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)

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

We previously reported that pharmacologic doses of 1,25 dihydroxyvitamin D3 (1,25(OH)2D3) given for 2-3 days, inhibited osteoblastic collagen synthesis in young rats. In this study, we tested the effects of 5, 25, and 125 ng of 1,25(OH)2D3 injected subcutaneously into 6-week-old rats for 12 or 18 days. In rats given 125 ng, cortical bone of distal half femurs exhibited decreased calcium (Ca) content but dry weight and hydroxyproline (Hyp) content were no different from control. Trabecular bone Ca was not different from control but dry weight and Hyp were increased. When cortical and trabecular bone were combined, there was a decrease in Ca, an increase in Hyp, and a 50% decrease in Ca:Hyp. Fluorescent labels given after 8 days of treatment were either diffuse or absent in calcified sections from rats given 125 ng, indicating impaired mineralization. The 25 and 125 ng doses produced hypercalcemia with normal serum phosphate. There was a dose-related increase in serum immunoreactive bone gla protein (BGP) and serum 1,25(OH)2D3 and a decrease in serum 25(OH)D3. At the 5 ng dose, no adverse effects were seen on body growth. With 25 ng and 125 ng, growth was inhibited. Increased serum urea nitrogen and histologic evidence of nephrocalcinosis occurred at the 125 ng dose. When 125 ng was given for 12 days and then withdrawn for 6 days, systemic toxicity decreased and bone Hyp and Ca increased so that Ca:Hyp remained low and comparable to that of rats treated with 1,25(OH)2D3 continuously.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Stimulation of undermineralized matrix formation by 1,25 dihydroxyvitamin D3 in long bones of rats. 308 98

The hypothesis that chronic metabolic acidosis encountered in some patients with primary hyperparathyroidism is due to inhibition of proximal HCO3 reabsorption has recently been challenged. Indeed, this action of parathyroid hormone (PTH) has only been observed in acute studies, whereas in animal models of chronic hyperparathyroidism a metabolic alkalosis has been induced, probably owing to the release of alkaline salts from bone tissue, and to the stimulation of tubular acid secretion by hypercalcaemia. Studies were, therefore, performed to determine the effect of PTH on the renal handling of HCO3 in an animal model in which changes in plasma calcium and phosphate, and nephrocalcinosis, all known to affect tubular acidification, did not occur. Thyroparathyroidectomized (TPTX) rats were infused with synthetic bovine hormone fragment bPTH 1-34 via Alzet minipumps at the rate of 0.7 U h-1 to simulate normal endogenous production of PTH (group I) and at the three-fold higher rate of 2.1 U h-1 (group II). In order to prevent changes in serum calcium and phosphate, and nephrocalcinosis, animals of group II were fed a Ca- and P-free diet prior to TPTX (compared with a regular diet for group I) and both groups were treated with dichloromethylene-diphosphonate (Cl2MDP, 10 mg kg-1 day-1) and a Ca-free diet during PTH infusion. During the course of PTH infusion both groups of animals had stable and normal levels of plasma calcium and phosphate.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Parathyroid hormone directly inhibits tubular reabsorption of bicarbonate in normocalcaemic rats with chronic hyperparathyroidism. 312 45

Peptides containing residues 1-34 of the human parathyroid hormone (PTH)-like hypercalcemic factor (hHCF), termed hHCF-(1-34)-NH2, produce effects similar to those of PTH in several biological systems in vitro and in vivo. However, there is conflicting evidence regarding the potency of hHCF on bone and, by implication, its role in calcium mobilization and the skeletal contribution to tumor-associated hypercalcemia. To resolve this conflict, the effects of infusing either hHCF-(1-34)-NH2 or a peptide containing residues 1-34 of bovine PTH [bPTH-(1-34)] into unrestrained thyroparathyroidectomized rats on a low calcium diet were compared. Direct effects on bone histology and serum calcium levels, which are totally dependent on calcium mobilization from bone in these animals, were examined. bPTH-(1-34) and hHCF-(1-34)-NH2 were equipotent in producing dose-dependent calcium mobilization from bone. At an infusion rate of 0.1 nmol/hr, both peptides produced hypercalcemia and extensive nephrocalcinosis. Histomorphometric analysis of tibiae from these animals after 48 hr of peptide infusion showed a dose-related increase in osteoclast number from 3-5 cells per mm2 at 0.01 nmol/hr to approximately equal to 32 cells per mm2 at 0.1 nmol/hr of hHCF or bovine PTH. These findings indicate that hHCF has a direct PTH-like effect on bone and, in this model system, the hHCF-(1-34)-NH2 is equipotent to bPTH-(1-34).
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PMID:Direct action of the parathyroid hormone-like human hypercalcemic factor on bone. 339 7

