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 33 year old man presented with symptoms of one week's duration; he had a serum calcium of 22.5 mg/dl and a markedly hypercellular bone marrow. Despite therapy with saline diuresis, furosemide mithramycin, total parathyroidectomy and corticosteroids, symptomatic hypercalcemia was poorly controlled. Inappropriate serum parathyroid hormone (PTH) levels were found before and after parathyroidectomy whereas assays of the peripheral blood for osteoclast-activating factor and prostaglandin E (PGE2) were negative. An elevated leukocyte alkaline phosphate level, the inability to aspirate marrow, the marked generalized hyperplasia of all hematopoietic marrow elements, the focal accumulations of blastic cells and increasing reticulin fiber formation led to the diagnosis of acute myelofibrosis. A single course of cytosine arabinoside and thioguanine therapy was followed by profound hyperphosphatemia, hypocalcemia and death. The rarity of hypercalcemia with myeloproliferative disorders is documented by a review of the world literature, and the possible mechanism for hypercalcemia in this patient is discussed.
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PMID:Acute myelofibrosis and malignant hypercalcemia. 84 61

Chondrocalcinosis is known to be common in hyperparathyroidism. In order to discover the effect of parathyroidectomy on chondrocalcinosis and to investigate this association further, we studied two groups of patients. In one group were 41 postparathyroidectomy patients, and in the other 100 admissions to the acute geriatric unit. The total incidence of chondrocalcinosis in the parathyroidectomy group was 32%, and in the elderly control group 11%. There was little or no osteoarthrosis in these patients. It was found that chondrocalcinosis occurred in the normal population from the age of 75 and in the hyperparathyroid group from the age of 45. In both groups the incidence rose steadily with age. In the hyperparathyroid group alone, preoperative serum calcium levels were no different in those without chondrocalcinosis, suggesting that hypercalcaemia alone is not a sufficient stimulus for chondrocalcinosis. Those with chondrocalcinosis had higher mean preoperative alkaline phosphatase levels, nearly twice as much radiological bone disease, and were older. Parathyroidectomy had no effect on attacks of pseudogout or on preexisting cartilage calcification. A connection with high levels of circulating parathyroid hormone is suggested, and a link with physical age-related changes in cartilage postulated.
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PMID:Chondrocalcinosis in primary hyperparathyroidism. Influence of age, metabolic bone disease, and parathyroidectomy. 85 41

The relatives of 25 index patients with primary parathyroid hyperplasia were tested for hypercalcemia. At least 13 of these patients had one or more first degree relatives with hypercalcemia. Two familial syndromes each with autosomal dominant transmission were recognized. Two index patients were part of large kindreds categorized as having familial hypocalciuric hypercalcemia (FHH). Manifestations of multiple endocrine neoplasia type I were present in the kindreds of at least four other index patients (FMEN I). In seven other kindreds there were too few affected members to allow definitive classification. Differences between manifestations of FHH and FMEN I were described. Among offspring of affected persons in kindreds with FHH, as distinct from FMEN I, the prevalence of hypercalcemia approached the theoretic maximum of 50 per cent during the first two decades. In FHH, nephrolithiasis and peptic disease were unusual; moderate hypercalcemia occurred without hypercalciuria; and subtotal parathyroidectomy did not abolish hypercalcemia. Concentrations of peptide hormones other than parathyroid hormone (PTH) were normal in those with FHH; in FMEN I high concentrations of glucagon in plasma were found in five of six patients tested, and high concentrations of gastrin were found in three of 12 patients. Hypergastrinemia generally accompanied obvious peptic disease. Distinction of the two conditions is important since patients with FHH may not benefit from subtotal parathyroidectomy, but they generally have a better clinical prognosis than do patients with FMEN I.
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PMID:Family studies in patients with primary parathyroid hyperplasia. 87 Nov 27

A 25-year-old white woman with sporadic hypophosphatemic rickets presented with a 7 year history of chronic mild hypercalcemia, osteitis fibrosa cystic and hypercalcemic nephropathy. Serum immunoreactive parathyroid hormone was elevated by greater than 100-fold and a 3.5 g parathyroid tumor was found at operation. Survey of the literature reveals that of 9 previous cases in which hypercalcemic hyperparathyroidism occurred in association with hypophosphatemic rickets, only two had classical x-linked familial hypophosphatemic rickets. It appears more than likely that this unusual combination of skeletal diseases represents the chance occurrence of primary hyperparathyroidism in patients with underlying x-linked familial hypophosphatemic rickets rather than a complication of phosphate therapy.
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PMID:Hypercalcemic hyperparathyroidism in hypophosphatemic rickets. 87 68

