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

Vitamin D intoxication was induced in chicks by treatment with large amounts of radioactive cholecalciferol (vitamin D3) either by s.c. injections or by stomach tube. Hypercalcemia and nephrocalcinosis were present, confirming toxicity. The distribution of cholecalciferol and its metabolites in the tissues of the intoxicated birds was compared with that in birds that were treated with physiological amounts of radioactive cholecalciferol. Treatment with pharmacological doses resulted in marked elevation of cholecalciferol and its metabolites in all tissues examined, including elevation of 1 alpha,25-dihydroxycholecalciferol in the intestine. The predominant form of cholecalciferol in these birds was found to be the unchanged vitamin, whereas in birds treated with physiological doses 25-hydroxycholecalciferol was the predominant metabolite. The route of vitamin administration was found to be of importance only when pharmacological doses were given: generally, higher levels were noted when administered via s.c. injections than via stomach tube, except in the arteries. It is suggested that in vitamin D intoxication, the factor responsible for the pathological changes in soft tissues is cholecalciferol itself. High levels of 1 alpha,25-dihydroxycholecalciferol may be responsible for the hypercalcemia.
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PMID:Metabolism of cholecalciferol in vitamin D intoxicated chicks. 628 28

Renal impairment in sarcoidosis is usually due to hypercalcaemia and nephrocalcinosis but can also be caused by granulomatous nephritis or interstitial nephritis without sarcoid granulomata. A variety of types of glomerulonephritis have also been described in sarcoidosis but these rarely cause impaired renal function. Renal failure as an isolated manifestation of sarcoidosis is uncommon. A 66-year-old woman presented with a 1-year history of lethargy, polyuria and nocturia. Clinical examination was unremarkable and she had impaired renal function (urea 18 mmol/l (108 mg%) and creatinine 380 mumol/l (4.3 mg%)). As her kidneys were normal in size, she underwent renal biopsy, which revealed granulomatous interstitial nephritis. Reevaluation showed no other evidence of sarcoidosis and she had impaired urinary acidification and concentrating capacities. Therapy with corticosteroids produced a marked improvement in symptoms and renal function. This case confirms the view that granulomatous sarcoid nephritis is steroid sensitive and that full recovery can be expected provided interstitial fibrosis and scarring do not occur.
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PMID:Reversible renal failure due to isolated renal sarcoidosis. 646 14

A 49-year-old woman at recent climacterium was admitted to our hospital for a dyspeptic-type symptomatology, weight loss, bone pain, moderate polyuric-polydipsic syndrome and in a marked astheno-depressive state. Paraclinical explorations revealed constant hypercalcemia with hypophosphoremia, calciuria, chronic renal failure in the polyuric phase with retention of nitric bases. X-ray films showed diffuse osteoporosis, right nephrocalcinosis and diffuse calcifications of the galactophorous ducts in both breasts. Computerized tomography revealed and surgery confirmed the presence of tumoral tissues on the anterior aspect of the trachea. Histopathologic examination revealed a parathyroid adenoma.
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PMID:Primary hyperparathyroidism associated with galactophorous ducts calcification. 649 88

A patient with end-stage renal disease and hypercalcemia was referred for a radionuclide bone imaging study. Deposition of Tc-99m hydroxymethylenediphosphonate was apparent in the lungs and myocardium as well as in the skeleton. Renal uptake was also noted, despite anuria. Computed tomography demonstrated nephrocalcinosis but no myocardial calcification. The cause of myocardial uptake of tracer is unknown. Amyloidosis is suggested as a possibility but is not validated in this case.
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PMID:Myocardial uptake of a bone tracer associated with hypercalcemia. 650 34

Bilateral dense rings in the renal medulla were found on noncontrasted computed tomography in a patient with marked hypercalcemia and suspected primary hyperparathyroidism. The rings were not present on plain radiographs and were obscured on contrasted scans, and may represent occult nephrocalcinosis. Associated findings--renal insufficiency induced by hypercalcemia and interstitial nephritis--may be reversible with early recognition of this CT finding.
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PMID:Renal medullary "rings": possible CT manifestation of hypercalcemia. 670 30

