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

A women with hypercalcemia and a hypernephroma confined to the left kidney underwent nephrectomy and subsequent resolution of hypercalcemia. Serum parathyroid hormone was undetectable in peripheral blood as well as in the left renal vein at surgery. Parathyroid hormone was also undetectable in the tumor extract using three different antisera to parathyroid hormone. Measurement of plasma prostaglandin E and 13, 14-dihydro-15-keto-prostaglandin E2 revealed levels within the normal range. The serum 1,25-dihydroxyvitamin D concentration was below normal and nephrogenous cyclic adenosine monophosphate was markedly elevated. The humoral agent responsible for hypercalcemia in this patient was not identified. This case emphasizes the need to search for new hypercalcemic factors in patients with hypercalcemia of malignancy.
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PMID:Humoral hypercalcemia of malignancy: a syndrome in search of a hormone. 629 89

Parathyroid hormone, 1,25-dihydroxyvitamin D, and calcitonin are the three primary calcium-regulating hormones. Physiological changes in these occur throughout normal life but it is when levels remain excessively high or low, or when their target organs are diseased, that hypocalcaemia or hypercalcaemia may develop.
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PMID:Fluid and electrolyte disorders. Calcium. 654 32

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

The relationship between the concentration of phosphate in plasma and parotid saliva was studied in six conscious sheep and a goat, either intact or thyroparathyroidectomized (t.x.p.t.x.), under conditions designed to minimize marked fluctuations in flow rate of saliva. A linear relationship between acutely induced changes in plasma phosphate concentration and the phosphate level in saliva has been demonstrated in both intact and t.x.p.t.x. animals. Dietary phosphorus depletion caused adaptation of salivary phosphate concentration so that less was secreted at a given concentration of plasma phosphate. Attention is drawn to the similarity between this phenomenon and that already described for the proximal renal tubule. Parathyroid hormone (PTH) was shown to reduce the salivary phosphate concentration with little or no effect on phosphataemia. The administration of 1,25-dihydroxycholecalciferol (1,25(OH)2CC) also caused a reduction in salivary phosphate concentration despite hyperphosphataemia and hypercalcaemia. It is suggested that salivary phosphate concentration can be influenced directly by the concurrent level of plasma phosphate but that this relationship can be modified by the circulating concentration of 1,25(OH)2CC and indirectly by PTH via increased production of 1,25(OH)2CC.
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PMID:Factors affecting the secretion of phosphate in parotid saliva in the sheep and goat. 689 39

Secondary hyperparathyroidism is a universal complication of chronic renal failure. It has been proposed that the markedly elevated levels of immunoreactive parathyroid hormone (i-PTH) in uremia may represent a "uremic toxin" responsible for many of the abnormalities of the uremic state. Plasma i-PTH consists of a mixture of intact hormone, a single-chain polypeptide of 84 amino acids, and smaller molecular weight hormonal fragments from both the carboxy- and amino-terminal portion of the PTH molecule. The hormonal fragments arise from metabolism of intact PTH by peripheral organs as well as from secretion of fragments from the parathyroid glands. The structural requirements for the known biological actions of PTH reside in the amino-terminal portion of the PTH molecule. Carboxy-terminal fragments, biologically inactive at least in terms of adenylate cyclase activation, hypercalcemia, or phosphaturia, depend on the kidney for their removal from plasma, and thus accumulate in the circulation in chronic renal failure. It is unknown at the present time if other biological effects of these carboxy-terminal fragments may contribute to some of the biochemical alterations observed in uremia. The most significant consequence of increased PTH levels in uremia is the development of bone disease characterized by osteitis fibrosa. In addition, it would appear that PTH plays an important role in some of the abnormal electroencephalographic patterns observed in uremia. This may be due to a potential role of PTH in increasing calcium content of brain. Parathyroid hormone also has been implicated as a pathogenetic factor in many other alterations present in uremia, i.e., peripheral neuropathy, carbohydrate intolerance, hyperlipidemia, and other alterations. Unfortunately, outstanding clinical research is lacking in this field and conclusive experimental data are practically nonexistent. Further studies are necessary if one is to accept the concept of PTH being a significant "uremic toxin."
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PMID:Parathyroid hormone metabolism and its potential as a uremic toxin. 699 9

Twenty-one patients with severe coccidioidomycosis, including eight with osseous lesions, were admitted to the University of California, Davis, Medical Center, during a recent epidemic. Transient mild ionized hypercalcemia occurred in only two patients, and a tendency toward low normal ionized calciums was noted. Parathyroid hormone levels appeared to be appropriate for the ionized calcium in these patients. There were no significant differences in ionized calcium levels of parathyroid hormone levels among patients with and without osseous coccidioidomycosis. We conclude that hypercalcemia is rare in coccidioidomycosis, even with extensive bony involvement.
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PMID:Total ionized serum calcium and parathyroid hormone levels in patients with disseminated coccidioidomycosis. 723 97

