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

A series of 38 cases of primary hyperparathyroidism seen at a single hospital within a four a half year period is reported. The importance of hypercalcemia in the diagnosis of this syndrome and its screening in cases of arterial hypertension, gout, osteoporosis, and families with type I multiple endocrine neoplasia are underlined. The patients in the present series had a florid clinical history with a mean duration of 14 years. Main symptoms were urolithiasis (52%), arterial hypertension (28.9%), bone involvement and pain (23.7%), and peptic ulcer (18.4%). There were a high proportion of patients with hyperuricemia (26.3%), some with classical symptoms of gout. One patient presented simultaneous pituitary and pancreatic involvement. Surgical therapy was undertaken in 25 patients, of whom 24 (96%) were cured, one of them after reoperation. There were no cases of relapse, hypoparathyroidism, or postoperative death. Surgery is the only rational and definitive form of treatment of hyperparathyroidism; both experienced surgeons and pathologists are necessary to deal with the anatomic and histologic subtleties of this interesting endocrine disorder.
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PMID:[Comments on a series of 38 cases of primary hyperparathyroidism (author's transl)]. 724 69

Two women ahd acromegaly due to a pituitary adenoma associated with phaeochromocytoma. Eight additional patients with this combination of tumours have been described by others. Our first patient had sustained hypertension, mild hypercalcaemia, and elevated basal levels of parathyroid hormone and calcitonin associated with malignant phaeochromocytoma and parathyroid hyperplasia. The second patient had episodic hypertension and normal basal serum calcium, parathyroid hormone, and calcitonin levels with a benign cystic phaeochromocytoma. Four of the ten patients died from causes related to the phaeochromocytoma. Three patients had parathyroid hyperplasia. A separate group of four patients with phaeochromocytoma and pituitary adenoma without acromegaly has also been reported. These fourteen patients probably represent a non-familial variant of the multiple endocrine neoplasia syndrome. Our findings suggest that acromegalic patients with hypertension should be screened for phaeochromocytoma.
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PMID:Acromegaly and pituitary adenoma with phaeochromocytoma: a variant of multiple endocrine neoplasia. 729 6

The clinical spectrum of 100 consecutive cases of surgically proved primary hyperparathyroidism treated from 1974 through 1978 was analyzed. Their laboratory test results were compared with 64 cases of other form of hypercalcemia using multivariate discriminant analysis. The clinical spectrum has dramatically shifted during the past three decades from renal calculi and bone disease to the asymptomatic patient discovered by routine serum chemical analysis. Hypertension was twice as common among hyperparathyroid patients as in the general population but failed to improve in 92% after parathyroidectomy. The most useful discriminant laboratory test in descending order of value were the serum chloride, serum calcium, hematocrit, serum phosphorus, and parathormone. Multivariate discriminant analysis of the serum calcium, phosphorus, chloride, and Hct provided a 98% degree of accuracy in separating hyperparathyroidism from other forms of hypercalcemia.
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PMID:Primary hyperparathyroidism. Changing clinical spectrum, prevalence of hypertension, and discriminant analysis of laboratory tests. 731 24

Rhabdomyolysis occurred in 25 of 1,000 patients (2.5%) with phencyclidine (PCP) intoxication. 10 of these 25 patients (40%) developed acute renal failure and another 7 had mild impairment in renal function. Marked hyperuricemia was present in all 17 patients, and marked hyperphosphatemia and hypocalcemia were noted in the 10 patients with acute renal failure; 3 of the latter developed hypercalcemia during the diuretic phase of the illness. Fever, tachycardia and hypertension were frequent findings among the 25 patients with rhabdomyolysis and all had leukocytosis. The data show that rhabdomyolysis with and without acute renal failure is not infrequent among abusers of PCP.
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PMID:Rhabdomyolysis with and without acute renal failure in patients with phencyclidine intoxication. 734 47

Hyperparathyroidism and hyperaldosteronism coexisted in association with medullary sponge kidneys in a 27-year-old woman with severe hypertension. A modest fall in systolic and diastolic pressure followed removal of a parathyroid adenoma. Blood pressure was controlled with spironolactone therapy and restored to normal after removal of an aldosterone-secreting adrenal tumor. Elevated levels of aldosterone may have been responsible for the severe hypertension, while hypercalcemia may have had a synergistic effect on the arteriolar response to circulating vasoactive peptides.
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PMID:Hyperaldosteronism, hyperparathyroidism, medullary sponge kidneys, and hypertension. 741 8

