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Query: UMLS:C0020437 (hypercalcemia)
 10,293 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To provide further understanding of humoral hypercalcemia in Hodgkin's disease (HD) the authors describe the clinical features and laboratory investigation of three patients recently treated at Massachusetts General Hospital. All were middle-aged men who presented with symptomatic hypercalcemia which led to a diagnosis of bulky intraabdominal HD. None had evidence of bone involvement or hyperparathyroidism. In the two cases tested 1,25(OH)2D3 was elevated at the time of diagnosis. These characteristics are remarkably similar to those of ten patients with HD and probable humoral hypercalcemia described in the literature. The diagnosis of HD was supported in Cases 1 and 3 by genomic blot analysis which showed no evidence of T-cell or B-cell tumor origin. In an in vitro assay, primary tumor medium from Case 1 stimulated dose-dependent bone resorption which was not entirely ascribable to 1,25(OH)2D3. The authors conclude that humoral hypercalcemia in HD predominantly affects males of middle age, that intraabdominal bulky disease is common, and that hypercalcemia appears to be mediated by tumor related production of 1,25(OH)2D3 in concert with a second factor.
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PMID:Humoral hypercalcemia in Hodgkin's disease. Clinical and laboratory evaluation. 253 88

The adult T cell leukemia (ATL) is a T cell neoplasm etiologically associated with human T lymphotropic virus type I (HTLV-I) infection. ATL cells often abnormally express interleukin 2 (IL-2) receptors, and ATL patients may show clinical evidence of hypercalcemia, osteolytic bone lesions, or increased bone turnover. Whereas interleukin 1 (IL-1) is not generally recognized as a product of T cells, this cytokine is capable of both altering IL-2 receptor expression and activating osteoclasts. Thus, we investigated the possibility that primary ATL leukemic T cells and HTLV-I-infected long-term ATL cell lines produce IL-1. S1 nuclease protection assays demonstrated that primary leukemic ATL cells from five out of six patients, as well as one patient with T4+ chronic lymphocytic leukemia, contained considerable quantities of IL-1 beta messenger RNA (mRNA) and small amounts of IL-1 alpha mRNA. These primary leukemic T cells also released biologically active IL-1 protein as evaluated in the murine thymocyte comitogenesis bioassay. In contrast to primary tumor cells, four out of six long-term ATL cell lines produced variable amounts of IL-1 alpha mRNA in the absence of detectable IL-1 beta mRNA as measured by S1 nuclease protection. These data demonstrate that IL-1 gene (especially IL-1 beta) expression occurs in many primary HTLV-I-infected leukemic T cells raising the possibility that this mediator may play a role in the pathological changes associated with this leukemia. Also, these studies show that the pattern of IL-1 alpha and IL-1 beta gene expression differs between primary ATL tumor cells and long-term cultured ATL cell lines, indicating an interesting biological difference in these two HTLV-I-infected cell populations.
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PMID:Interleukin 1 gene expression in adult T cell leukemia. 288 87

When grown as sc tumors in the nude (nu/nu) mouse, cells of the established human renal carcinoma cell line 786-0 produce hypercalcemia; this has an apparent humoral basis because it is reversed by resection of the primary tumor. We have investigated the pathogenesis of hypercalcemia in this model. Tumor-bearing mice were hypercalcemic (13.4 +/- 0.9 vs. 9.52 +/- 0.13 mg/dl in control mice) and hypophosphatemic (10.0 +/- 0.8 vs. 13.8 +/- 1.5 mg/dl in control mice; all values are mean +/- SEM). The serum concentration of 1,25-dihydroxyvitamin D was increased in tumor-bearing animals (70.0 +/- 9.3 vs. 43.8 +/- 4.8 pg/ml in control animals). Urinary excretion of cAMP was similar in control (33.7 +/- 1.4 nmol/mg creatinine) and tumor-bearing mice (38.2 +/- 4.7 nmol/mg creatinine). However, in the latter, the acute response of urinary cAMP to PTH was blunted. Although intestinal calcium transport in everted duodenal sacs in vitro was increased in tumor-bearing mice, hypercalcemia was unaffected by feeding the animals for 8 days a diet containing less than 0.02% calcium. Hence, absorption of dietary calcium did not play a significant role in maintenance of hypercalcemia. In hypercalcemic animals, the calcium content of the humerus was decreased (2.95 +/- 0.08 vs. 3.29 +/- 0.13 mg in controls; P less than 0.05). Quantitative histomorphometric analysis of the distal femoral metaphysis disclosed a significant reduction in trabecular bone volume in tumor-bearing mice (12.0 +/- 1.1% vs. 16.1 +/- 1.1% in controls; P less than 0.02). A strong trend for increased osteoclast surface and number was observed, suggesting that bone resorption was increased. Osteoblast surface and number were also somewhat increased, as was the rate of mineral apposition (2.55 +/- 0.14 vs. 1.91 +/- 0.04 micron/day in controls; P less than 0.01). Thus, the decrease in trabecular bone volume was associated with high turnover of bone, with an apparent net increase in bone resorption. We conclude that hypercalcemia in the nude mouse bearing human renal carcinoma cells is associated with increased bone resorption, high bone turnover, hypophosphatemia, and increased serum levels of 1,25-dihydroxyvitamin D.
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PMID:Pathogenesis of hypercalcemia in nude mice bearing a human renal carcinoma. 301 91

