control of hypercalcaemia in thyrotoxicosis. 54 53

We have undertaken a study of 24 hypercalcemic patients with the use of salmon calcitonin as a therapeutic agent. Seventy-five percent of the patients exhibited a clinically significant decrease in serum calcium and approximately half became normocalcemic within 2 hr. Throughout salmon calcitonin administration, the mean serum calcium of the patients was lower than the pretreatment values. Although the drug did not always lower the calcium level to normal, it often brought the hypercalcemia to more tolerable levels. During the course of calcitonin therapy, the number of patients with normal or near-normal serum calcium ranged from 31.3% (at 96 hr) to 82.4% (at 30 hr). Many of the patients improved symptomatically. The only significant side effects were nausea and vomiting in 12.5% of the patients, which necessitated cessation of therapy in only one. The drug was well tolerated in patients with azotemia. Calcitonin-induced hypocalcemia was not encountered. Salmon calcitonin can be used safely alone or in conjunction with other hypocalcemic therapies.
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PMID:Salmon calcitonin in hypercalcemia. 56 8


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