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

A review of 51 successful reoperations for persisting hypercalcaemia due to primary hyperparathyroidism shows that inadequate anatomical knowledge, inadequate surgical technique and unusual localizations of the parathyroids are the most frequent causes of failure of the primary operation. The majority of these failures are therefore preventable. There is a frequent need for cervical thymectomy in parathyroid surgery. Sternotomy is only very rarely necessary.
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PMID:Causes of failure in the surgical treatment of primary hyperparathyroidism: lessons from 51 successful reoperations. 64 90

Various hormones have been implicated in the genesis of hypercalcemia in patients with malignancy. Ectopic secretion of PTH by tumor has been documented in only a few patients; rather, elevated levels of circulating iPTH have been presumed to reflect tumor production of hormone in most patients. Small fragments of PTH, as well as polypeptides larger than native PTH, have been described; their biological roles are unclear. The pattern of immunoreactivity, however, has been used to differentiate patients with ectopic hyperparathyroidism from patients with concomitant primary hyperparathyroidism. Vitamin D-like sterols produced by breast cancer seldom reach plasma levels necessary for physiological effects. Members of the prostaglandin family have been proposed to induce hypercalcemia through osteoclast activation or alteration of the immune system and also to affect the frequency of bone metastases. At present, no direct evidence is available to prove a direct role for these effects and prostaglandins are most useful as possible indicators of disease activity.
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PMID:Mechanisms of hypercalcemia in malignancy. 65 92

In 44 patients, all suffering from a malignant disease with hypercalcaemia, plasma parathormone was measured by a radioimmunoassay measuring the intact PTH molecule. The results as a function of plasma calcium were compared with those in 38 patients suffering from proven primary hyperparathyroidism and with those in 9 cases of hypercalcaemia of other origin. PTH was indetectable in 14 cases of malignant disease and normal in 25 cases. In 5 patients only could PTH and plasma calcium not be separated from primary hyperparathyroidism. 3 patients had an increased PTH level when plasma calcium was lowered by treatment of the underlying disease. In patients with malignant disease hypercalcaemia is rarely caused by increased secretion of PTH. In these cases either primary hyperparathyroidism or ectopic secretion of PTH may be the cause of hypercalcaemia.
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PMID:[Determination of plasma parathyroid hormone in the differential diagnosis of hypercalcemias associated with malignant tumors]. 66 97

Of 365 patients surgically treated for hyperparathyroidism at the University of Toronto hospitals, 3 had hypercalcemia due to an abnormal and ectopic fifth parathyroid gland. Autopsy studies have shown that a fifth gland may be present in 3% to 5% of patients with hyperparathyroidism. The possibility of an abnormal fifth gland as the cause of primary hyperparathyroidism should be considered when four glands of normal size and histology have been found in the neck, and such a gland should be sought in all patients with the diffuse hyperplasia of secondary hyperparathyroidism. The fifth gland is usually in the lower neck or upper mediastinum, frequently within the thymus. If present, it can usually be recognized and excised.
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PMID:Importance of a fifth parathyroid gland in the surgical treatment of hyperparathyroidism. 67 81

The thyroidal content of calcitonin was investigated in patients with euthyroid goitre, patients undergoing laryngectomies or neck operations and finally patients with primary hyperparathyroidism using method of biological titration. Patients with primary hyperparathyroidism had markedly decreased content of calcitonin in the thyroid gland when compared with the content of calcitonin of both groups of patients without calcium metabolism disturbance. Decreased content of calcitonin in patients with primary hyperparathyroidism can be explained by long lasting hypercalcaemia during which the rate of biosynthesis of calcitonin in the C cells does not keep up with the rate of release of calcitonin into the circulation.
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PMID:Calcitonin activity of the thyroid gland in primary hyperparathyroidism. 69 67