A 70-year-old white woman had a lower abdominal mass and hypercalcemia. Physical and radiologic evidence was found for the presence of nonmetastatic pelvic tumor. Biochemical tests confirmed the presence of hypercalcemia with evidence of active bone resorption. Plasma parathyroid hormone (PTH) and the nephrogenic urinary cyclic AMP excretion were low; levels of plasma prostaglandins were elevated. Bone biopsy revealed histologic evidence of extensive osteoclastic bone resorption. At operation, a papillary serous cystadenocarcinoma of the ovary was removed. Postoperatively, the serum calcium fell to normal, and plasma prostaglandins became undetectable. Short-term incubation of ovarian tumor fragments demonstrated the production by tumor tissue of a substance causing bone resorption in an in vitro bioassay. The production of this substance was blocked by indomethacin. Radioimmunoassay of the incubation medium revealed significant amounts of prostaglandins of the E + F series. Parathyroid hormone was not detected in the medium. These data implicate tumor-produced prostaglandins as mediators of the hypercalcemia in this patient.
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PMID:Hypercalcemia with ovarian carcinoma: evidence of a pathogenetic role for prostaglandins. 727 55

Thirty-nine patients with primary hyperparathyroidism were studied four to eight years after their initial operation. In six patients, both the pathologist and surgeon agreed on the diagnosis of solitary adenoma; in 16 patients, the surgeon diagnosed solitary adenoma and the pathologist parathyroid hyperplasia (microscopic hyperplasia). In 16 patients, primary chief cell hyperplasia was agreed upon by the pathologist and surgeon. In the 16 patients with microscopic hyperplasia, there have been no long-term recurrences of hypercalcemia, but, in two patients, plasma parathyroid hormone levels are high. Parathyroid hormone--total calcium regression curves demonstrate significant preoperative correlation in solitary adenoma, p less than 0.01, and primary chief cell hyperplasia, p less than 0.05. After operation, significant correlations were not found between parathyroid hormone and total calcium. T-testing slope differences of pre- and postoperative parathyroid hormone--total calcium regression curves demonstrates a significant (p less than 0.01) shift to the right of the microscopic hyperplasia patients after operation, moving them to a broader range of total calcium per picogram parathyroid hormone. We conclude that 1) in primary hyperparathyroidism, positive regulation of total calcium by autonomously released parathyroid hormone exists in patients with solitary adenoma and chief cell hyperplasia; 2) autonomously functioning parathyroid tissue has been removed by operation for solitary adenoma with coexistent microscopic parathyroid hyperplasia. In this four- to eight-year follow-up period, it is clear that microscopic parathyroid hyperplasia is not associated with recurrent hypercalcemia. Two functionally distinct forms of parathyroid suppression are suggested; positively regulated microscopic hyperplasia and negatively regulated pathologically suppressed glands.
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PMID:Primary hyperparathyroidism: four- to eight-year postoperative follow-up demonstrating persistent functional insignificance of microscopic parathyroid hyperplasia and decreased autonomy of parathyroid hormone release. 728 4

A patient with a phaeochromocytoma associated with hypercalcemia is described. The hypercalcaemia was corrected by removal of the phaeochromocytoma. Parathyroid hormone-like peptide was isolated from the tumour suggesting that ectopic parathyroid hormone production from the phaeochromocytoma was the explanation of the hypercalcaemia.
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PMID:Hypercalcaemia and phaeochromocytoma. 731 45

Concentrations of the hormones and ions involved in calcium homeostasis were analyzed in simultaneous samples of amniotic fluid and maternal blood obtained from normal pregnant women between 14 weeks' gestation and term. Amniotic fluid total calcium, magnesium, and phosphorus levels fell progressively and markedly despite constant or only declining maternal serum levels. Ionized calcium was constant in both amniotic fluid (mean 2.22 mEq/L) and maternal serum (mean 2.33 mEq/L) throughout gestation. Parathyroid hormone levels in amniotic fluid declined after 20 weeks' gestation, despite rising maternal serum levels, consistent with suppressed fetal parathyroid activity secondary to the relative hypercalcemia of late fetal life. Calcitonin levels in both amniotic fluid and maternal serum were unchanged throughout gestation, with amniotic fluid levels being significantly lower than those in maternal serum.
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PMID:Calcium-regulating hormones and ions in amniotic fluid. 735 41


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