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)

Serum calcium (s-Ca) was measured in 245 patients with bronchial carcinoma. Mean s-Ca (+/- SD) was 2.52 +/- 0.14 mmol/l in the cancer patients, compared to 2.48 +/- 0.14 mmol/l in a control group (p less than 0.01). Sixty-one (25%) of the patients with bronchial carcinoma had hypercalcaemia (s-Ca greater than or equal to 2.60 mmol/l), compared to 16% of the controls. Squamous cell carcinoma was the histological type most often associated with hypercalcaemia. Patients with hypercalcaemia were not overrepresented among those with bone metastases. During follow-up another 32 patients developed hypercalcaemia. Altogether 93 patients (38%) became hypercalcaemic at some time in the course of the disease. In 20 patients s-Ca fell below 2.60 mmol/l after radiotherapy, after operation, or spontaneously. The survival time was significantly shorter for patients with s-Ca above 2.68 mmol/l on admission than for those with s-Ca below this value.
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PMID:Serum calcium in bronchial carcinoma: a population-based study. 381 68

Primary squamous cell carcinoma of the thyroid is an extremely rare, aggressive neoplasm with a uniformly poor prognosis. Described herein is a case of a 66-year-old man with primary squamous cell carcinoma of the thyroid associated with hypercalcemia (13 mg/dL [3.24 mmol/L]) and unexplained leukocytosis (28,400/mm3 [28.4 X 10(9)/L]). The histogenesis of squamous cell carcinoma of the thyroid remains controversial. The associated hypercalcemia and leukocytosis most likely represent a form of paraneoplastic syndrome; possible mechanisms will be discussed in the light of recent studies on tumor-derived mediators.
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PMID:Primary squamous cell carcinoma of the thyroid associated with leukocytosis and hypercalcemia. 382 45

We have purified peptides with PTH-like bioactivity from a rat Leydig cell tumor (H-500) and a human squamous cell carcinoma, both associated with a syndrome of humor-induced hypercalcemia. Tumor extracts were shown to be active in an in vitro renal cytochemical bioassay and in an in vitro osteosarcoma cell (UMR 108) adenylate cyclase assay; activity in both assays could be reduced by the PTH antagonist [norleucine-8,18,tyrosine-34]bovine PTH-(3-34)-amide. Partially purified extracts of both tumors and of rat tumor-conditioned culture medium were active in vivo in thyroparathyroidectomized rats in preventing hypocalcemia and increasing fractional phosphorus excretion and cAMP excretion. Ion exchange chromatography demonstrated that active peptides were basic in character. Employing reverse phase HPLC and gel permeation HPLC, active peptides of approximately 9,000 and 9,500 daltons were purified from extracts of the human and rat tumors, respectively, which had similar but not identical compositions. Two additional bioactive peptides were detected in rat tumor extract, and the more active had a mol wt of approximately 28,000. The results demonstrate that peptides that mimic PTH in a variety of in vivo and in vitro bioassays can be extracted from malignancies associated with hypercalcemia, that multiple molecular species may be detected in tumors that demonstrate PTH-like activity, and that at least one of these peptides may be similar in two tumors of highly divergent cell and species origin.
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PMID:Purification of peptides with parathyroid hormone-like bioactivity from human and rat malignancies associated with hypercalcemia. 394 72

A case of hypercalcemia associated with documented squamous cell carcinoma of the renal pelvis without bone metastasis is reported. High levels of cross-reacting parathyroid hormone-like material in serum and its presence in tumoral tissue were detected. To our knowledge this is the fourth case described in the literature and the first in which tumoral production of parathyroid hormone-like material is demonstrated.
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PMID:Squamous cell carcinoma of the renal pelvis associated with hypercalcemia and the presence of parathyroid hormone-like substances in the tumor. 399 1

A case of a patient with burn scar carcinoma of an extremity associated with hypercalcemia and without bone metastasis is presented. From the data presented, it seems reasonable to assume that this squamous cell carcinoma of a burn scar secreted some type of parathyroid hormone-like substance or substances which posessed calcium-increasing biological activity resulting in hypercalcemia.
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PMID:Burn scar carcinoma and hypercalcemia. 483 62

Hypercalcaemia due to malignant disease, in the absence of bone metastases, is generally regarded as a rare event. It occurred in 16% of a series of cases of bronchial carcinoma coming to necropsy. Hypercalcaemia is a relatively common complication of bronchial carcinoma. The hypercalcaemia is usually accompanied by hypophosphataemia and, in this respect, must be distinguished from the hypercalcaemia that may be found with breast carcinoma. It is frequently accompanied by hypokalaemic alkalosis; this must not be confused with the metabolic disorder that results from the production of ectopic ;ACTH'. The bones sometimes show changes of osteitis fibrosa akin to those seen in hyperparathyroidism. Cystic disease of bone recognizable radiologically is rare, probably because of the relatively short duration of the metabolic disturbance. The parathyroids are usually mildly atrophic. There is no evidence that the main pathogenetic mechanism is stimulation of the parathyroids by the tumour. Acceptable instances of parathyroid hyperplasia are very rare: the significance of these exceptional cases awaits further study.Squamous carcinoma of the bronchus is the type mainly incriminated. Oat-cell carcinoma and bronchial adenocarcinoma are involved less frequently than expected by chance. The significance of the tumour types implicated is discussed in relation to the possible pathogenesis.
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PMID:Bronchial carcinoma and hypercalcaemia. 536 47