A prospective series of 200 patients with persistent hypercalcemia had an abbreviated diagnostic work-up consisting of parathormone radioimmunoassay, chest roentgenogram, intravenous pyelography, and serum protein electrophoresis. All patients with hypercalcemia and hyperparathormonism had neck exploration if roentgenograms failed to reveal evidence of ectopic hyperparathyroidism. Serum iPTH proved to be at least 96% accurate in predicting parathyroid disease while at the same time resulting in considerable diagnostic economy. An elevated iPTH was particularly helpful in distinguishing between hypercalcemia due to destruction of bone by malignancy and primary hyperparathyroidism with a coexisting malignancy. Further, measurement of parathormone was useful in evaluation of postoperative hypercalcemia.
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PMID:Serum parathormone in the identification and surgical management of hyperparathyroidism. 70 2

The authors studied the presence of visceral calcification as evidenced by the visceral uptake of bone-seeking radionuclides during the course of a bone scan among 22 patients with terminal renal failure maintained on dialysis, nine patients with hypercalcemia secondary to malignancy, and nine patients with primary hyperparathyroidism. Uptake by the lungs or stomach was observed in 11 renal failure patients (50%) and in four of those with malignancy and hypercalcemia (44%). None of the patients with primary hyperparathyroidism had evidence of visceral calcification. The serum CaXP product was significantly higher among those with visceral calcification than those without. The results of this study indicate that a CaXP product of 60 represents the saturation product of calcium phosphate in serum above which spontaneous precipitation of this salt may occur in such viscera as stomach and lungs.
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PMID:Visceral calcification and the CaXP product. 71 4

Hypercalcemia occurred in 4 dogs with renal failure. Primary causes of hypercalcemia previously described in the dog (primary hyperparathyroidism, pseudohyperparathyroidism, vitamin D toxicosis) were not identified. Increased concentrations of circulating immunoreactive parathormone were found in 2 dogs, and thyroparathyroidectomy of 1 dog resulted in decreased serum concentrations of that hormone as well as of calcium. The latter observations indicated that hypercalcemia was related to increased parathormone activity, but the possibility of other homeostatic imbalances was not excluded. It was concluded that renal failure should be considered as a primary cause of hypercalcemia, along with other causes previously identified.
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PMID:Hypercalcemia secondary to chronic renal failure in the dog: a report of four cases. 72 83

Of 51 patients with primary hyperparathyroidism (2 patients with MEN, Type 1 clinical symptomatology, diagnostic procedures, differential diagnosis, operative strategy and long-term results are being reported. Aside from clinical findings and radiologic signs in our hands determination of the ionized serum calcium fraction, results of chrest bone biopsies and parathormone determinations are best parameters to substantiate the diagnosis of PHPT. Parathormone radioimmunassay determination is very helpful in localizing the adenoma, especially in cases of reoperations. Five patients were seen in acute hypercalcemic crises, in which emergency operations are absolutely indicated. Postoperative hypercalcemia and recurrencies were observed in 3.9%. Successful extirpation of parathyroid adenomas (15% multiple adenomas were found) is the therapy of choice in PHPT, only in cases with hyperplasia subtotal parathyroidectomy is indicated.
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PMID:[Diagnosis and therapy of primary hyperparathyroidism (author's transl)]. 72 76

On the basis of 100 cases of hypercalcemia, the authors attempt to elucidate the criteria of the etiologic diagnosis. Kidney lithiasis or nephrocalcinosis suggested a primary hyperparathyroidism (HPT I) or an intoxication due to vitamin D. X rays of the skeleton and quantitative histological exams of the bone were not useful in the diagnosis of HPT I. The level of parathormone in the plasma is the best parameter to be used in distinguishing HPT I from other diseases. In the absence of renal insufficiency or severe intestinal disorders, a phospharemia below 2.6 mg/100 ml, a chloremia above 103 m EG/l and bicarbonates below 25 m Eg/l indicate an HPT I or a paraneoplasic. A phosphoremia above 3.2 mg/100 ml runs counter to this diagnosis. The chloremia/phosphoremia ratio is not more helpful than the phosphoremia alone.
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PMID:[Etiologic diagnosis of hypercalcemia. A study of 100 cases]. 72 66


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