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

Forty-five patients with biochemically documented primary hyperparathyroidism as part of multiple endocrine neoplasia syndrome types 1 or 2 were surgically treated from 1960 through 1980. Hyperplasia occurred in 69% of the patients, single adenoma in 27%, and double adenomas in 4%. All but two patients with hyperplasia underwent subtotal parathyroidectomy. In this group, the cure rate was 93% and the incidence of permanent postoperative hypoparathyroidism 23%. In the adenoma group, treatment included excision of the adenoma and biopsy of at least one other gland. The cure rate was 76%, with no postoperative hypoparathyroidism. Analysis of patients with persistent hyperparathyroidism suggested that failure to recognize multiple gland disease was the principal cause of postoperative hypercalcemia. In view of the high incidence of hypocalcemia after subtotal parathyroidectomy, approximately 500 mg of tissue should be cryopreserved to allow transplantation should hypocalcemia ensue postoperatively.
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PMID:Primary hyperparathyroidism in patients with multiple endocrine neoplasia syndromes. Surgical experience. 613 93

Elucidation of the vitamin D endocrine system and the availability of potent metabolites have led to new approaches to vitamin D therapy. The traditional management of exogenous (sunlight) or endogenous (malabsorption) vitamin D deficiency without evidence of disordered vitamin D metabolism has not changed, since it consists of treatment with vitamin D itself--a therapy which preserves the normal intrinsic mechanisms for regulating the rate of production of 1,25-dihydroxycholecalciferol. 1,25-DHCC and the analogue compound 1 alpha-CC should be reserved for treatment of hypocalcemia consequent on chronic renal failure or hypoparathyroidism, where 1-hydroxylation is lacking or impaired. Hypophosphatemic rickets has been treated with 1-hydroxylated compounds, with promising results; this use of the latter metabolites warrants further investigation. The use of vitamin D metabolites and of pharmacological doses of vitamin D itself must be regarded as substitution of a hormone or hormone precursors. Therefore, careful monitoring of serum and urine calcium is required in every patient receiving these compounds, in order to avoid excessive dosage. Special attention must be paid to patients with sarcoidosis since they often develop hypercalcemia after vitamin D or UV-light exposure, as a result of an intrinsic regulation defect in 1,25-DHCC synthesis.
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PMID:[Therapy with vitamin D and D-metabolites]. 626 26

Phosphate indices (serum phosphate, tubular reabsorption of phosphate, renal threshold phosphate concentration (TmP/GFR) and index of phosphate excretion) were studied in 88 hypercalcaemic subjects: 64 with primary hyperparathyroidism (HPT) and 24 with hypercalcaemia from other causes, predominantly malignant disease. HPT patients as a group could easily be separated from normal subjects (n = 16) and patients with functional hypoparathyroidism (n = 7) by use of the phosphate variables but these indices were of little discriminating value for the differential diagnosis between HPT and hypercalcaemia from other causes. There was no difference in the urinary cyclic adenosine monophosphate (cAMP) excretion between the two hypercalcaemic patient groups, but HPT patients had clearly elevated serum parathyroid hormone (PTH) levels compared with normal PTH concentrations in patients with other causes of hypercalcaemia. A positive correlation between cAMP and serum calcium and an inverse relationship between cAMP and TmP/GFR were found in patients with hypercalcaemic malignant disease. These findings suggest the existence of a humoral factor with PTH-like effects in malignant disease. Since PTH levels were low, the physiological actions were apparently not mediated by circulating PTH. No difference in the values for phosphate variables, PTH, cAMP or serum calcium was found between renal stone-forming and stone-free patients with HPT.
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PMID:Clinical studies on phosphate handling in hypercalcaemia. 629 62

