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

A positive correlation was found between serum urate and elevated serum calcium in patients with hypercalcaemic primary hyperparathyroidism. No such correlation was detected in normocalcaemic controls, matched with respect to age and sex. Neither was such a correlation confirmed either in subjects with normalized serum calcium levels after extirpation of parathyroid adenomata, or in subjects with hypercalcaemia due to other conditions than primary hyperparathyroidism, such as various malignancies, sarcoidosis and hyperthyroidism. The positive correlation between elevated serum calcium and serum urate (within normal limits) in subjects with hypercalcaemic hyperparathyroidism is suggested in subjects with hypercalcaemic hyperparathyroidism is suggested to be a clue to the explanation of an association between hyperparathyroidism and urate retention.
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PMID:Serum urate in subjects with hypercalcaemic hyperparathyroidism. 91 19

Despite its earlier reputation as a relentlessly progressive disease, hyperparathyroidism may actually remain asymptomatic for many year. If its possible presence is signaled by hypercalcemia and supported by other laboratory findings, surgery is often indicated because no medical treatment is effective, and long-term follow-up of this frequently malignant condition is difficult; the surgical cure rate is about 95%.
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PMID:The changing face of hyperparathyroidism. 91 73

A woman with hyperthyroidism, hypercalcemia, and a parathyroid adenoma is described. Various studies indicate that in hypothyroid subjects given an acute dose of calcium, the serum calcium levels remain elevated for longer periods than in control subjects. In part, this may be due to diminished bone uptake. Despite these studies which would tend to support the contention that hypothyroid patients "have a propensity to hypercalcemia" (Lowe et al), overt and significant hypercalcemia is unusual. Hypothyroidism is listed as a possible cause of hypercalcemia. This does not seem to be warranted by a review of the literature. The reference most often cited is that of Lowe et al. In their particular case, the hypercalcemia improved with thyroid replacement therapy. This also happened in our case. However, the measurement of IPTH levels led to the correct diagnosis. IPTH levels were not available at the time of Lowe's report and hyperparathyroidism was not completely excluded. Therefore, at this time, the reported association of hypercalcemia with adult hypothyroidism needs further examination to determine if this association is real.
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PMID:Hypothyroidism and hypercalcemia: report of a case with a parathyroid adenoma and review of the literature. 91 7

Fifty eight patients with thyrotoxicosis were examined as well as 9 patients with hypothyroidism and 40 healthy subjects. A tendence towards hypercalcemia and hyperphosphatemia, hypercalciuria, hyperhydroxiprolinuria, elevated alkaline phosphatase were found in hyperthyroidism. In hypothyroidism--hypocalcemia, hypocalciuria, hypohydroxiprolinuria. The changes are associated with the direct effect of thyroid hormones upon bone system (intensified bone metabolism with predominance of destruction). Calciuria and HOP-uria in thyrotoxicosis depend on the severity of the disease. The elevated calcium excretion in thyrotoxicosis speaks for the presence of ostemalacic component. TRP, PEI, mean diametrically opposite in hyper- and hypothyroidism, support the hypothesis of the secondary hypoparathyroidism in thyrotoxicosis and hyperparathyroidism--in the hypothyroidism.
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PMID:[Studies of calcium-phosphorus metabolism in thyrotoxicosis]. 91 16

The newborn infant of a mother with hypoparathyroidism following thyroidectomy showed transient hypercalcemia and hypermagnesemia. Hypophosphatemia, as found in adult hyperparathyroidism, was not noted in this case, or in three of five other reported cases of neonatal hyperparathyroidism secondary to maternal hypoparathyroidism.
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PMID:Transient neonatal hyperparathyroidism associated with maternal hypoparathyroidism. 93 15

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

Total and ionized calcium concentrations as well as parathyroid hormone levels were measured in a group of hyperthyroid persons. Ionized and total calcium levels were elevated in 21 of 45 (47%) and in 12 of 45 (27%) thyrotoxic patients, respectively. Mean ionized and total calcium levels were higher in these 45 patients than in normal persons. Using two different radioimmunoassay systems for a total of 44 determinations, mean parathyroid hormone levels were lower in thyrotoxic patients than in subjects with proved hyperparathyroidism. These data suggest that [1] elevations of both ionized and total calcium concentrations occur frequently in thyrotoxic patients; [2] ionized calcium concentrations may be elevated in a higher percentage of hyperthyroid subjects than are total calcium concentrations; and [3] the hypercalcemia associated with thyrotoxicosis is not associated with elevated parathyroid hormone levels.
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PMID:Ionized and total serum calcium and parathyroid hormone in hyperthyroidism. 93 77

