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

Two patients with transient hypercalcaemia during recovery from acute renal failure are described. The literature is reviewed and possible pathophysiological mechanisms discussed. Patients with renal failure following muscle damage should have regular measurement of plasma calcium.
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PMID:Transient hypercalcaemia following acute renal failure. 87 19

Five patients who had gross abnormalities of calcium and phosphorus metabolism due to long standing renal failure are described to illustrate the difficulties with the term "tertiary hyperparathyroidism". One patient who had unequivocal biochemical tertiary hyperparathyroidism was found histologically to have nodular hyperplasia of all four glands even though one gland weighed twice as much (12g) as the combined weight of the other three. Another patient was not hypercalcaemic but had all the other features of the condition including rapid onset of osteitis fibrosa, vascular calcification and a probable parathyroid adenoma, with hyperplasia of the three glands. The other three had hypercalcaemia only after a reduction in the plasma inorganic phosphorus due either to renal transplantation or aluminum hydroxide therapy. The bone histology of the five patients varied from severe osteomalacia to severe osteitis fibrosa. A consideration of the factors involved in causing hypercalcaemia in these patients and a review of the literature leads to the conclusion that the term tertiary hyperparathyroidism is often misleading and best avoided.
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PMID:What is tertiary hyperparathyroidism? 106 86

Thyrocalcitonin (TCT) is useful as a diagnostic and therapeutic agent in selected human diseases. Elevated plasma levels of TCT occur in patients with medullary carcinoma of the thyroid gland. Asymptomatic relatives of these patients harboring microscopic foci of tumor may have abnormal plasma levels of TCT in the basal state or after provocative stimuli. In both instances the plasma levels of TCT can be used in the diagnosis and management of this thyroid neoplasm. Elevated plasma levels of TCT have also been described recently in subjects with certain extrathyroidal neoplasms or renal failure. Moderate elevations are seen during normal pregnancy and in the neonatal period. Although exogenous TCT has actions on several organs, including bone, the kidneys and the gastrointestinal tract, its physiological role in man, if any, is still unknown. The recently reported measurements of TCT in normal subjects should facilitate the clarification of this issue. TCT has been used as a therapeutic agent in Paget's disease of bone, hypercalcemia of diverse etiologies, osteopenia and several other skeletal disorders. The dramatic improvement of patients with Paget's disease has been a unique therapeutic action of TCT. The therapeutic responses in hypercalcemic subjects given TCT are encouraging but more information is needed about the pharmacology of the hormones in these subjects before conclusions can be formed. At present the therapeutic role of TCT in osteopenia is hypothetical and the results of ongoing and future studies are needed to determine its effects.
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PMID:Clinical aspects of thyrocalcitonin. 109 26

The presence of hypercalcemia in patients with known cancers may be due to the cancers themselves, or to co-existing primary hyperparathyroidism. The differentiation of primary hyperparathyroidism from the hypercalcemia of malignancy is important since the relief of distressing symptoms and prevention of hypercalcemic crises and renal failure can be accomplished relatively easily by parathyroid surgery in the former condition, and only with difficulty, at times, with fluids and drugs in the latter condition. The histories of three recent patients are presented, which demonstrate the difficulties inherent in the differentiation of these conditions. These patients were ultimately found at operation to have primary hyperparathyroidism in addition to malignancies of the cervix, adrenal gland and kidney. In our experience the following have been helpful in establishing a diagnosis; history of hypercalcemia prior to development of cancer, the type of cancer itself, the effect of cancer therapy on the hypercalcemia, and selective venous sampling with radioimmunoassay for parathyroid hormone.
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PMID:The differentiation of primary hyperparathyroidism from the hypercalcemia of malignancy. 111 56

A case is reported of a twenty-one year old man who developed severe hypercalcemia late in the diuretic phase of acute reversible renal failure secondary to severe trauma. Hypercalcemia persisted for approximately five months. Serum immunoreactive parathyroid hormone levels were undetectable and sub-total parathyroidectomy had no appreciable effect on the serum calcium. The most likely source of this patient's hypercalcemia was resorption of calcium from metastatic deposits in soft tissue and possibly from bone. Failure to incorporate calcium into bone during the period of immobilization may explain the prolonged hypercalcemia.
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PMID:Prolonged hypercalcemia following acute renal failure. 115 48

In a case of primary hyperparathyroidism, ocular changes were observed as vacuoles in the basal cells of the corneal epithelium, and by staining procedures, calcium was found in the corneal and conjunctival epithelia, the corneal endothelium and in the sclera. By electron microscopy, needle-like crystals of calcium hydroxyapatite precursors were found intracellularly, also in keratocytes. The crystals in the epithelial cells were often confined to the nucleus. In a case of idiopathic hypercalcaemia of infancy, similar crystals were found intracellularly in the corneal epithelial and stromal cells, and in this case extracellular deposits, morphologically identical with extracellular deposits in conjunctival biopsies from patients with renal failure, were also seen. These extracellular aggregations were probably also composed of hydroxyapatite. The difference in morphology between intracellular and extracellular deposits is discussed in the light of the serum values of the mineral ions found in the three groups of cases.
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PMID:Ouclar calcifications in primary hyperparathyroidism. Histochemical and ultrastructural study of a case. Comparison with ocular calcifications in idiopathic hypercalcaemia of infancy and in renal failure. 117 99