The effects of small oral doses (1-2 microgram/day) of 1alpha-hydroxycholecalciferol, given for 1 to 2 years, have been examined in four nondialysed adolescents with chronic renal failure and bone disease. Treatment increased calcium retention and plasma calcium, and decreased plasma levels of alkaline phosphatase, hydroxyproline, and immunoreactive parathyroid hormone. X-ray abnormalities of bone regressed, and 2 patients underwent successful surgical correction of knock-knees; bone histology in these 2 was normal at the time of operation. 2 patients developed hypercalcaemia which promptly reversed when 1alpha-hydroxycholecalciferol was withdrawn. In one patient treatment was initially successful, but later there was biochemical, radiographic, and histological evidence of relapse. Long-term treatment of such patients with 1alpha-hydroxycholecalciferol may be effective and facilitate the surgical correction of deformities, but this is not invariable. Toxic effects are similar to those of vitamin D itself, but are more readily reversible.
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PMID:Renal osteodystrophy in nondialysed adolescents. Long-term treatment with 1alpha-hydroxycholecalciferol. 87 33

Serial measurements of serum calcium and immunoreactive parathyroid hormone (PTH) were performed in two young patients with hypercalcemia of immobilization. Serum PTH was elevated in both patients. With mobilization, both serum PTH and serum calcium returned to normal levels and remained so during six months of follow-up. The hyperparathyroidism of immobilization is an unexplained, reversible disorder that should be treated by medical measures and aggresive attempts at early mobilization.
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PMID:Parathyroid hormone and the hypercalcemia of immobilization. 90 94

Fourteen patients with renal osteodystrophy were treated for at least one year with 1-alpha-hydroxycholecalciferol (1-alpha-OHD3) in a dose varying from 1 microgram/week to 3 microgram/day. Plasma calcium and inorganic phosphorus concentrations increased significantly. The plasma alkaline phosphatase concentration fell in 11 of the 12 patients in whom it was initially raised and returned to normal in seven. Serum parathyroid hormone concentrations were initially raised in all patients, but they decreased significantly with treatment and became normal in eight patients within one year. The 10 patients with radiological abnormalities showed some improvement. Hypercalcaemia occurred in 11 patients, and necessitated a reduction in the dose of 1-alpha-OHD3 in some. 1-alpha-OHD3 was effective in reducing the biochemical and radiological abnormalities of renal osteodystrophy, but it should be used wtih care, and plasma calcium concentrations should be monitored.
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PMID:1-alpha-hydroxycholecalciferol for renal osteodystrophy. 91 69

The syndrome of hypercalcemia in patients with renal cell carcinoma without metastasis to bone, in association with elevated levels of immunoreactive prostaglandin E and normal parathyroid hormone levels, prompted the investigation of an etiologic relationship of increased prostaglandin in this syndrome. Ethyl acetate extracts of tissue culture effluents, primary and metastatic renal cell carcinoma, and plasma were chromatographed on silicic acid columns and assayed by double antibody immunoprecipitative methods for immunoprecipitative methods for immunoreactive prostaglandins A and E. Increased levels of immunoreactive prostaglandins A and E were found 1) to be generated in parallel with cell growth during a period of time by renal cell carcinoma in monolayer growth, 2) in extracts of primary and metastatic renal cell carcinoma tissue and 3) in the venous effluent of a kidney bearing a renal cell carcinoma. These findings support the hypothesis that renal cell carcinoma can produce prostaglandins. Furthermore, reported syndromes of patients with renal cell carcinoma associated with elevated prostaglandin levels may result from the autonomous production of prostaglandins in vivo by the tumor.
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PMID:Prostaglandin: increased production by renal cell carcinoma. 91 87

Hypocalcemia is a frequent accompaniment of acute renal failure, but paradoxically hypercalcemia also has been described in association with acute renal failure. In this paper we describe two patients who provide some insights into both the potential clinical importance and mechanism of the hypercalcemia associated with acute renal failure. The clinical significance is emphasized by the presence of diffuse metastatic calcification observed at postmortem examination in one patient. In both patients the increase in serum calcium concentration was not coincident with a decrease in serum phosphorus concentration; when measured in one patient, serum levels of parathyroid hormone were undetectable. These findings, along with the consistent association with rhabdomyolosis, support the proposal that the hypercalcemia of acute renal failure is caused by dissolution of dystrophic calcifications in traumatized muscle and may lead to severe metastatic calcifications.
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PMID:Hypercalcemia of acute renal failure. Clinical significance and pathogenesis. 93 62

Described here is a patient with esophageal carcinoma who had hypercalcemia, an elevated serum level of parathyroid hormone and normal parathyroid glands. A review of the literature reveals that a total of 25 other patients with ectopic hyperparathyroidism in esophageal malignancy have been described, four of whom had documented elevations of serum parathyroid hormone levels. Esophageal neoplasms should be added to the list of tumors associated with ectopic secretion of parathyroid hormone.
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PMID:Ectopic hyperparathyroidism (pseudohyperparathyroidism) in esophageal malignancy. Report of a case and a review of the literature. 93 65


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