The relative contributions of Ca++, phosphorus, and parathyroid hormone (PTH) on insulin secretion were evaluated in three groups of dogs. Dogs were studied with glucose infusions (group I) or standard intravenous glucose tolerance tests (IVGTT) (group II) before and after the development of diet-induced hypophosphatemia. Mean serum phosphorus levels for both groups fell from 4.1 to 1.1 mg/100 ml. Animals in group I demonstrated a fall in glucose disappearance rates (Kg) from 5.3+/-0.6% min to 3.5+/-0.5% after induction of hypophosphatemia (P less than 0.001). Mean insulin response was significantly greater in the hypophosphatemic animals than in controls in this group. In group II animals, mean insulin areas obtained during the IVGTT increased from 1,426+/-223 to 2,561+/-141 muU/ml/60 min after induction of hypophosphatemia, and were unaffected by Ca++ or PTH administration. Ca++ administration, but not hypophosphatemia or PTH infusion, increased significantly the mean insulin response to tolbutamide. Secondary hyperparathyroidism was induced by dietary manipulation in four dogs (group III). Mean PTH values increased from 71.4+/-2.1 to 3,012+/-372 pg/ml (P less than 0.001). Mean insulin response to an IVGTT was similar to group III animals, but increased from 1,352+/-128 to 1,894+/-360 muU/ml/60 min after the excessive dietary phosphorus was reduced for 3 mo, and plasma phosphorus fell from 3.2+/-0.1 to 2.8+/-0.3 mg/100 ml. PTH values decreased to 647+/-53 pg/ml. The insulin response to tolbutamide was comparable to that in group II animals, but increased significantly after calcium administration. Immunoreactive insulin disappearance rates were unaffected by hypophosphatemia or diet-induced secondary hyperparathyroidism. These data demonstrate that hypophosphatemia is associated with an augmented glucose-stimulated insulin release, without any effect on tolbutamide-stimulated insulin release. Hypercalcemia produces an augmented tolbutamide-stimulated insulin release with no apparent effect on glucose-stimulated insulin release. Finally, PTH does not appear to be an insulin antagonist and has no apparent effect on either glucose- or tolbutamide-stimulated insulin release in animals with dietary-induced secondary hyperparathyroidism.
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PMID:The relative roles of calcium, phosphorus, and parathyroid hormone in glucose- and tolbutamide-mediated insulin release. 95 71

Investigation of multiple serum and urinary factors in 44 patients with calcium urinary stone disease confirmed a number of defects that have been described previously: elevation of mean serum calcium and uric acid above normal, and depression of mean serum magnesium. Urinary excretion of calcium and uric acid was increased and was increased and was probably related to food ingestion. Urinary magnesium also increased after eating but less than calcium, with the result that for most patients the magnesium to calcium x 100 ratio approached levels observed in stone formation. Urinary oxalate excretion was constant during the entire observation period and apparently was not affected by ingestion of a defined diet. Nine additional patients had persistent hypercalcemia owing to hyperparathyroidism (5 confirmed, 1 suspected), malignancy (2) and drug ingestion (1). Metabolic evaluation of patients with calcium urinary calculi continues to contribute to decisions regarding their best therapeutic regimen.
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PMID:Contribution to therapeutic decisions of ratios, absolute values and other measures of calcium, magnesium, urate or oxalate balance in stone formers. 95 3

In 82 patients, a preoperative diagnosis of primary hyperparathyroidism has been established by means of transfemoral neck vein catheterization and measurement of serum immunoreactive parathyroid hormone (iPTH). Twenty-five of these patients have had cancer in other parts of the body but with no evidence of recurrence or metastasis. One patient had carcinoma of the colon with metastases, and four were members of families with multiple endocrine adenomatosis (MEA, Types I and II). In six other hypercalcemic patients, high levels of iPTH were found also in the effluent blood from cancer sites other than the parathyroid gland, secondary to ectopic hormone production or pseudohyperparathyroidism. In addition, a high serum level of iPTH was found in the superior vena cava of a seventh patient who had carcinoma of the breast but no clinical or radiological signs of recurrence or metastasis with the exception of an enlarged liver. This iPTH finding was interpreted as being, probably, the result of parathyroid adenoma in either the neck or the mediastinum. At the time of operation, a transcervical mediastinal search was made. Four normal cervical parathyroid glands were found; three were removed. Hypercalcemia persisted after operation, and the patient died. At postmortem examination, microscopic study revealed that the disease had metastasized to lungs and hilar lymph nodes. There was massive metastasis in the liver; the liver contained a large amount of iPTH. The results of these investigations suggest that (1) venous catheterization of the neck veins and the effluent blood from extraparathyroid tumors aid in identifying and localizing iPTH production; (2) primary benign hyperparathyroidism is not uncommon in patients with cancer, and its co-existence must be recognized; (3) high serum iPTH level in the superior vena cava may be found in patients with metastatic or primary cancer of the thoracic cavity; and (4) hyperparathyroidism may be the first hint of a familial multiple endocrine syndrome.
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PMID:Hypercalcemia in patients with known malignent disease. 96 5


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