The principal maternal physiologic adjustment with respect to calcium metabolism is increasing PTH secretion, which maintains the serum ionic calcium level within its characteristically narrow physiologic limits in the face of an expanding extracellular fluid volume, increased urinary excretion, and calcium transfer to the fetus. Additionally, PTH promotes increased renal synthesis of 1,25-(OH)2D3, which acts in concert with PTH to meet the calcium demands of gestation. Whether or not calcitonin secretion increases as well is not clear; if so, this effect may be important in protecting the maternal skeleton. The primary characteristic of perinatal calcium metabolism is the active placental transport of calcium ions from mother to fetus, making the fetus relatively hypercalcemic. Since none of the calcitropic hormones cross the placenta, hypercalcemia apparently suppresses either secretion or activity of PTH by the fetus and stimulates fetal calcitonin release, creating an environment (high calcium, low PTH, high calcitonin) favorable to skeletal growth. With birth, the transplacental calcium source terminates abruptly and the serum calcium level declines for 24 to 48 hours, after which it stabilizes and then rises slightly. Neonatal calcium homeostasis probably reflects multiple influences, including the respective calcitropic hormones and other involved ions such as magnesium and phosphate. The physiologic mechanisms regulating calcium homeostasis during pregnancy and the perinatal period generally operate very effectively. Thus, aberrations leading to clinically evident disease states are relatively infrequent. Maternal hyperparathyroidism causes several complications, notably hypocalcemic tetany in the newborn, and maternal hypoparathyroidism may be associated with perinatal hyperparathyroidism. Diabetic pregnancy leads to altered calcium metabolism in mother, fetus, and newborn; the primary feature may be chronic hypomagnesemia, which leads to hypoparathyroidism to mother and fetus. There is some suggestion of an etiologic role for calcium in hypertensive disorders, and, in any event, magnesium sulfate therapy influences calcium homeostasis. Finally, leg cramps in the pregnant woman may reflect alterations in calcium metabolism.
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PMID:Endocrine regulation of calcium homeostasis during pregnancy. 636 Apr 69

The influence of changes in the serum calcium concentration on TSH secretion was evaluated in patients with primary hyperparathyroidism and idiopathic hypoparathyroidism and in normal subjects. Serum calcium concentrations were 12.7 +/- 0.8, 9.0 +/- 0.4, and 5.7 +/- 0.5 mg/100 ml in hyperparathyroid, normal, and hypoparathyroid subjects, respectively, and were significantly different from each other. Serum T3 and T4 concentrations were comparable among the three groups. The basal serum TSH concentration was highest in hypoparathyroid, lowest in hyperparathyroid, and intermediate in normal subjects. However, all values were within normal limits and were not significantly different from each other. TRH-stimulated TSH secretion was significantly greater in hypoparathyroid patients and significantly less in hyperparathyroid patients than in normal subjects, respectively. The TSH response to TRH was normalized when the serum calcium concentration was normalized by parathyroidectomy in a hyperparathyroid patient or by 1 alpha-hydroxyvitamin D3 administration in a hypoparathyroid patient. To further clarify the mechanism responsible for the modified TSH response to TRH in the hypercalcemic state, rats were made chronically hypercalcemic by the administration of 1 alpha-hydroxyvitamin D3 (0.2 micrograms/100 g BW, ip, for 10 days) and 3% calcium chloride in drinking water. The pituitary TSH content of hypercalcemic rats was significantly greater than that of control rats. The results suggest that decreased TSH secretion produced by chronic hypercalcemia is due to diminished TSH release, rather than to decreased pituitary TSH reserve.
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PMID:Thyrotropin secretion in patients with hyperparathyroidism or hypoparathyroidism: effect of serum calcium on thyrotropin release. 640 63

Treatment of hypoparathyroidism usually requires the use of pharmacological doses of parent vitamin D or near physiological amounts of the hydroxylated metabolites, calcitriol or alphacalcidol. Vitamin D intoxication and hypercalcaemia may be a problem but can be minimised by the use of small doses of vitamin D or its metabolites combined with large amounts of oral calcium. The response to treatment can be easily monitored by measuring serum and urinary calcium and creatinine concentrations. This allows the derivation of two simple indices reflecting calcium load presented to the kidney (calcium excretion in mmol/l glomerular filtrate) and renal tubular calcium reabsorption (TmCa/GFR). These can be used to predict the requirement of calcium supplements and also identify those patients at particular risk of hypercalcaemia.
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PMID:Renal handling of calcium in hypoparathyroidism. 641 28