Of 123 patients with sarcoidosis observed from 1971 to 1986, 4 had histologically proven renal involvement. Hypercalcemia was present in all of these 4 patients, hypercreatinemia in 3 and urolithiasis in one. Histologically renal interstitial nephritis or fibrosis was found in all 4 cases, and 3 cases showed sarcoid-like renale granulomas. In addition, nephrocalcinosis or mesangioproliferative glomerulonephritis was present in one patient each. Corticosteroid therapy corrected hypercalcemia in 3 patients and improved renal function in the patient with glomerulonephritis and in the case with interstitial fibrosis. One patient died of granulomatous myocarditis, renal insufficiency having been unaffected by corticosteroids.
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PMID:[Sarcoidosis of the kidney]. 343 93

The factors responsible for the frequent occurrence of hypertension in patients with primary hyperparathyroidism have not been elucidated. Suggested mediators have included hypercalcemia, renal insufficiency, and increased plasma renin activity. However, experimental results have not been reported in any species that test the hypothesis that sustained hypertension in this clinical syndrome is due to consequences of parathyroid hormone (PTH) excess versus unrelated factors (e.g., primary hypersecretion of other hormones, NaCl sensitivity, genetic factors). Moreover, no systematic evaluation of the renin or adrenal cortical responses to chronic PTH excess has been reported in any species. Accordingly, the present studies assessed the effects of chronic (12 days) continuous intravenous b-(1-34) PTH infusion in normal human subjects (n = 4). PTH infusion resulted in persistent hypercalcemia and hypertension, reversible during a 4-8-day recovery period. Transient but significant increases in urinary tetrahydroaldosterone excretion and plasma cortisol concentration were observed as hypercalcemia and hypertension developed. No significant changes in plasma potassium concentration or plasma renin activity were observed, suggesting that hypercalcemia-induced transient hypersecretion of ACTH was responsible for both cortisol and aldosterone responses. The present results suggest that hypertension associated with clinical primary hyperparathyroidism results from either direct or indirect effects of PTH excess, per se, and requires neither the long-term consequences/complications of the clinical disorder (e.g., severe nephrocalcinosis, renal insufficiency) nor primary hypersecretion of additional hormones. These results are consistent with the hypothesis that hypercalcemia alone or in combination with at least permissive levels of PTH can generate short-term, but persistent (12 days) hypertension in human subjects and thus may be the initiating mechanism for hypertension in clinical primary hyperparathyroidism.
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PMID:Chronic continuous PTH infusion results in hypertension in normal subjects. 354 30

The metabolic manifestations and operative findings in 10 patients with a diagnosis of parathyroid carcinoma were analyzed to determine whether they differ from those in patients with parathyroid adenomas and similar degrees of hypercalcemia. Two groups of patients with parathyroid adenomas were used for comparison. Group A consisted of eight patients with "atypical" benign adenomas (mean preoperative level of serum calcium: 13.4 mg/dl); group B consisted of 13 patients with benign typical adenomas--all with preoperative serum calcium levels greater than or equal to 13.0 mg/dl (mean: 14.2 mg/dl). The patients with carcinoma (mean preoperative level of serum calcium: 15.3 mg/dl) had a frequency of osteoporosis and osteitis fibrosa cystica (50%) comparable with that of group A (33%) and group B (62%). Seventy percent of the patients with carcinoma had renal disease (nephrolithiasis, nephrocalcinosis, or impaired renal function), whereas only 38% of group A and 15% of group B had similar disorders. The patients with carcinomas had the highest frequency of combined bone and renal disease (50% versus 14% in group A and 15% in group B). Anemia, peptic ulcer disease, and hypertension occurred with similar frequencies in the three groups. Three patients with recurrent parathyroid carcinoma died of profound hypercalcemia, renal failure, or cardiac arrhythmia. In general, although patients with parathyroid carcinomas have more profound metabolic abnormalities than do patients with primary hyperparathyroidism, the metabolic manifestations in patients with parathyroid carcinoma are comparable with those in patients with parathyroid adenomas and profound hypercalcemia. Furthermore atypical adenomas share many anatomic and histopathologic features with parathyroid carcinomas, and distinguishing between the two is sometimes possible only in cases of tumor recurrence.
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PMID:Parathyroid carcinoma versus parathyroid adenoma in patients with profound hypercalcemia. 358 61

