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)

Fifteen patients with the diagnosis of multiple endocrine adenomatosis, type II, syndrome (MEA II) were reported from a single center to discuss the dilemmas of early detection and treatment of the adrenal medullary, thyroid, and parathyroid gland diseases. Ten patients came from three families. Three of the patients died, none in hypertensive crisis. Bilateral adrenal medullary disease was present in six patients. Five patients with proved pheochromocytoma had hypertension. All had diagnostic urinary catecholamine values. Nine normotensive patients without proved pheochromocytoma but in a high-risk category for adrenal medullary disease, have multiple suspicious urinary cathecholamines suggestive of adrenal medullary hyperplasia. Bilateral adrenalectomy is recommended for proved adrenal medullary disease in the MEA II syndrome. Medullary carcinoma of the thyroid gland was found in 13 patients and is believed to be present in two others. Five of the proved cases were occult, being discovered by elevation of pentagastrin-stimulated serum calcitonin levels, justifying total thyroidectomy. Parathyroid hyperplasia was found in three patients with preoperative hypercalcemia and in four others with preoperative normocalcemia. Conservative treatment of parathyroid gland hyperplasia in the MEA II syndrome is substantiated. Metachronous phenotypic expression of the syndrome components was significant.
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PMID:Dilemmas in the early diagnosis and treatment of multiple endocrine adenomatosis, type II. 1 7

Four patients with thyrotoxicosis, hypercalcaemia and metabolic bone disease are described. One of them had a 'hot nodule', T3 toxicosis and a parathyroid tumour and another had thin bones, subperiosteal cortical bone erosions and complete dysphagia. Hypercalcaemia persisted during treatment with antithyroid drugs in two patients, both of whom had hyperparathyroidism. The administration of salmon calcitonin to these two patients before starting antithyroid treatment produced an immediate and sustained fall in serum calcium and urinary hydroxyproline levels. Calcitonin administration should be of value in the early management of hypercalcaemic patients.
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PMID:Thyrotoxicosis and hypercalcaemia: response to antithyroid drugs and salmon calcitonin. 6 11

Thyroglobulin-like immunoreactivity of the parafollicular cells was studied by an immunoperoxidase bridge technique using antisera against dog thyroglobulin fragments. 1. The dog parafollicular cells were specifically stained by anti-peak I (27S and larger components fraction) antiserum absorbed with peak II (19S fraction). By this method, they were easily distinguishable from the non-reactive follicular cells and colloid droplets. More sensitive staining of the parafollicular cells was possible with anti-peak I'' (larger components fraction) antiserum. The staining reactions indicated that the antigenic material responsible for immunoreactivity of the parafollicular cells was due to larger molecular components of thyroglobulin corresponding to 32S, 37S or greater than 37S, and was not due to either the 19S thyroglobulin or to the 27S iodoprotein. 2. A conspicuous decrease of the immunoreactive material in the parafollicular cells occurred in the dog after both chronically induced hypercalcemia and antithyroid drug treatment. This coincided with movement of secretory granules containing calcitonin as shown by staining with silver impregnation, HCl-basic dye, and lead-hematoxylin. 3. The antisera against larger molecular components of dog thyroglobulin showed a high degree of cross-reactivity to the parafollicular cells of most of the mammalian species investigated; rats, rabbits, hamsters, mice, cats, lions, goats, cows, and human.
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PMID:Immunohistochemical study of a large molecular fragment of thyroglobulin in parafollicular cells. 7 16

The hypercalcemia observed during the acute calcitonin test reflects the size and the activity of the osteoclastic population throughout the entire skeleton. Several calcitonins of animal origin (pork, salmon) have already been used for this test in human pathology, but the results can be flawed by the presence of anti-calcitonin antibodies. The authors demonstrate that human synthetic anti-calcitonin in man has a hypocalcemia effect identical to salmon synthetic calcitonin, with an equipotential dose for the rat. The systematic study of acute salmon calcitonin in various osteopathies makes it possible to note a certain number of paradoxical responses with prolonged hypercalcemia in the hours following injection. This is observed especially in the "hyperosteoidosis states" and the authors attempt to give it a physiopathological explanation. Finally, the acute salmon calcitonin test can be used as a mean of surveillance of the anti-osteoclastic activity of the disphosphonates in the treatment of Paget's disease.
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PMID:[The hypocalcemia test, using human and salmon synthetic calcitonins. Paradoxical hypercalcemic responses. Responses in patients with Paget's disease treated with EHDP]. 11 60

Rhesus monkey (Macaca mulatta) were subjected to hypercalcaemia by daily intramuscular injections of vitamin D2 (100,000 IU) and by providing them gram soaked in 1% CaCl2 solution for eating and 1% CaCl2 solution (prepared in tap water) for drinking. After 10, 15, 20 and 30 days of such treatment the serum calcium level recorded a rise (18.24 +/- 0.56, 26.20 +/- 1.30, 17.25 +/- 0.25 and 20.50 +/- 0.55 mg/dl respectively) as compared to those of control animals (12.80 +/- 1.00, 12.30 +/- 0.50, 12.70 +/- 0.20 and 12.30 +/- 0.30 mg/dl). Serial sections of thyroid parathyroid complex and isthmus were subjected to selective staining for lcalising the C cells. The structure and behaviour of these cells both under normal and experimental conditions has been studied. Hypercalcaemia resulted in the increase of these cells. Mitotic figures of the C cells were also encountered after 10 days of hypercalcaemia. The specimens subjected to 30 days treatment showed complete degranulation of these cells. Chronic hypercalcaemia inhibits the activity of parathyroid cells which display degenerative changes. The anterior and posterior poles, the peripheral regions of thyroid and isthmus are completely devoid of calcitonin cells.
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PMID:Thyroid calcitonin cells and parathyroid gland of the Indian rhesus monkey Macaca mulatta in response to experimental hypercalcaemia. 11 36