A case of malignant ameloblastoma with hypercalcemia in a 67-year-old Japanese woman is presented. The tumor of the maxilla was removed and diagnosed as a follicular ameloblastoma. The tumor recurred in the lower orbita-zygoma region, and multiple tumors of the lungs and hypercalcemia were detected eight months after the second operation. The recurrent tumor resembled the primary tumor but was less well differentiated. Autopsy revealed widespread lung metastasis of the malignant ameloblastoma, nephrocalcinosis, and sigmoid colon cancer. Histologic examination showed the metastatic ameloblastoma to be composed of nests and strands of basaloid and spindle-shaped cells surrounded by columnar cells arranged in palisade formation, with focal areas of squamous differentiation and occasional cystic degeneration. Only two cases of malignant ameloblastoma with hypercalcemia have previously been reported. This is the first case of malignant ameloblastoma with hypercalcemia and sigmoid colon cancer. In addition, prostaglandin E2 assay revealed that ameloblastoma produces prostaglandin E2, which results in hypercalcemia.
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PMID:Malignant ameloblastoma with pulmonary metastasis and hypercalcemia. Report of an autopsy case and review of the literature. 305 19

The success of cancer therapy depends on the destruction of all viable cancer cells in the primary site, as well as in metastatic areas. Surgery alone can do little for the patient whose tumor has produced distant involvement except in those situations where surgical excision, radiotherapy, chemotherapy, or immunotherapy can be relied on to eradicate metastatic disease. Because of the paucity of systemic therapy for renal cell carcinoma, an aggressive surgical approach to the primary tumor is justifiable when all metastatic lesions can be excised or otherwise definitively treated and in experimental protocols in which adjuvant therapy of possible benefit can be combined with palliative nephrectomy. There is no evidence, however, in reported studies to suggest that routine palliative nephrectomy in patients who will not be offered adjuvant systemic therapy or radiation is beneficial. Such practice is also associated with a higher incidence of complications and mortality than is expected for resection of localized renal cell carcinoma. For these reasons, it is reasonable to recommend adjunctive nephrectomy only in certain selected instances, which include (1) the control of a patient's current symptoms related to the primary disease, for example, flank pain, hematuria, fever and toxicity, anemia, erythrocytosis, and hypercalcemia; (2) nephrectomy with the excision of a solitary metastasis; and (3) the patient who is willing to undergo experimental therapy, part of which involves removal of the primary tumor.
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PMID:The failure of infarction and/or nephrectomy in stage IV renal cell cancer to influence survival or metastatic regression. 331 66

Hypercalcemia is associated with a few primary malignant neoplasms and with a variety of tumors that have spread by metastases. Hyperparathyroidism is a diagnosis that is usually not considered in these patients. At our institution, 18 patients with malignant tumors presented over a 6-year period with hypercalcemia caused by hyperparathyroidism. There were five men and 13 women with a mean age of 48 years (range 24-87 years). Primary tumors in these patients included colon carcinoma (four cases), breast carcinoma (four cases), lymphoma (four cases), thyroid carcinoma (four cases), Paget's disease (one case), and lung carcinoma (one case). Metastases of the primary tumor occurred in seven patients, and in 11 patients the tumor was not metastatic or recurrent. Serum levels of calcium, phosphate, and chloride averaged 11.8 mg/dl, and 100 mEq/liter, respectively. C-terminal parathyroid hormone (PTH) levels ranged from 300 to 1,900 pg/ml with an average of 1,150 pg/ml (normal 50-340 pg/ml). At operation, a single parathyroid adenoma was discovered in 15 patients, and four-gland hyperplasia was noted in three patients. In all cases, serum levels of calcium returned to normal after operation. We conclude that patients with malignant tumors and concomitant hypercalcemia should be evaluated for the possibility of hyperparathyroidism. In cases of primary hyperparathyroidism, elevated C-terminal PTH level should be diagnostic. If hyperparathyroidism is determined to be the cause of hypercalcemia, neck exploration and parathyroidectomy are indicated.
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PMID:Malignancy and concomitant primary hyperparathyroidism. 333 14

