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

A case is presented of nephrolithiasis in a patient with no other symptoms than the urological ones and in which considerable hypercalcemia led to a study being carried out on his phospho-calcium metabolism and the diagnosis reached was primary hyperparathyroidism caused by a parathyroid adenoma. Surgical treatment was performed on the lithiasis and the adenoma as a result of which the symptoms completely disappeared and the biochemical readings returned to normal.
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PMID:[Parathyroid adenoma and renal lithiasis. Report of a case]. 52 57

The leading symptom in patients with primary hyperparathyroidism (pHPT) is renal lithiasis and not osteopathy. The most abundant circulating forms of parathyroid hormone in pHPT represent COOH-terminal fragments with molecular weights ranging from 4000 to 7000. Radioimmunnoassays making use of antibodies directed to CCOH-terminal parts of human parathyroid hormone are therefore suitable in distinguishing patients with pHPT from control subjects and patients with hypercalcemia unrelated to hyperfunctioning parathyroid glands.
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PMID:[Diagnosis of primary hyperparathyroidism and differential diagnosis of hypercalcemia]. 53 70

In order to investigate the frequency of fasting hypergastrinaemia in primary hyperparathyroidism (A) and in chronic hypercalcaemia (B), in 40 and 16 patients respectively gastrin, parathyroid hormone (PTH) and serum calcium levels were measured and compared with those of a control group (40 subjects) with similar distribution of sex and age. Moreover, possible linear relationships between these parameters were investigated. Notwithstanding significant differences in calcium and PTH levels between the three groups (A: high PTH, high Ca++; B: low PTH, high Ca++; C: normal PTH and Ca++ levels), no significant difference in gastrin levels were found. However, in the first group, a marked increase of gastrin was observed in one patient, very probably affected by a gastrin-secreting tumor (positive secretin test). While no linear relationship between PTH and gastrin values was present in all the three groups, a significant correlation between serum calcium and fasting gastrin was detectable in the group A, ruling-out the above mentioned patient. Present data suggest that PTH does not modify gastrin levels and that chronic moderate hypercalcaemia does not raise serum fasting gastrin, at least in clinical conditions. Moreover, the frequency of hypergastrinaemia in hyperparathyroidism is very low and it seems to be present only in patients with gastrin-secreting tumors.
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PMID:Fasting serum gastrin in primary hyperparathyroidism and in chronic hypercalcemia. 54 29

Hypercalcaemia would seem to be rare during immobilisation, whilst osteoporosis and hypercalciuria are constant. In fact, it often goes unnoticed. The case presented here confirms its predominance in the adolescent male. The reason for immobilisation seems to be irrelevant. The clinical symptoms are very variable: polydipsia, nausea, headache, apathy, anorexia. Blood calcium levels are raised, up to 14 mg%. This hypercalcaemia is due to very marked bone loss in adolescents, secondary to hyper-resorption and a temporary stoppage in osseous formation. The differential diagnosis from primary hyperparathyroidism is sometimes difficult but is aided by laboratory and histological findings. The essential is to consider the possibility of immobilisation hypercalcaemia in the presence of any suggestive symptoms in an immobilised adolescent. Treatment includes a return to weight bearing, adequate water intake and the administration of phosphorus, calcitonin, furosemide, and corticosteroids.
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PMID:[Immobilisation hypercalcaemia (author's transl)]. 59 68

The surgical management of primary hyperparathyroidism with severe bone disease (and tertiary hyperparathyroidism) has frequently been complicated by severe and prolonged post-operative hypocalcaemia. In seven such cases a short-pre-operative course of 1alpha-hydroxyvitamin D3 has been found to abolish these adverse features virtually completely and even to diminish pre-operative symptoms where present. Exacerbation of hypercalcaemia has not occurred and this regimen is thus recommended as a routine measure.
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PMID:1alpha-hydroxyvitamin D3 in primary hyperparathyroidism. 60 19

The results of radio-immunoassay of parathormone in peripheral venous blood (using an anti-serum preferentially recognising fragments from the carboxyl-terminal pole) were compared with those of blood calcium measured on the same day in 33 cases of primary hyperparathyroidism. In the 28 patients with hypercalcaemia, PTH was invariably high (27 cases) or at the upper limit of normal (1 case). In the 5 patients with normal blood calcium levels, it was normal in 3 cases. It is thus important to take blood calcium levels into account in the interpretation of PTH estimation, that latter being more valid during a hypercalcaemic phase.
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PMID:[The relationship between parathormone and calcium blood levels in primary hyperparathyroidism. Diagnostic value (authors transl)]. 60 36

