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)

Prostaglandin synthetase inhibitors have, in the past, been shown to inhibit osteolysis caused by breast carcinoma tissue in vitro. We therefore assessed the effect of Indomethacin and aspirin on some parameters of calcium metabolism in patients with breast cancer. Neither drug reduced the serum calcium in pateints with hypercalcemia, nor reduced skeletal destruction as measured by the urinary hydroxy proline: creatinine ratio and urinary calcium in normocalcemic or hypercalcemic patients with osteolytic metastases. A possible reason for the discrepancy between results obtained in vitro and in vivo is that there are two phases of bone destruction in breast cancer; the early phase dependent and the late phase independent of prostaglandin synthesis.
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PMID:Failure of indomethacin to reduce hypercalcemia in patients with breast cancer. 100 35

The clinical findings of bone marrow necrosis in 13 patients undergoing bone marrow examination to investigate a peripheral blood cytopenia or leukoerythroblastic blood smear were reviewed and compared to those in the literature. Excluding sickle cell disease, all cases of bone marrow necrosis diagnosed during life were associated with a neoplastic process involving the marrow. A myeloproliferative disorder was found in five patients, metastatic carcinoma in five patients, a lymphoma in two patients, and both a myeloproliferative disorder and metastatic carcinoma in one patient. Marrow necrosis was found to involve the marrow at multiple sites in a piecemeal fashion with areas of necrotic marrow and structurally intact marrow adjacent to each other. Severe bone pain without roentgenographic abnormality was the major symptom in 85% of the patients. Marrow and fat emboli, hypercalcemia and peripheral blood cytopenias were identified as direct complications of marrow necrosis. The prognosis of patients with marrow necrosis secondary to neoplastic disease was found to be extremely poor with a median survival of less than one month. However, one patient responded to antineoplastic chemotherapy and showed healing of the bone marrow.
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PMID:Bone marrow necrosis. 106 33

Hypercalcemia associated with nonmetastatic malignancy has been reported most frequently with lung or kidney tumors, while among gynecologic malignancies, the ovary has been the most common primary site. The pertinent clinicopathologic features of 2 cases of nonmetastatic vulvar carcinoma producing hypercalcemia are described in the present report. Including 3 previously reported cases, the vulva is seen to be the second most common site in the female genital tract for production of this paraendocrine syndrome. The clinician should be aware of the association of hypercalcemia and mental confusion with bulky vulvar tumors, so that surgery will not needlessly be delayed in a futile attempt to correct the hypercalcemia medically,
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PMID:Vulvar carcinoma with hypercalcemia. 111 57

Of 13 patients treated surgically for familial medullary thyroid carcinoma in whom parathyroid tissue was availabe, the majority showed parathyroid abnormalities (hyperplasia in sis, tumors in five). Two patients had had renal calculi. No correlation was evident between the presence of the parathyroid tumors and peripheral blood levels of parathyroid hormone. Hyperparathyroidism is usually mild, but occasionally it results in complications of hypercalcemia. Hyperparathyroidism has not appeared to date following removal of medullary thyroid carcinoma associated with normal-sized but microscopically hyperplastic parathyroids. Evidence of parathyroid abnormalities has not been recognized in eight patients with sporadic medullary carcinoma, making genetic factors dominant in explaining the association of parathyroid hyperplasia and this carcinoma. At operation, parathyroid glands should be evaluated and those that are grossly enlarged removed while preserving parathyroid function.
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PMID:Management of parathyroid glands in surgery for medullary thyroid carcinoma. 113 Oct 5

The VX2 carcinoma produces profound hypercalcemia (17-22 mg/100 ml) in the rabbit about 3-4 wk after transplantation. A bone resorption-stimulation factor (assayed in vitro with mouse calvaria in culture) has been extracted with diethyl ether from the tumor tissue and from the medium of a clonal strain of VX2 cells grown in culture. Serologic methods reveal that the tumors contain 294 plus or minus 51 ng/g fresh weight (mean plus or minus SE, 25 tumors) of prostaglandin E2 (PGE2), a potent bone resorption-stimulating agent. VX2 cells in culture produce 0.5-3.0 mug PGE2 per mg cell protein per 24 hr. The production of bone resorption-stimulating activity and PGE2 by VX2 cells in culture were both inhibited by indomethacin (100 ng/ml). Tumors from normocalcemic, indomethacin-treated rabbits (10-40 mg/rabbit/24 hr) contained little or no bone resorption-stimulating activity nor PGE2. Tumor-bearing rabbits receiving indomethacin continuously did not develop hypercalcemia, however, following cessation of indomethacin administration, hypercalcemia developed rapidly and was again reversed by reinstitution of indomethacin feeding. In untreated, hypercalcemic, tumor-bearing rabbits, initiation of indomethacin treatment was followed by a rapid return of the plasma calcium to the normal range. Systemic venous plasma from hypercalcemic tumor-bearing plasma contained higher concentrations of PGE2 than plasma from normocalcemic control rabbits. Venous drainage of the tumor contained even higher plasma PGE2 concentrations than systemic venous plasma in hypercalcemic animals; plasma PGE2 concentrations locally and in systemic plasma were unmeasurable (less than 70 pg/ml) in normocalcemic, indomethacin-treated, tumor-bearing rabbits. We conclude that PGE2 is a bone resorption-stimulating factor produced by VX2 tumor cells, and that secretion of PGE2 by the tumor in vivo may well be responsible for the hypercalcemia observed in tumor-bearing rabbits.
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PMID:Hypercalcemia and tumor-prostaglandins: the VX2 carcinoma model in the rabbit. 114 92