Twenty-nine patients with acute hypercalcemia secondary to carcinoma, myeloma and parathyroid adenoma have been treated with large doses of furosemide, mithramycin, or salmon calcitonin perfusion. With furosemide administration the treatment was successful in 6 of 10 patients. Furosemide was injected intravenously at the rate of 125 mg every 3 hours. With mithramycin perfusion only 2 of 8 patients have a return of the serum calcium levels to normal. With salmon thyrocalcitonin 3 of 10 patients obtained a good result. It can be interesting to suggest the association of furosemide and salmon calcitonin infusion to treat hypercalcemia of myeloma.
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PMID:Furosemide, mithramycin, and salmon calcitonin in hypercalcemia. 13 Feb 39

Three patients with malignant disease received the usual recommended doses of mithramycin and calcitonin, either concurrently or concomitantly, because of severe life-threatening hypercalcemia. All three patients developed severe, symptomatic hypocalcemia. The mechanisms for this phenomenon are discussed. A possible synergism between calcitonin and mithramycin may prove to be hazardous in such patients and this possibility must be kept in mind when these agents are being considered as a combination treatment for hypercalcemia.
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PMID:Symptomatic hypocalcemia following combined calcitonin and mithramycin therapy for hypercalcemia due to malignancy. 15 45

Hypercalcemia is very uncommon in small cell (oat cell) carcinoma of the lung. Two cases of this neoplasm associated with symptomatic hypercalcemia are described. Despite normal skeletal roentgenograms, metastatic bone disease was demonstrated by abnormal bone scans and bone biopsies in both patients. The combination of conventional antihypercalcemia therapy, cytotoxic cancer chemotherapy, and synthetic salmon calcitonin corrected the hypercalcemia despite progression of the small cell carcinoma. One patient with elevated serum immunoreactive parathyroid hormone (PTH) had a parathyroid adenoma at autopsy. This association emphasizes that in cases of bronchogenic small cell carcinoma with hypercalcemia, conincidental primary hyperparathyroidism should be considered.
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PMID:Hypercalcemia in small cell (oat cell) carcinoma of the lung. Coincident parathyroid adenoma in one case. 17 Oct 50

Although hypercalcemia, osteoporosis, and increased bone turnover are associated with thyrotoxicosis, no direct effects of thyroid hormones on bone metabolism have been reported previously in organ culture. We have now demonstrated that prolonged treatment with thyroxine (T4) or triiodothyronine (T3) can directly increase bone resorption in cultured fetal rat long bones as measured by the release of previously incorporated 45Ca. T4 and T3 at 1 muM to 10 nM increased 45Ca release by 10-60% of total bone 45Ca during 5 days of culture. The medium contained 4 mg/ml of bovine serum albumin to which 90% of T4 and T3 were bound, so that free concentrations were less than 0.1 muM. The response to T4 and T3 was inhibited by cortisol (1 muM) and calcitonin (100 mU/ml). Indomethacin did not inhibit T4 response suggesting that T4 stimulation of bone resorption was not mediated by increased prostaglandin synthesis by the cultured bone. Matrix resorption was demonstrated by a decrease in extracted dry weight and hydroxyproline concentration of treated bones and by histologic examination which also showed increased osteoclast activity. The effects of thyroid hormones were not only slower than those of other potent stimulators of osteoclastic bone resorption (parathyroid hormone, vitamin D metabolites, osteoclast activating factor, and prostaglandins), but the maximum response was not as great. We conclude that T4 and T3 can directly stimulate bone resorption in vitro at concentrations approaching those which occur in thyrotoxicosis. This effect may explain the disturbances of calcium metabolism seen in hyperthyroidism.
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PMID:Direct stimulation of bone resorption by thyroid hormones. 18 21

Studies of calcium metabolism in 38 patients with cancer indicated that: 1) intestinal absorption of calcium was reduced in patients with skeletal metastases and in those with hypercalcemia; 2) calcium-47 space (a measurement of bone turnover rate) was high in the patients with skeletal metastases; 3) hypercalcemic patients had higher urinary and endogenous fecal excretion of calcium than those who were normocalcemic; 4) levels of plasma immunoreactive parathyroid hormone were similar in normo- and hypercalcemic patients, but the levels for a given serum calcium in malignant disease were lower than those in primary hyperparathyroidism; and 5) some patients had elevated calcitonin levels. Hypercalcemia complicating malignant disease is therefore not due to hyperabsorption or diminished excretion of calcium, and a low calcium diet is unlikely to benefit these patients. Measurement of 47Ca space could be of use in monitoring therapy of patients with skeletal metastases, and measurement of plasma parathyroid hormone could be useful in the differential diagnosis of hypercalcemia.
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PMID:Calcium metabolism in cancer. Studies using calcium isotopes and immunoassays for parathyroid hormone and calcitonin. 18 80


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