Neonatal hyperparathyroidism usually presents as a "failure to thrive" syndrome. It may be transmitted as an autosomal dominant trait and may involve more than one offspring. We report on two brothers with neonatal primary hyperparathyroidism. One underwent a total parathyroidectomy and has lived for 14 years. Hyperparathyroidism was found in their father, suggesting autosomal dominant inheritance. The disease is fatal unless recognized early and treated. The characteristic pathological change is chief cell hyperplasia of the parathyroid glands. Near-total parathyroidectomy is the minimal operation required to control the hypercalcemia. Permanent hypoparathyroidism may be the sequel of appropriate surgical management. Treatment of the totally parathyroidectomized infant, however, is possible and can result in normal growth and development.
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PMID:Hereditary neonatal hyperparathyroidism. 61 57

Scintiscanning to detect the uptake of bone-seeking radioactive isotopes by soft tissue is a promising technique for the in vivo study of visceral calcification. Visceral uptake of such radioisotopes was studied in 40 patients: 22 undergoing long-term dialysis, 9 with malignant disease and hypercalcemia and 9 with primary hyperparathyroidism and hypercalcemia.Fifteen patients, 11 undergoing dialysis and 4 with malignant disease, had radioisotope uptake in the lungs, and 5, 3 undergoing dialysis and 2 with malignant disease, had uptake in the stomach. None of the patients with primary hyperparathyroidism had visceral uptake, nor did the patients with uptake have radiologic evidence of pulmonary or gastric calcification. The dialysis patients with visceral uptake had a mean calcium x phosphate product of 84.3 +/- 23.7 (standard deviation), which was significantly greater (P < 0.001) than that of patients without such uptake (59.2 +/- 14.0). Similarly, in patients with malignant disease and visceral uptake the Ca x P product was 72.2 +/- 6.4 - significantly greater (P < 0.005) than that of patients without such uptake (49.3 +/- 6.7).These findings indicate that scintiscanning for the visceral uptake of a bone-seeking radioisotope is a simple and effective technique for the in vivo study of visceral calcification. An elevation in the Ca x P product seems to be the single most important factor in the production of visceral calcification.
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PMID:Detection and pathogenesis of visceral calcification in dialysis patients and patients with malignant disease. 62 Mar 83

Our results with radioimmunoassay studies for parathyroid hormone performed during the last 6 years are compared retrospectively to results of the laboratory tests customarily secured when hyperparathyroidism is suspected. The results obtained in patients with known primary hyperparathyroidism and in patients with unconfirmed but presumptive hyperparathyroidism are compared to the results obtained from a group of normal controls. Despite the fact that certain discrepant results were noted in the earlier assay techniques the over-all results and, in particular, those of more recent years have been highly sensitive and reproducible corroboratives of the existence of primary hyperparathyroidism. About two-thirds of the patients with primary hyperparathyroidism will present to the urologist. All patients with calcium-containing stones should have at least 3 determinations of the serum calcium in screening for primary hyperparathyroidism. The radioimmunoassay for parathyroid hormone provides the most reliable confirmation. The patient with calculous disease, elevation of the immunoreactive parathyroid hormone level and hypercalcemia is virtually certain to have primary hyperparathyroidism.
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PMID:Experience with the radioimmunoassay for parathyroid hormone in the diagnosis of primary hyperparathyroidism. 63 70

The influence of hypercalcemia on renal function was studied retrospectively in 13 patients suffering from primary hyperparathyroidism, sarcoidosis, vitamin D intoxication, malignant lymphoma or chronic lymphatic leucemia. Different kinds of treatment, depending upon the primary disease, often induced a rapid fall in the serum calcium concentration. The serum creatinine concentration always fell simultaneously. The serum phosphate concentration fell in all but two patients. Changes in serum calcium and serum creatinine correlated significantly (p less than 0.001), as did changes in serum calcium and serum phosphate concentrations (p less than 0.05). Serum calcium/serum creatinine and serum calcium/serum phosphate ratios were significantly higher in patients with primary hyperparathyroidism than in patients with hypercalcemia of non-hyperparathyroid origin (p less than 0.01, p less than 0.001). This suggests a different effect of calcium on the glomerular filtration rate in hyperparathyroid and non-hyperparathyroid patients, the latter group being more sensitive to the influence of hypercalcemia. Possible explanations for this difference, such as a protective effect of PTH on the glomerular filtration, are discussed.
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PMID:Reversible renal failure caused by hypercalcemia. A retrospective study. 64 44


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