An experimental model of hyperparathyroidism was developed in the rat to simulate primary hyperparathyroidism in humans. In this model thyroparathyroidectomized (TPTX) or parathyroidectomized (PTX) animals were infused for 6 days with an amount of bovine synthetic parathyroid hormone (PTH)-(1-34) fragment to restore plasma calcium levels to normal (0.7 U X h-1) or with PTH at twofold (1.4 U X h-1) or threefold (2.1 U X h-1) this basal level. Animals infused with 2.1 U X h-1 of bovine PTH-(1-34) exhibited hypercalcemia, hypophosphatemia, a reduction in theoretical renal threshold for phosphate and an increase in 1,25-dihydroxyvitamin D plasma levels that were approximately threefold the control value. In addition, these animals demonstrated nephrocalcinosis and changes of bone histology that were typical of the findings in patients with primary hyperparathyroidism. In contrast, in animals infused at 1.4 U X h-1, plasma calcium, phosphate, and theoretical renal threshold for phosphate remained within normal limits, but plasma 1,25-dihydroxyvitamin D was increased above control, suggesting that increased activity of 1 alpha-hydroxylase may be the most sensitive index of increased PTH levels. This animal model permits sustained elevation of PTH plasma levels at basal or pathologically elevated levels and should provide an effective means by which to evaluate the consequences of chronic hyperparathyroidism on epithelial function, bone, and other organ systems.
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PMID:Animal model of primary hyperparathyroidism. 359 40

Renal impairment in sarcoidosis is unusual: cases with granulomatous interstitial nephritis (GIN) and without associated glomerular disease, nephrocalcinosis and hypercalcemia have rarely been described. We report 2 such cases, one of whom is the first patient documented as surviving following presentation in dialysis dependent renal failure. Review of the literature revealed a further 20 patients. Of the 22 patients, including our own, 3 failed to respond to treatment, all dying in acute renal failure. Relapse occurred in 4, in association with rapid reduction or early cessation of treatment. No relapse was reported later than 9 months after starting treatment with corticosteroid. The majority of patients (15/19) who responded to treatment had residual renal impairment after up to 30 months of steroid treatment.
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PMID:Renal impairment in sarcoidosis: granulomatous nephritis as an isolated cause (two case reports and review of the literature). 380 88

Acute primary hyperparathyroidism is an unusual form of primary hyperparathyroidism characterized by life-threatening hypercalcemia. Forty-three cases reported in the literature since 1974 are reviewed, along with five new cases. The average age of the patients was 55 (27 to 82), with an even distribution between men and women. Marked hypercalcemia (17.5 +/- 2.1 mg/dl) was accompanied by parathyroid hormone levels 20 times normal. Virtually all patients had symptoms. Hyperparathyroid bone disease occurred in 53 percent of patients; even more (69 percent) had nephrolithiasis or nephrocalcinosis. Combined renal and skeletal involvement was seen in 50 percent. Only three deaths were recorded. The pathophysiology of the acute hyperparathyroid state is unknown but appears to consist of uncontrolled parathyroid hormone secretion followed by cycles of hypercalcemia, polyuria, dehydration, reduced renal function, and worsening hypercalcemia. These features of acute primary hyperparathyroidism are compared with the features reported in the literature antedating multichannel screening, and with the features of the common form of primary hyperparathyroidism. Clinical guidelines by which the diagnosis may be suspected are also reviewed.
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PMID:Acute primary hyperparathyroidism. 381 20


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