A case of 53-year-old woman with a parathyroid adenoma and a parathyroid carcinoma with functioning metastases to the lungs, mediastinum and pleura is reported. The administration of inorganic phosphate solution failed to control hypercalcemia. The therapeutic methods available to deal with metastases are discussed.
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PMID:Functioning metastatic parathyroid carcinoma. 114 93

Nonparathyroid humoral hypercalcemia is becoming an increasingly more common problem associated with carcinoma. Carcinomas of the head and neck may elaborate parathormone or parathormone-like humors that in the absence of bone metastases, renal disease, parathytoid tumors, or secondary hyperparathyroidism may produce hypercalcemia, which if unrecognized, complicates and prevents the appropriate management of the patient. This report deals with the production of parathyroid hormone and the first reported case, to our knowledge, of carcinoma of the larynx associated with nonparathyroid hypercalcemia.
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PMID:Production of parathyroid hormone by laryngeal cancer. Report of a case. 114 29

We have compared the effects of oral and intravenous ethanol on the secretion of both thyrocalcitonin and gastrin in five patients with medullary carcinoma of the thyroid. Ethanol caused a moderate rise in plasma thyrocalcitonin to 316% +/- 343% of baseline when given intravenously and to 197% +/- 106% of baseline when given orally. Only oral ethanol caused a measurable rise in serum gastrin levels. Serum calcium did not change significantly from baseline during either oral or intravenous administration. The results suggest that stimulation of thyrocalcitonin secretion by ethanol is not secondary to increased secretion of gastrin nor to the induction of hypercalcemia. Neither oral nor intravenous ethanol appears to be as effective as intravenous pentagastrin in testing for the presence of medullary carcinoma.
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PMID:Stimulation of thyrocalcitonin secretion by ethanol in patients with medullary thyroid carcinoma--an effect apparently not mediated by gastrin. 118 95

The effect of magnesium chloride or magnesium sulfate infusion on circulating levels of immunoreactive calcitonin (iCT) was evaluated on nine occasions in three patients with metastatic medullary carcinoma of the thyroid. One patient was normocalcemic and had normal circulating levels of immunoreactive parathyroid hormone (iPTH), one patient was hypocalcemic and had surgical hypoparathyroidism, and one patient had mild to moderate hypercalcemia associated with bone metastases. The basal serum iPTH levels were undetectable in the latter two patients. In every instance magnesium administration produced a rapid and striking fall in circulating iCT and usually a detectable fall in serum calcium. During the hypermagnesemic state, serum iPTH fell from normal to undetectable in the patient with normal parathyroid function, while serum iPTH levels remained undetectable in the hypoparathyroid patient and in the patient with hypercalcemia associated with bone metastases. The results of these studies indicate that: (a) contrary to what has been reported in normal experimental animals, magnesium administration lowers circulating iCT in human subjects with thyroid medullary carcinoma and (b) the calcium-lowering effect produced by magnesium in patients with medullary carcinoma may, in part at least, be due to a redistribution of body calcium that is not mediated by the actions of either parathyroid hormone or clacitonin.
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PMID:Serum calcitonin-lowering effect of magnesium in patients with medullary carcinoma of the thyroid. 120 87

Stimulation of tumor growth and induced hypercalcemia both may occur during the initiation of estrogen therapy in breast cancer. This study was conducted to determine whether cyclophosphamide (CTX) as an adjuvant to estrogen therapy might (1) prevent induced hypercalcemia or (2) achieve a higher tumoricidal effect during the phase of tumor stimulation. Fifty postmenopausal women with inoperable or recurrent disseminated breast carcinoma were divided into two random groups. Results could be evaluated in 44 patients; 21 received diethylstilbestrol (DES), and 23 received DES plus a 4-week course of cyclophosphamide (DES + CTX). The response rate was 5/21 (24%) in the DES group and 8/23 (35%) in the DES + CTX group (p greater than 0.05). The median duration of response for both groups was 9 months. The survival rate at 24 months was 52% in the DES group and 25% in the DES + CTX group (p = 0.05). Induced hypercalcemia occurred in 3 patients treated with DES + CTX. Short-term cyclophosphamide adjuvant to estrogen therapy did not prevent induced hypercalcemia nor prolong the duration of response or survival.
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PMID:The effect of short-term cyclophosphamide on estrogen therapy in metastatic breast cancer. 123 33


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