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 case is presented of a 52-year-old man with a swelling in the neck and dysphagia resulting from an intrathyroid cystic parathyroid adenoma. Hypercalcaemia and unusually high parathyroid hormone levels were detected preoperatively. The adenoma was removed by partial hemithyroidectomy. The literature is reviewed.
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PMID:Intrathyroid cystic parathyroid adenoma: a rare case of hyperparathyroidism. 58 75

The high circulating concentrations of immunoassayable parathyroid hormone observed in chronic renal failure are due to a number of factors. These include altered metabolism of the hormone and also end-organ unresponsiveness which may, indirectly, cause increased secretion of parathyroid hormone. The response of the overactive parathyroid glands to changes in plasma calcium and magnesium is variable and caution is needed in evaluating the suppressibility of parathyroid hormone secretion in acute studies. 1alpha-Hydroxylated derivatives of vitamin D can effectively suppress parathyroid gland overactivity. This effect may not necessarily be medicated through hypercalcaemia and vitamin D metabolites may act directly on the parathyroid glands.
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PMID:Hyperparathyroidism in chronic renal failure. 60 26

Experiments were performed on 36 plasma-expanded Munich-Wistar rats to examine the effects of acute hypercalcemia on the determinants of glomerular ultrafiltration. Elevation of total plasma calcium concentration to an average value of 13.2 +/- 0.5 mg/dl, by acute infusion of calcium chloride into nonthyroparathyroidectomized (non-TPTX) rats, resulted in significant declines in single nephron and whole kidney glomerular filtration rate. These declines were due primarily to a fall in the glomerular capillary ultrafiltration coefficient (Kf), to a mean value approximately 60% below that determined in the pre-infusion period. These changes were not seen in a separate group of sham-treated non-TPTX rats. It is of interest that these effects of acute hypercalcemia were largely abolished in rats that underwent acute TPTX before hypercalcemia. Infusion of a submaximally phosphaturic dose of parathyroid hormone, together with calcium chloride, into a second group of acute TPTX rats, however, had the effect of reproducing the striking declines in filtration rate and Kf noted in non-TPTX rats given calcium chloride alone. These findings suggest that the decline in filtration rate associated with hypercalcemia is due largely to the reduction in Kf, the latter dependent upon the presence of parathyroid hormone.
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PMID:Evidence for a parathyroid hormone-dependent influence of calcium on the glomerular ultrafiltration coefficient. 61 12

A patient with adrenocortical carcinoma had three major endocrine abnormalities attributable directly to the tumor: hypercortisolism (Cushing's syndrome), hyperestrogenism (feminization), and hypercalcemia (pseudohyperparathyroidism). There were higher levels of immunoreactive parathyroid hormone in venous effluent from the tumor or its abdominal metastases compared to that found in the veins draining the parathyroid glands. This, together with the presence of normal parathyroid glands on autopsy, established the diagnosis of pseudohyperparathyroidism as the cause of hypercalcemia in this patient.
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PMID:Feminizing adrenocortical carcinoma with Cushing's syndrome and pseudohyperparathyroidism. 62 58

Chronic administration of lithium salts is associated with hypercalciuria in the rat. To study the renal and extrarenal mechanisms of this phenomenon, we utilized balance and clearance techniques in rats pair-fed diets with or without Li2CO3 (0.5 meq/day per rat). Lithium induced hypercalcemia (mean +/- SE: 5.40 +/- 0.09 VS. 5.06 +/- 0.05 meq/liter) and hypercalciuria (Ca/creatinine = 0.28 +/- 0.04 vs. 0.13 +/- 0.03) only during feeding. When CaCO2 supplement to a calcium-deficient diet was abruptly withdrawn, hypercalciuria was abolished. However, polyuria and polydipsia persisted. No significant changes in serum phosphate, urine phosphate, sodium, pH, or citrate were observed. Chronic parathyroidectomy (PTX) also abolished this effect. During clearance studies, fasting excretion of calcium was similar between treated and control animals. Superimposed acute PTX resulted in comparable changes, hence arguing against primary changes in renal calcium reabsorption or changes in parathyroid hormone effects on the renal tubule. Thus, lithium produces absorptive hypercalciuria by a mechanism dependent on intact parathyroid glands and adequate diet calcium, but independent of urine sodium, phosphate, or pH. The active component of gut calcium transport may be involved, possibly via alterations of vitamin D metabolism.
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PMID:Mechanism of lithium-induced hypercalciuria in rats. 62 44