A patient with familial hypocalciuric hypercalcaemia (FHH) is reported. Seven years after total parathyroidectomy he remained hypocalcaemic, with biochemical evidence of hypoparathyroidism (enhanced renal tubular reabsorption of phosphate, low nephrogenic cyclic AMP excretion, and reduced serum concentration of 1,25-dihydroxycholecalciferol in the presence of normal renal function and normal serum 25-hydroxyvitamin D levels). Iv infusions of calcium were given before and 6 years after total parathyroidectomy. The renal tubular reabsorption of calcium was compared in these two situations. No difference was found. Before and after parathyroidectomy there was enhanced renal tubular reabsorption of calcium. It is concluded that the enhanced renal tubular reabsorption of calcium in FHH is independent of parathyroid hormone. Total parathyroidectomy corrects the hypercalcaemia in FHH by a reduction in the input of calcium into the extra-cellular fluid from gut and or bone perhaps as a result of reduced renal synthesis of 1,25-dihydroxycholecalciferol.
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PMID:Familial hypocalciuric hypercalcaemia: evidence for continued enhanced renal tubular reabsorption of calcium following total parathyroidectomy. 647 56

Primary hyperparathyroidism during pregnancy is associated with significant risk of fetal loss and neonatal and maternal morbidity. Neonatal hypocalcemia probably results from transient hypoparathyroidism consequent to abnormal suppression by fetal hypercalcemia. Loss of the protective effect provided by the placental calcium transport mechanism produces significant maternal risk for development of acute hypercalcemia and possible crisis immediately postpartum. Management of maternal primary hyperparathyroidism diagnosed during pregnancy should be based on the patient's symptoms, severity of the disease, and gestational age of the fetus. Patients without symptoms and those with mild hypercalcemia may be managed effectively and safely for a short time with oral phosphate therapy, postponing operation until after delivery. More severe disease characterized by progressive symptoms and inadequately controlled hypercalcemia should be treated surgically after control of hypercalcemia has been achieved with diuretic and/or other medical therapy. Maternal operative morbidity is low and risk to the fetus is slight once organogenesis has been completed. Maternal parathyroidectomy should be performed preferably after the first trimester and should not be deferred unless delivery is imminent.
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PMID:Primary hyperparathyroidism during pregnancy. 650 64

The records of 400 patients operated on for primary hyperparathyroidism during 10 years were reviewed. Seventy-three per cent of the patients were women. The mean age at operation was 58 years. Renal stones was the main indication for surgery in 52 per cent of the men, but only in 17 per cent of the women. Forty-four per cent of the women and 22 per cent of the men had neuromuscular symptoms. Fifteen per cent of the patients were asymptomatic. Hypercalcemia was moderate in most cases with mean S-Ca less than 3.0 mmol/l in 80 per cent. A conservative surgical approach with microscopical identification of one or two glands only was used in 2/3 of the cases. Subtotal parathyroidectomy was performed in less than 10 per cent. Single adenoma was found in 70 per cent, double adenomas in 4 per cent, hyperplasia in 17 per cent and cancer in 1 per cent. The outcome of the operation was normocalcemia in 86 per cent. Seven per cent had persistent hypercalcemia. Seven per cent were hypoparathyroid and had to take calcium or vitamin D to be normocalcemic. The frequency of hypoparathyroidism was highest in the group of patients where all four parathyroid glands had been biopsied during the operation. The results support a conservative surgical strategy with careful bilateral exploration without biopsy of all four glands.
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PMID:Surgery for primary hyperparathyroidism. Experience with 400 patients during 10 years (1972-1981). 659 66

Three cases of metastatic carcinoma of the breast are described in patients who presented with hypercalcaemia. They achieved an excellent regression of their disease with combination chemotherapy but despite this they clinically deteriorated. Investigation showed them to be hypocalcaemic due to temporary hypoparathyroidism. Correction of their serum calcium resulted in good symptomatic relief. The possible mechanisms for these changes are discussed and we feel that this unusual complication of successful chemotherapy should be remembered when patients fail to improve symptomatically despite a good disease response.
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PMID:Hypocalcaemia--an unusual complication of successful chemotherapy for metastatic breast cancer. 666 56


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