Mithramycin given as a single dose for the treatment of hypercalcemia has not been reported to cause renal dysfunction. A case is presented of nephrotoxicity following a single 25 micrograms/kg dose in a patient with underlying squamous cell carcinoma, obstructive uropathy, and hypercalcemia. Underlying renal impairment may magnify the nephrotoxicity of mithramycin.
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PMID:Nephrotoxicity following single dose mithramycin therapy. 622 49

Tumor tissue from a patient with squamous cell carcinoma of the lung and hypercalcemia has been serially implanted into athymic mice. Tumor-bearing mice develop cachexia, hypercalcemia without bone metastases, hypophosphatemia, increased urinary cyclic adenosine monophosphate (cAMP) to creatinine ratio, and undetectable human immunoreactive parathyroid hormone levels. Radiographs of spines in the tumor-bearing mice demonstrate demineralization, suggesting skeletal resorption as the source of the hypercalcemia. Within 4-8 hours following tumor removal, hypercalcemia is reversed, suggesting that a relatively short-acting humoral substance is responsible for the hypercalcemia. The animals gain weight and become essentially normal within 4 days following tumor removal. The studies demonstrate that this animal model is similar in many aspects to human malignancy-associated humoral hypercalcemia (MAHH) and can provide a useful tool for further investigation of the pathogenesis and treatment of this syndrome.
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PMID:A model for malignancy-associated humoral hypercalcemia. 644 30

Hypercalcemia is a well-recognized phenomenon in squamous cell carcinoma of the head and neck, but the incidence of hypercalcemia in this group of patients is not clear. We have reviewed the records of 166 patients with squamous cell carcinoma of the head and neck presented at the Boston VA Medical Center over a 2-year period (October 1981 to September 1983). Hypercalcemia (greater than 11 mg/dl), for which a benign etiology could not be identified, occurred in the clinical course of seven patients (4.2%). Of the hypercalcemic patients, 5/7 (71.4%) had advanced stage IV disease and serum calcium levels ranging from 11.2 to 15 mg/dl at presentation. The incidence of hypercalcemia in this stage IV group was 5/78 (6.4%). On the basis of concomitant serum alkaline phosphatase, x-ray films, and radionuclide bone scans in these patients, bone metastases or a humoral factor were felt to be the etiologic agent. Six of the seven patients died within 77 days of the onset of the hypercalcemia despite vigorous antihypercalcemic and chemotherapeutic measures, and the remaining patient is under chemotherapy at present. We conclude that hypercalcemia is a late manifestation of advanced squamous cell carcinoma of the head and neck and is an ominous prognostic sign. Hypercalcemia without bone metastases is presumably due to the production of ectopic parathormone (PTH)-like substances from the tumor. To control this hypercalcemia, the underlying tumor must be treated vigorously in conjunction with symptomatic treatment.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The incidence of hypercalcemia in squamous cell carcinoma of the head and neck. 651 40

Two human malignant tumors, which we previously reported to produce colony-stimulating factors (CSFs), were found to be accompanied by remarkable hypercalcemia. A patient with a CSF-producing lower jaw cancer (squamous cell carcinoma) developed a marked granulocytosis (150,000/microliters) and hypercalcemia (more than 215 mg/dl). The tumor was successfully transplanted into nude mice, which developed marked granulocytosis (300,000/microliters) and hypercalcemia (20 mg/dl). White blood cell and serum calcium concentrations of these mice decreased promptly to normal levels when the tumor was excised. Treatment with prednisolone (1.5 mg/kg) or indomethacin (5 mg/kg) had no effect on the serum calcium level of these mice. Parathyroid hormone or prostaglandin E was not increased in the serum of the mice or in the tumor tissue. However, the mice bearing the tumor excreted extremely large amounts of calcium in their urine, and their bony tissues contained less calcium and phosphorus than controls. Moreover, histology of bony tissues of these nude mice clearly demonstrated the decrease in trabecular tissues and cortical thickness as well as remarkable activation of osteoclasts. Another patient with a CSF-producing bronchogenic squamous cell carcinoma showed mild granulocytosis and hypercalcemia. The biopsied tumor tissue was transplanted into nude mice, which developed marked granulocytosis (300,000/microliters) and also severe hypercalcemia (18 mg/dl). These results suggest the presence of a new syndrome of granulocytosis and hypercalcemia associated with CSF-producing tumors. The causal mechanism of the hypercalcemia was shown to be some humoral factor which activates osteoclasts other than parathyroid hormone. Neither prostaglandins nor osteoclast-activating factor seemed to be the cause of the hypercalcemia.
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PMID:Association of hypercalcemia with tumors producing colony-stimulating factor(s). 660 Sep 66


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