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

We describe a boy who presented at 4 years of age with radiological hyperparathyroidism, osteosclerosis, and necrosis of the femoral heads. Plasma biochemistry was normal but the parathyroid hormone (PTH) level was very high. He was deaf and had an unusual facies but did not have the phenotype of Albright's hereditary osteodystrophy. Plasma and urine cyclic AMP reponses to bovine PTH were markedly subnormal. Vitamin D produced sustained hypercalcaemia and a fall in plasma phosphorus. After four hyperplastic parathyroid glands were removed he became hypocalcaemic and plasma phosphorus rose. After operation he remained unresponsive to exogenous PTH; We suggest that he had a form of pseudohypoparathyroidism without the phenotype of Albright's hereditary osteodystrophy and with some residual skeletal and renal responsiveness to PTH.
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PMID:Normocalcaemic pseudohypoparathyroidism with unusual phenotype. 64 42

Autopsy examination of a patient with well-documented supravalvular aortic stenosis and other characteristic features of the idiopathic infantile hypercalcemia syndrome revealed previously unreported hyperplasia of parafollicular cells (C cells). Immunohistochemical analysis demonstrated up to 30 calcitonin-containing cells per high power field, whereas normal glands contain only 4 to 10 cells per low power field in areas of highest concentration. The parathyroid glands were found to be normal both grossly and microscopically, whereas the bones showed thickened trabeculas, normal Haversian canals and no apparent increase in osteoblast or osteoclast activity, suggesting normal parathyroid hormone, but increased thyrocalcitonin activity. We suggest that C-cell hyperplasia has occurred in response to a persistent, rather than transient, elevation in serum calcium levels and that thyrocalcitonin function is augmented, rather than impaired in this disorder. The primary biochemical defect promoting hypercalcemia remains to be clarified, as well as the role, if any, such a defect plays in producing significant pathology in the central nervous system and in the cardiovascular, renal and skeletal systems.
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PMID:Supravalvular aortic stenosis with parafollicular cell (C-cell) hyperplasia. 65 98

We studied the effects of vitamin D metabolites on parathyroid hormone (PTH) secretion. Test materials were injected into the cranial thyroid artery of the dog, and immunoreactive PTH was measured frequently in serum samples from the inferior thyroid vein and the femoral vein. This model for the study of secretion had previously been validated with the use of known modulators on PTH secretion. In control experiments, injection of 100% ethanol, the vehicle in which cholecalciferol (D(3)) metabolites were suspended, resulted in no change in PTH secretion. Likewise, native vitamin D(3), in doses ranging from 250 to 1,250 ng had no effect on PTH secretion. 25-Hydroxycholecalciferol, 25-(OH)D(3), in doses of 125-240 ng, caused complete suppression of PTH secretion. When 24,25-dihydroxycholecalciferol, 24,25-(OH)(2)D(3), was injected in doses of 50-250 ng, suppression of PTH secretion was again complete; in doses of 5 ng, injection of this metabolite resulted in significant but incomplete suppression of secretion. In doses of 50-250 ng, 1,25-(OH)(2)D(3) strongly stimulated PTH secretion, but in a dose of 5 ng this metabolite had no effects. Injection of equal doses of 1,25-(OH)(2)D(3) and 24,25-(OH)(2)D(3) resulted in significant suppression of PTH secretion. Hypocalcemia-induced stimulation of PTH secretion was suppressed by 24,25-(OH)(2)D(3) while hypercalcemia-induced suppression of PTH secretion was stimulated by 1,25-(OH)(2)D(3). In all experiments showing suppression of PTH secretion, peripheral PTH decreased. Arguments are presented for considering the suppressive effects of D(3) metabolites as physiologic modulators. However, this stimulating effect of 1,25-(OH)(2)D(3) occurred only in pharmacologic doses and hence probably has no physiologic relevance.
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PMID:Inhibition of parathyroid hormone secretion by 25-hydroxycholecalciferol and 24,25-dihydroxycholecalciferol in the dog. 65 99

A patient with hypercalcemia, hypophosphatemia, and an undifferentiated lymphoma involving only the bone marrow was treated by us. The finding of an elevated serum parathyroid hormone (PTH) level in the presence of normal parathyroid glands and increased metabolic bone activity on bone biopsy suggests an ectopic PTH syndrome. To our knowledge, no previous case of ectopic PTH syndrome associated with a lymphoma with bone marrow involvement only has been reported.
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PMID:Ectopic parathyroid hormone syndrome. Occurrence in a case undifferentiated lymphoma with bone marrow involvement. 67 91


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