Hypocalcemia is a well known finding in critically ill patients. Subsequent occurrence of mild hypercalcemia has also been reported. In order to investigate the incidence and nature of critical care hypercalcemia serum calcium was measured in 83 critically ill ICU patients (TISS score > or = 40) and related to the occurrence of acute renal failure (ARF) and severity of illness, evaluated by the APACHE-II and the multiple organ failure scoring systems. Thirty-two percent of the patients developed hypercalcemia (serum calcium > or = 2.60 mmol/l) during their ICU stay. These hypercalcemic episodes (mean maximal value 2.71 +/- 0.12 mmol/l) were more common and occurred earlier in patients with co-existing ARF. However, multiple regression analysis showed the number of failing organ systems in the first days to be the best predictors for later occurrence of hypercalcemia (p < 0.0001). When serum parathyroid hormone (PTH) was measured in 6 of the patients without ARF during their hypercalcemic episodes, PTH was not suppressed but slightly elevated, to a similar extent as in patients with mild primary hyperparathyroidism. In conclusion, a high incidence of hypercalcemia was found in critically ill ICU patients. The hypercalcemia was mild and was more frequently found in patients with co-existing renal failure. The most powerful predictor to later occurrence of hypercalcemia was however the severity of the illness in itself. The raised levels of PTH found during the hypercalcemic episodes suggest ICU hypercalcemia to be caused by parathyroid overactivity.
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PMID:Critical care hypercalcemia--a hyperparathyroid state. 130 66

We studied the effect of converting 100 established CAPD patients from aluminium- to calcium-based phosphate binders. After a follow-up of 1 year only 60% of patients remained on calcium carbonate. Hypercalcaemia was the major problem, with more than 40% of patients having a serum calcium in excess of 3.0 mmol/l. Several patients required hospitalization for symptomatic hypercalcaemia. Hypercalcaemia was more common in patients with normal serum parathyroid hormone concentrations (65 versus 25%, P less than 0.01). Serum phosphate control was better prior to commencing calcium carbonate when patients were treated with aluminium phosphate binders mean 1.71 +/- 0.15 mmol/l (SEM) than at the time of maximum serum calcium concentration, 1.81 +/- 0.25, P less than 0.05. This study does not confirm the findings of others, which have suggested that calcium carbonate is a safe and effective phosphate binder for patients with end-stage renal failure.
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PMID:Audit of the use of calcium carbonate as a phosphate binder in 100 patients treated with continuous ambulatory peritoneal dialysis. 838 46

We evaluated the degree of secondary hyperparathyroidism (SHPT) in the patients undergoing long-term hemodialysis treatment. Most patients showed improvement of SHPT by administration of the active vitamin D3 analogue. However, some patients developed overt SHPT even under intensive treatment. Pulse therapy with large dose of vitamin D3 for those who suffered from overt SHPT was an effective treatment modality at the initial stage, however, hypercalcemia which developed in the majority of the patients at the later stage of this treatment became an obstacle for the continuation of this treatment. Therefore, early detection of the hypersecretion state of parathyroid hormone (PTH) as well as earlier initiation of intensive therapy are important factors in preventing overt SHPT. Establishment of a suitable assay system for early detection of SHPT is an important task and the high sensitivity-PTH assay system may be the most desirable. Though diabetic patients were not likely to develop overt SHPT, this system could detect even the mild chronological increase of serum PTH level in diabetic patients. On the other hand, relatively earlier initiation of vitamin D3 therapy to the predialysis patients from the conservative treatment stage caused aggravation of deterioration of renal function. Therefore, we should be prudent to initiate vitamin D3 therapy on predialysis patients suffering from renal failure. Strict management of the patients by vitamin D3 as well as calcium supplement therapy along with evaluation of the serum PTH level is still an important measure to avoid overt SHPT.
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PMID:[Evaluation of secondary hyperparathyroidism in the patients undergoing hemodialysis--focused on parathyroid hormone assay system]. 133 62

Much interest is currently centered on the use of calcium acetate as a phosphorus binder in patients with renal failure. Therefore, this compound in subjects previously stable on calcium carbonate and undergoing high-efficiency hemodialysis with a dialysate calcium of 2.5 mEq/L was evaluated. Twenty subjects were switched from generic calcium carbonate to a single calcium carbonate preparation for a period of 2 months. This was followed by a phase (1 month) in which calcium acetate was substituted for calcium carbonate at a dose containing half the amount of elemental calcium. Subjects then continued calcium acetate for 6 months. It was found that calcium acetate allowed comparable control of immunoreactive parathyroid hormone, calcium, and phosphorus levels compared with calcium carbonate. This occurred with half the amount of elemental calcium ingested in the form of calcium acetate (349 +/- 25 versus 699 +/- 75 mmol/day; P less than 0.001). With this lower dose, the overall incidence of hypercalcemia was the same with each formulation. In the eight subjects concurrently receiving i.v. calcitriol, the incidence of hypercalcemia was significantly higher during the first month of calcium acetate compared with that in those not receiving this compound (P less than 0.05). Of those four subjects receiving the high dose of calcitriol (2 micrograms thrice weekly), all required either reduction in the dose or discontinuation of the drug. Thus, mineral metabolism could be controlled adequately with calcium acetate despite using half as much elemental calcium compared with calcium carbonate. This, however, did not result in a lower incidence of hypercalcemia, particularly in those receiving i.v. calcitriol.
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PMID:Calcium acetate as a phosphorus binder in hemodialysis patients. 139 13


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