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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 known transitional cell carcinoma of the bladder and hypercalcemia was evaluated for urinary prostaglandin levels when no bone metastases or elevated parathormone levels could be demonstrated. Urinary levels of prostaglandin E metabolite were assessed in relation to serum and urinary calcium levels during treatment. The serum calcium levels decreased from the 13.0 mg. per cent range whenever the rpimary tumor was manipulated (transurethral resection) or when other treatments directed at the tumor were used (radiation therapy and chemotherapy). Serum and urinary calcium levels, and urinary prostaglandin E metabolite decreased when 3 gm. aspirin were given daily. These data suggest that the somewhat unusual hypercalcemia in our patient was caused by a prostaglandin-secreting transitional cell carcinoma. Prostaglandin-secreting tumors are reviewed herein.
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PMID:Prostaglandin-mediated hypercalcemia in transitional cell carcinoma of the bladder. 66 Jul 46

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.
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PMID:Role of prostaglandins in the production of hypercalcemia by tumors. 69 57

The results of morphologic studies performed in 18 patients who had total parathyroidectomy and autotransplantation of parathyroid tissue into the forearm muscle are presented. All patients had long-standing renal disease with azotemia, hyperphosphatemia and high levels of parathyroid hormone. The histologic findings after total parathyroidectomy, before gland transplantation, are important for selection of parathyroid tissue for surgery. Diffuse hyperplasia with the development of multiple nodules of the parathyroids can possibly be adverse for the transplant. In one case, nine month after autotransplantation we found a tumor in the forearm, measuring 2.0 X 3.0 X 2.2 cm in diameter. Morphologic findings in this case before implantation showed diffuse hyperplasia with adenomatous nodules but no signs of carcinoma. The grafted parathyroid tissue after excision was seen with blood vessel invasion in the normal skeletal muscle. In the case of primary renal disease with secondary parathyroid hyperplasia, the light microscopic examination revealed an autonomous tumorlike adenomatous formation in the autografted parathyroid tissue, with graft-dependent hypercalcemia. The invasive growth with some signs of neoplasia following autotransplantation raises the question of the development of certain neoplasia.
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PMID:[Morphological aspects of parathyroid gland transplantation. Contribution on the clinical relevance of induced, invasive tissue growth]. 72 Jan 63

Renal cell adenocarcinoma can be one of the great masqueraders in medicine. More common extrarenal manifestations of renal cell carcinoma include fever, anemia and gastrointestinal symptoms. Other rarer systemic symptoms are caused by amyloidosis, neuromyopathy and tumor thrombus. Humoral manifestations include polycythemia, hypercalcemia, galactorrhea and Cushing's syndrome. Metastatic disease commonly presents as the initial symptom.
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PMID:Extrarenal manifestations of renal cell carcinoma. 85 Mar 16

The VX-2 carcinoma in 32 New Zealand white rabbits was studied morphologically with respect to the osseous effects induced by the innoculation and subsequent growth of tumour in the soft tissues over periods ranging from 1 to 5 weeks. Although more severe changes were noted in bones of tumor-bearing than in non-tumor-bearing limbs, effects could be seen in both experimental situations. Severe bone marrow hyperplasia was noted consistently in tumor-bearing animals. A marked increase in numbers of osteoclasts over control rabbit bones was observed along the surface of bones near and distant from the tumor. Resorptive changes were also noted in the cortex of tumor-bearing rabbits. The increase in osteoclast numbers was related chronologically to the development of hypercalcemia and was proportional to the degree of hypercalcemia at the time the animals died. The number of osteoclasts was inversely proportional to the serum creatinine. A diminution of osteoclast numbers was noted in the latter stages of the disease. These changes may be the morphologic expression of humoral hypercalcemia accompanying the VX-2 carcinoma.
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PMID:Changes in bone and bone marrow of rabbits bearing the VX-2 carcinoma. A comparison of local and distant effects. 86 13

A 25-year-old white woman with sporadic hypophosphatemic rickets presented with a 7 year history of chronic mild hypercalcemia, osteitis fibrosa cystic and hypercalcemic nephropathy. Serum immunoreactive parathyroid hormone was elevated by greater than 100-fold and a 3.5 g parathyroid tumor was found at operation. Survey of the literature reveals that of 9 previous cases in which hypercalcemic hyperparathyroidism occurred in association with hypophosphatemic rickets, only two had classical x-linked familial hypophosphatemic rickets. It appears more than likely that this unusual combination of skeletal diseases represents the chance occurrence of primary hyperparathyroidism in patients with underlying x-linked familial hypophosphatemic rickets rather than a complication of phosphate therapy.
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PMID:Hypercalcemic hyperparathyroidism in hypophosphatemic rickets. 87 68

In rabbits bearing the prostaglandin-producing VX2 carcinoma, the plasma concentration of 13,14-dihydro-15-keto-PGE2 (PGE2-M) was elevated within one week after tumor implantation and preceded the development of hypercalcemia. Both the rate of rise and magnitude of the increase were greater for the metabolite than for PGE2; at the time of peak hyercalcemia (about 4 to 5 weeks after tumor implantation), the increase over basal in plasma PGE2-M was about 75 fold whereas it was previously shown that the increase in PGE2 was less than 2 fold. Indomethacin, which inhibits PGE2 synthesis in VX2 cells in culture, lowered in parallel plasma calcaium and PGE2-M in tumor-bearing rabbits. Administration of hydrocortisone to rabbits bearing the VX2 tumor prevented the development of hypercalcemia when given at the time of tumor implantation and reversed the elevated plasma calcium in previously untreated animals; the steroid hormone also lowered plasma concentrations of PGE2-M. These findings are consistent with our hypothesis that the hypercalcemic syndrome in VX2 tumor-bearing rabbits is due to the secretion of PGE2 by the tumor.
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PMID:Plasma concentrations of 13,14-dihydro-15-keto-prostaglandin E2 in rabbits bearing the VX2 carcinoma: effects of hydrocortisone and indomethacin. 89 22

Prostaglandin biosynthesis and metabolism were studied in the VX2 carcinoma-bearing rabbit, an animal model of prostaglandin-mediated hypercalcemia. All the identification and quantification of the prostaglandins were done by gas chromatography-mass spectrometry. The tumor incubated in vitro converted exogeneous arachidonic acid principally to PGE2. Biosynthesis from endogenous precursor lipids yields mainly PGE2 and PGF2alpha. The 100,000 x g supernatant fluid of the tumor did not contain any metabolizing enzymes. Significant hypercalcemia developed between the first and second week after tumor implantation. The levels of the major plasma metabolite of PGE2, 15-keto-13,14-dihydro-PGE2, became elevated at one week, had risen 25-fold by the end of the second week, and at the fourth week were elevated to 256 times the pre-incubation levels. The concentration of 15-keto-13,14-dihydro-PGF2alpha in plasma rose in parallell but to a lesser degree. 7alpha-hydroxy-5,11-diketotetranor-prostane-1,16-dioic acid, the major urinary metabolite of the E prostaglandins, was elevated two weeks after tumor implantation and rose until the fifth week. Indomethacin treatment lowered both serum calcium and the plasma level of 15-keto-13,14-dihydro-PGE2.
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PMID:Prostaglandin-mediated hypercalcemia in the VX2 carcinoma-bearing rabbit. 89 23


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