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)

The therapeutic armamentarium in the treatment of cancer is now expanded to include surgery, radiotherapy, chemotherapy and immunotherapy. The aim is to achieve cure where possible. For some cancers the concept of cure can be questioned, and for many patients, cancer must be regarded as a chronic disease. A vigorous approach to palliation, particularly in regard to special problems such as hypercalcaemia, yields good dividends. Human values remain of paramount importance, and active antitumour treatment with attendant side effects must not be continued where there is no expectation of worthwhile response.
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PMID:The current approach to cancer treatment. 7 59

Hypercalcaemia is often associated with malignant disease. Causes of elevated serum-calcium levels in the absence of bony metastases include parathyroid-hormone production by the tumour, osteolytic factors made by the tumour, and coexistent primary hyperparathyroidism. By measuring nephrogenous cyclic-A.M.P. excretion to assess parathyroid-hormone function, we have determined the mechanism of such hypercalcaemia in 15 patients. Nephrogenous cyclic A.M.P. ranges from 0.05 to 2.40 mumol/g of creatinine in normal subjects, from 2.27 to 8.45 mumol/g in patients with primary hyperparathyroidism, and from 0.50 to 1.30 mumol/g in patients with proven non-hyperparathyroid hypercalcaemia without malignancy. 9 patients (60%) with hypercalcaemia and malignancy had normal levels of nephrogenous cyclic A.M.P. (range 0.35-2.07 mumol/g creatinine). The other 6 (40%) had elevated nephrogenous cyclic A.M.P. (range 2.70-5.55 mumol/g) consistent with increased parathyroid-hormone secretion. Surgical exploration of the neck in these patients showed that the increased parathyroid-hormone secretion was secondary to primary hyperparathyroidism, not ectopic hyperparathyroidism. Thus, the data indicate that coexistent hyperparathyroidism may be common in patients with hypercalcaemia and malignancy and that the measurement of nephrogenous cyclic A.M.P. is very useful in identifying patients at risk for hyperparathyroidism.
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PMID:Primary hyperparathyroidism in paraneoplastic hypercalcaemia. 7 31

A specific receptor for 1,25-dihydroxyvitamin D has been demonstrated in a cultured human breast cancer cell line. This is the first such demonstration in any cancer cell. It may explain the high incidence of metastatic bone destruction and hypercalcaemia in this common malignancy, and the limited success of other steroid-receptor assays in predicting the response of breast cancer to therapy.
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PMID:1,25-dihydroxyvitamin-D-receptor in breast cancer cells. 9 76

A patient with metastatic islet cell carcinoma of the pancreas, recurrent peptic ulcer disease, and hypergastrinemia (Zollinger-Ellison syndrome) developed symptomatic hypercalcemia and renal insufficiency; she was treated with streptozotocin after parathyroidectomy failed to control her hypercalcemia. Shortly after somewhat less than the usual recommended dose of streptozotocin was administered, the serum calcium concentration fell to near normal with complete resolution of symptoms. Seven months after therapy, mild hypocalcemia, consistent with her degree of renal impairment was noted. However, mild hypercalcemia recurred 13 months after therapy. Shortly after streptozotocin therapy, the mean serum gastrin concentration fell to near normal with radiographic disappearance of the anastomotic ulcer. At 7 and 13 months after therapy, serum gastrin levels were normal. Streptozotocin therapy was accomplished without major complications; specifically, without a detrimental effect on the creatinine clearance. Thus, although hypercalcemia in patients with pancreatic islet cell tumors is often due to associated primary hyperparathyroidism, in some patients it may be due to secretion of a hypercalcemic substance from the tumor and may respond to streptozotocin. Similarly, hypergastrinemia in patients with islet cell tumors may also respond to streptozotocin.
Cancer 1976 Dec
PMID:Pancreatic islet cell carcinoma with hypercalcemia and hypergastrinemia: response to streptozotocin. 13 70

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.
Cancer Treat Rep 1978 Oct
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.
Cancer 1975 Sep
PMID:Hypercalcemia in small cell (oat cell) carcinoma of the lung. Coincident parathyroid adenoma in one case. 17 Oct 50

Measurement of total urine cyclic 3':5'-adenosine monophosphate (cyclic AMP) only incompletely discriminates between normal, hyperparathyroid, and nonparathyroid hypercalcemic patients. Only a fraction of total urine cyclic AMP is contributed by parathyroid hormone (PTH) action on the proximal nephron (renal cyclic AMP); the remainder is derived from plasma by glomerular filtration. We dtermined total urine and plasma cyclic AMP and PTH (by carboxy-terminal specific radioimmunoassay) in control, hyperparathyroid, nonparathyroid hypercalcemic, and surgically hypoparathyroid patients. Renal cyclic AMP was calculated as total urine cyclic AMP minus the filtered component. Of these determinations, only renal cyclic AMP segregated normal from hyperparathyroid, and hyperparathyroid from nonparathyroid hypercalcemic patients with complete accuracy. These data suggest that measurement of renal cyclic AMP provides an accurate index of parathyroid activity and allows clinical discrimination and appropriate treatment of the sub-groups of patients with malignancy and nonparathyroid hypercalcemia from those with hyperparathyroidism.
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PMID:Renal cyclic adenosine monophosphate: an accurate index of parathyroid function. 18 64

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.
Cancer 1976 Nov
PMID:Calcium metabolism in cancer. Studies using calcium isotopes and immunoassays for parathyroid hormone and calcitonin. 18 80

Evidence has been presented for prostaglandin-mediated hypercalcemia and bone resorption in malignancies of both, experimental animals and man. Occurence of hypercalcemia in cancer patients is known for a long time, but its pathogenesis has been poorly understood so far. Besides ectopic parathyroid hormone secretion by tumors, an osteoclast-activating factor released from leukocytes and direct bone destruction by tumor cells, prostaglandins of the E series have to be considered as one of the candicates involved in the pathomechanism of hypercalcemia and osteoclastic osteolysis in cancer patients. This new concept on the pathophysiology of cancer-associated hypercalcemia has implications for the diagnosis and management of this common complication of neoplastic disease.
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PMID:Prostaglandin-mediated hypercalcemia: a paraneoplastic syndrome. 20 5

Metastatic soft tissue calcification is known to occur in hypercalcemia and is usually present in the kidneys, stomach and lungs. 1--3 This case presents two unusual features: 1) ectopic parathormone production in association with poorly differentiated lymphocytic lymphoma; and and 2) uptake of 99mTc-pyrophosphate in the liver in the absence of demonstrable abnormality at autopsy. The more usual sites of metastatic calcification also showed uptake of the radionuclide. We will discuss metastatic soft tissue calcification, ectopic parathyroid hormone production, hypercalcemia in malignancy and bone scan agent localization in soft tissues.
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PMID:Poorly differentiated lymphocytic lymphoma with ectopic parathormone production: visulization of metastatic calcification by bone scan. 21 69


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