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)

A patient with poorly differentiated monocytic malignancy had extensive lytic lesions of bone and hypercalcemia. The patient's bone margins showed little evidence of osteoclast activity. Serum parathormone concentrations were slightly increased relative to the degree of hypercalcemia, consistent with impaired renal function. Serum concentrations of the relevant prostaglandins were normal. Supernatant medium from cultured tumor cells caused prominent bone resorption in vitro. The studies on this patient provide evidence that malignant cells of the monocyte-macrophage line are capable of direct bone resorption.
Cancer 1978 Jun
PMID:Production of bone resorbing activity in poorly differentiated monocytic malignancy. 65 6

The detection of specific hormone receptors in normal and tumor tissue has brought new insight into the mechanisms of action of hormones and anti-hormones. The Swiss Cooperative Cancer Study Group (SAKK) has evaluated the antitumor effect of the new antiestrogenic substance tamoxifen in metastatic breast cancer. 158 postmenopausal patients treated with 20 mg/d tamoxifen by mouth are evaluable at present time. Complete and good partial remissions were achieved in 39 patients (25%) largely with soft tissue but also lung and bone metastases. Tamoxifen was well tolerated and caused few serious complications such as thrombosis/pulmonary embolism and hypercalcemia. These results confirm already published experience with tamoxifen, which may replace the estrogens as the primary endocrine treatment in postmenopausal mammary carcinoma metastasizing to soft tissues, lung and bone.
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PMID:[Antiestrogens: a new endocrine treatment possibility in metastasizing breast neoplasms. Experiences of the Swiss Cooperative Cancer Study Group with tamoxifen]. 69 81

Hypercalcemia causes lethargy and coma in patients with head and neck cancer. It is important to realize that coma may be due to hypercalcemia and need not be a terminal event in the progress of the tumor. Also, the development of hypercalcemia in a previously normocalcemic patient requires investigation as to the cause of the hypercalcemia. I report two cases of comatose patients, hypercalcemic from bony metastases from tongue cancer, in whom treatment by furosemide and intravenous fluid diuresis, prednisone, sodium phosphate, and mithramycin produced worthwhile remissions. Hypercalcemia may be due to (1) bony metastases, (2) pseudohyperparathyroidism, (3) unrelated associated parathyroid tumors, or (4) a second primary tumor. Even with treatment, hypercalcemia is a bad prognostic sign in patients with head and neck cancer.
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PMID:Hypercalcemia and head and neck cancer. Bony metastases from tongue cancer. 69 40

This report summarizes the data from two animal and cell culture systems that serve as models that show how certain malignant tumors produce hypercalcemia by means of a humoral mechanism. Studies with the HSDM1 murine fibrosarcoma and the VX2 carcinoma in the rabbit have led to the conclusion that these two tumors produce hypercalcemia in the host by means of a mechanism that utilizes prostaglandin E2 as the mediator between the neoplasm and bone. Analogous or identical mechanisms may operate in a small number of human tumors.
Cancer Res 1978 Nov
PMID:Role of prostaglandins in the production of hypercalcemia by tumors. 69 57

A prospective series of 200 patients with persistent hypercalcemia had an abbreviated diagnostic work-up consisting of parathormone radioimmunoassay, chest roentgenogram, intravenous pyelography, and serum protein electrophoresis. All patients with hypercalcemia and hyperparathormonism had neck exploration if roentgenograms failed to reveal evidence of ectopic hyperparathyroidism. Serum iPTH proved to be at least 96% accurate in predicting parathyroid disease while at the same time resulting in considerable diagnostic economy. An elevated iPTH was particularly helpful in distinguishing between hypercalcemia due to destruction of bone by malignancy and primary hyperparathyroidism with a coexisting malignancy. Further, measurement of parathormone was useful in evaluation of postoperative hypercalcemia.
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PMID:Serum parathormone in the identification and surgical management of hyperparathyroidism. 70 2

The authors studied the presence of visceral calcification as evidenced by the visceral uptake of bone-seeking radionuclides during the course of a bone scan among 22 patients with terminal renal failure maintained on dialysis, nine patients with hypercalcemia secondary to malignancy, and nine patients with primary hyperparathyroidism. Uptake by the lungs or stomach was observed in 11 renal failure patients (50%) and in four of those with malignancy and hypercalcemia (44%). None of the patients with primary hyperparathyroidism had evidence of visceral calcification. The serum CaXP product was significantly higher among those with visceral calcification than those without. The results of this study indicate that a CaXP product of 60 represents the saturation product of calcium phosphate in serum above which spontaneous precipitation of this salt may occur in such viscera as stomach and lungs.
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PMID:Visceral calcification and the CaXP product. 71 4

The first case of primary hyperparathyroidism associated with renal cell carcinoma, nasopharynx carcinoma and thyroid carcinoma is reported. Selective venous sampling with radioimmunoassays for parathyroid hormone was helpful in the differentiation of primary hyperparathyroidism from hypercalcemia associated with malignancy.
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PMID:Primary hyperparathyroidism with triple cancers consisting of renal cell carcinoma, nasopharynx carcinoma and thyroid carcinoma. 83 5

Acute hyperparathyroidism should be distinguished from severe hypercalcemia of malignancy. In the former condition parathyroidectomy is often of vital importance; in the latter, the malignant neoplasm should be treated surgically or with radiation or cytostatics. The differential diagnosis is sometimes difficult because some patients with acute hyperparathyroidism have coexisting carcinoma elsewhere. Two patients subjected to parathyroidectomy because of severe hypercalcemia secondary to malignant neoplasms are described and compared with twelve similar cases from the literature. In patients with severe hypercalcemia medical treatment should always be tried first. If acute hyperparathyroidism cannot be excluded, subtotal parathyroidectomy should be performed after medical preparation.
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PMID:Differentiation of acute hyperparathyroidism from severe hypercalcemia of malignancy. 84 64

Peripheral plasma prostaglandin E (PGE) determinations were performed on a series of 79 patients with solid tumor neoplasms and correlated with their serum calcium levels. Fourteen patients were hypercalcemic and 11 of these had significant elevations in circulating plasma PGE. Ten of the hypercalcemic group had extensive metastases to bone. These findings support the recently developed hypothesis that prostaglandins are causally related to the genesis of hypercalcemia in malignancy.
Cancer 1977 Apr
PMID:Plasma prostaglandins in hypercalcemic patients with neoplastic disease. 85 45

Hypercalcemia was found in 19 (28%) of 67 patients with cancer of the esophagus. There was no evidence of bone metastases in 14 (20%) of the patients with hypercalcemia. The location of the lesion (upper, middle or lower esophagus) appears to have no bearing on the clinical features in this condition and the association of hypercalcemia with esophageal malignancy, even in the absence of bone metastases, should be recognized.
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PMID:Carcinoma of the esophagus and hypercalcemia. 86 Jul


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