Renal and systemic magnesium metabolism has not been adequately characterized in states of prolonged PTH excess in humans. Whereas acute experimental PTH administration uniformly results in enhanced renal magnesium reabsorption in many species, including humans, numerous clinical reports have documented renal magnesium wasting in human primary hyperparathyroidism. The possibility has been raised, therefore, that secondary consequences of sustained hyperparathyroidism (eg, hypercalcemia, nephrocalcinosis) might override the direct renal effects of PTH. Accordingly, the present studies assessed the effects of chronic (12 days) continuous intravenous (IV) b-(1-34)-PTH infusion in four normal human subjects on plasma, urinary, and intestinal magnesium and calcium homeostasis under metabolic balance conditions. Chronic PTH infusion resulted in a steady-state of hypercalcemia, hypercalciuria, and persistent negative calcium balance, which returned to baseline values in a recovery period. In contrast to plasma calcium concentration, plasma magnesium concentration was not altered by PTH infusion. Significant hypermagnesuria was observed during the period of PTH administration (control, 8.21 +/- 0.43 mEq/24 hours; PTH days 7-12, 10.75 +/- 0.74 mEq/24 hours, P less than 0.05) resulting in an initial, but transient, negative magnesium balance. During days 7-12 of PTH administration, net intestinal magnesium absorption increased sufficiently to result in a return to control magnesium balance. These findings suggest that hypermagnesuria associated with clinical primary hyperparathyroidism results from either direct or indirect effects of PTH excess, per se, and does not require the long-term consequences or complications of the clinical disorder (eg, nephrocalcinosis, renal insufficiency, acidosis).
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PMID:Renal and systemic magnesium metabolism during chronic continuous PTH infusion in normal subjects. 673 67

A case of metastatic ameloblastoma of the maxilla with secondary hypercalcemia in a 54-year-old man is presented. After treatment with surgery, chemotherapy, and radiotherapy, the patient was found to have multiple metastases and severe hypercalcemia associated with high levels of parathormone-like substance in the peripheral blood. At autopsy he was found to have widespread metastases and nephrocalcinosis.
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PMID:Ameloblastoma of the maxilla with distant metastases and hypercalcemia. 722 20

Sarcoidosis may involve the kidneys in several ways. Most commonly, aberrations of calcium metabolism, including hypercalcemia, hypercalciuria, and nephrocalcinosis, are responsible for the renal manifestations of sarcoidosis. Granulomatous infiltration of the renal interstitium may also produce severe derangements of renal function. Glomerulonephritis can occur with sarcoidosis, although the pathogenesis remains unclear. Besides renal insufficiency and frank renal failure, nephrotic syndrome, nephrolithiasis, hypertension, and a variety of tubular defects may complicate sarcoidosis. The sensitivity of "sarcoid nephropathy" to corticosteroids usually warrants therapeutic trial.
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PMID:Renal manifestations of sarcoidosis. 722 44

Of 570 patients operated on for hyperparathyroidism, 18 subsequently died (between one day and 12 yr after operation). Pathological findings at necropsy in these patients have been reviewed. Four necropsies on patients with untreated hyperparathyroidism have also been reviewed for comparison. Of these 22 cases, 14 had renal failure at the time of death. This was attributed to the following: nephrocalcinosis 6; chronic glomerulonephritis 4; analgesic nephropathy 1; cystinuria 1; sarcoidosis 1; and polycystic disease 1. Of those with renal failure due to nephrocalcinosis, three had persistent hypercalcaemia after operation; the other three survived only for a short time. There was no evidence of residual nephrocalcinosis producing progressive renal failure if the plasma calcium concentration was corrected. In those with chronic glomerulonephritis, cystinuria, and polycystic disease, the hyperparathyroidism was considered to be tertiary to the renal disease but renal failure was not always present at the time of diagnosis.
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PMID:Progressive renal failure in surgically treated hyperparathyroidism. 726 1

Primary hyperparathyroidism is a common entity that routinely lends itself to prompt surgical cure. Infrequently, multiple surgical explorations are required to effect a cure. A case is reported of a 27-year-old man with hypercalcemia and nephrocalcinosis. The initial surgical exploration failed to identify the abnormal parathyroid tissue. Hypercalcemia necessitated rigorous antihypercalcemic therapy; three subsequent operations, including a mediastinal exploration, were unsuccessful. On the fifth exploration, which took barely an hour, a 35-g adenoma was removed from the left superior posterior mediastinum. This report illustrates that a detailed knowledge of the possible locations of aberrant parathyroid tissue and the skills of the operating surgeon are the sine qua non for those patients requiring one or more parathyroid reexplorations.
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PMID:Management of acute hyperparathyroidism in a community hospital. 726 28


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