A patient with gastric carcinoma exhibited an excessive granulocytosis (58,000/microliter) preoperatively, in the absence of overt infection. After resection of the primary tumor, the peripheral leukocyte count decreased promptly to the normal value. In a search for a colony-stimulating factor (CSF), the tumor was transplanted into nude mice. A marked neutrophilia was observed in the tumor-bearing mice, suggesting the production of CSF by the tumor. Media conditioned by the primary culture of the tumor cells revealed the presence of CSF activity as well. CSF-producing carcinomas have been detected in various organs; nevertheless, no cases of gastric carcinoma have hitherto been described. It is of particular interest that in this patient hypercalcemia was not observed, although it often accompanied CSF-producing tumors reported previously. Therefore, it is suggested that this tumor secreted pure CSF and that the CSF produced by the tumor did not necessarily induce hypercalcemia.
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PMID:A case of gastric carcinoma associated with excessive granulocytosis. Production of a colony-stimulating factor by the tumor. 387 82

During a 14-year period, carcinoma of the anal sac apocrine glands was found in 52 pastel and 8 sapphire mink (Mustela vison) kept for studies on slow viral diseases. The pastel mink varied in age from 72 to 135 months (mean age 108 months), the sapphire mink from 63 to 100 months (mean age 81 months). All but one pastel mink were females. The primary tumor varied in size from masses that caused bulges in the perineum to those that were found only after microscopic examination of the anal sac glands. Although the primary tumor grew mainly by expansion with little local infiltration, 41 of the 60 tumors had metastasized to the regional lymph nodes and sometimes also to more distant sites. The striking propensity of the carcinoma to metastasize while still small, even microscopic, often resulted in massive secondary growths, notably in the iliac lymph nodes. Hypercalcemia did not accompany the carcinoma. Its varied microscopic appearance included solid, glandular, squamous cell, and spindle or round cell components. Combinations of them formed mixed or complex histologic patterns, no doubt largely attributable to neoplastic proliferation of myoepithelial cells and squamous metaplasia of the apocrine gland epithelium. Although its cause remains obscure, the carcinoma appeared to arise from small foci of hyperplastic apocrine glands, sometimes in relation to both anal sacs. The tumor is a common and distinctive expression of neoplasia in older ranch mink.
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PMID:Carcinoma of the anal sac glands in ranch mink. 400 34

We report a case of symptomatic hypocalcemia with a calcitonin-producing tumor. This case is unusual for two reasons. First, the primary tumor was a hepatocellular carcinoma that was producing large amounts of calcitonin. To our knowledge, well-defined cases of calcitonin-secreting hepatoma have not been previously reported. Second, the patient's hypercalcemia was shown to be secondary to hypomagnesemic inhibition of parathyroid function and not related to hypercalcitonemia.
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PMID:Hypocalcemia associated with a calcitonin-producing hepatocellular carcinoma. 626 11

We treated a case of hypercalcemia and primary liver tumor and reviewed a series of such cases treated at the Mayo Clinic (Rochester, Minn). Primary tumor of the liver was diagnosed in 192 patients (152 had hepatocellular carcinomas; 40, cholangiocarcinomas) between 1969 and 1980. Hypercalcemia of unknown cause was found in eight patients with hepatocellular carcinoma (5.3%) and seven with cholangiocarcinoma (17.5%). Five hypercalcemic patients had serum immunoreactive parathyroid hormone values consistent with ectopic hyperparathyroidism. An additional five patients had high serum calcium, low phosphate, and low chloride concentrations that met Lafferty's criteria for pseudohyperparathyroidism. Our results suggest that hypercalcemia associated with primary hepatic tumors is relatively common, and incidences vary according to the type of primary tumor. Hypercalcemia may be controlled when surgical excision of the primary tumor is possible.
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PMID:Hypercalcemia and primary hepatic tumors. 628 74


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