Forty-two patients with sarcoidosis were studied with special attention to renal disease and disturbance of calcium metabolism. Abnormal calcium metabolism was found in 19 patients and prednisone corrected hypercalcaemia in those affected within two weeks, except in one patient who had concomitant primary hyperparathyroidism. Renal failure was found in 19 patients, 15 of whom had hypercalcaemia. Prednisone had a beneficial effect on kidney function within four weeks in all patients except in one with co-existing glomerulonephritis. Arterial hypertension was found in six patients, proteinuria in six, and calcinosis in six. Among 14 patients who underwent renal biopsy, granulomas were found in five. In only one of these was granulomatosis extensive bringing out renal failure and death within two years after temporary remission with prednisone. Co-existent non-sarcoid diseases affecting the kidneys or calcium metabolism occurred in ten out of 23 patients with sarcoidosis and kidney disease/calcium abnormality. In most cases these conditions contributed more to the prognosis than did sarcoidosis. From the present series and review of the literature it appears that young males within the first two years of diagnosis are at the greatest risk of hypercalcaemia or kidney disease.
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PMID:Renal manifestations and abnormal calcium metabolism in sarcoidosis. 746 60

The pathogenesis of acute pancreatitis is poorly understood, despite well-recognised precipitating factors. Current evidence suggests that the earliest abnormalities of acute pancreatitis arise within acinar cells, but the key intracellular trigger has yet to be identified. Within the pancreas, physiological concentrations of secretagogues bind to G-protein-linked cell-surface receptors on acinar cells, evoking short, oscillatory spikes of acinar cytosolic-free ionised calcium ([Ca2+]i), an ubiquitous intracellular messenger. Specific effects within acinar cells include initiation of enzyme release through the phosphorylation cascades of stimulus-secretion coupling. Low resting levels of [Ca2+]i are restored by Ca(2+)-ATPase, which pumps calcium into the endoplasmic reticulum and out of the cell. If high concentrations of [Ca2+]i persist, toxicity results, intracellular signalling is disrupted, and cell damage occurs. Sustained elevations in acinar [Ca2+]i result from exposure to high concentrations of secretagogues, high doses of which also induce acute pancreatitis. Similarly, sustained elevations of [Ca2+]i may result from ductal hypertension, alcohol, hypoxia, hypercalcaemia, hyperlipidaemia, viral infection, and various drugs--all factors known to precipitate acute pancreatitis. We suggest that these factors precipitate acute pancreatitis by causing either excessive release of acinar [Ca2+]i, or damage to the integrity of mechanisms that restore low resting levels of [Ca2+]i, and that the consequent calcium toxicity is the key trigger in the pathogenesis of acute pancreatitis.
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PMID:Is an elevated concentration of acinar cytosolic free ionised calcium the trigger for acute pancreatitis? 747 53

This article begins with a discussion on changes in the maternal calcium-parathyroid axis in response to pregnancy, followed by calcium disorders that can take place during pregnancy. Hypercalcemia and its subsequent disorders, including hyperparathyroidism, hypocalciuric hypercalcemia, and thyroid disease, are reviewed. Also, hypocalcemia and its subsequent disorders, including hypoparathyroidism, vitamin D deficiency, and hypomagnesemia, are addressed. Concluding the article are discussions on bone status and osteoporosis, calcium metabolism in pregnancy-induced hypertension and preeclampsia, and nephrolithiasis in pregnancy.
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PMID:Calcium disorders of pregnancy. 778 23

In the period 1981-1993, 102 patients underwent surgery for primary hyperparathyroidism (HP). Parathyroid adenoma was found in 81, carcinoma in 4 and hyperplasia in 17 patients. HP was usually diagnosed late with marked skeletal or renal damage, psychiatric symptoms and hypertension. Following the first operation in our institution hypercalcemia was successfully reduced in 100 of 102 patients, in two hypercalcemia persisted after the operation and both were reoperated. Postoperative hypocalcemic syndrome (transitory hypoparathyroidism) due to advanced stage of HP and enormous calcium deficit in bones, occurred in 47% of patients (most frequently with skeletal and hypercalcemic form of the disease).
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PMID:[Results of surgical treatment of primary hyperparathyroidism]. 778 88

Paraneoplastic manifestations are signs and symptoms observed in patients with cancer, distant from the tumour or its metastases and not caused by invasion, obstruction or bulk mass. In children with cancer, paraneoplastic manifestations are rare and distinct from those observed in adults. Knowledge about paraneoplastic manifestations can be of great clinical importance because they may be the presenting sign of a tumour or its recurrence and hence facilitate early diagnosis. In contrast, they sometimes mask the symptoms of a tumour and cause diagnostic delay. In this review, paraneoplastic manifestations in children are described, including hypercalcaemia, Cushing syndrome, precocious puberty, opsoclonus/myoclonus, acquired von Willebrand disease, watery diarrhoea syndrome, and hypertension. The mechanisms causing these manifestations are also discussed.
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PMID:Paraneoplastic manifestations in children. 784 90


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