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

The TmMg and renal Mg threshold were assessed in normal subjects and in a number of pathological conditions. The TmMg in normal subjects was 1.4 mg/100 ml glomerular filtrate (GF) 1.73 m2 and numerically equalled the renal Mg threshold of 1.4 mg/100 ml. No significant difference was seen in patients with primary hyperparathyroidism or hypoparathyroidism. Patients with familial hypocalciuric hypercalcemia, however, tended to have an elevated renal Mg threshold. Investigation of 3 patients with idiopathic renal Mg wasting demonstrated a normal TmMg but reduced renal Mg threshold. Urinary Mg excretion was also assessed in normomagnesemic alcoholic patients. Retention of a parenterally administered Mg load and renal Mg retention were significantly greater than normal despite normal serum Mg concentrations. These data suggest that determination of TmMg and renal Mg threshold may provide useful information in understanding Mg homeostasis in normal subjects and in disorders which may result in abnormal Mg metabolism.
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PMID:TmMg and renal Mg threshold in normal man and in certain pathophysiologic conditions. 380 21

Two children with congenital hypoparathyroidism and two children with pseudohypoparathyroidism were given maintenance doses of 15 to 45 ng/kg/day 1,25-dihydroxyvitamin D3 for a total of 255 months. The urinary calcium excretion showed an upward elevation after the first 2 years of treatment but was not significantly higher than that in 10 normal control subjects. The renal threshold for phosphate excretion stayed within the normal ranges compared with control values. Two hypercalcemic and two hypocalcemic episodes occurred during this period of treatment. Hypercalcemia was reversed within 1 week after withdrawal of 1,25-dihydroxyvitamin D3. Hypocalcemia was countered by increasing the dose of 1,25-dihydroxyvitamin D3. Renal functions were not adversely affected, as estimated by creatinine clearance and reciprocals of serum creatinine concentrations. The mean serum calcium concentration during 1,25-dihydroxyvitamin D3 treatment was significantly higher (P = 0.001) compared with that obtained during vitamin D2 treatment at a dose of 500 to 3000 IU/kg/day. These data provide additional support for the long-term use of 1,25-dihydroxyvitamin D3 in idiopathic hypoparathyroidism and pseudohypoparathyroidism.
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PMID:Calcium and phosphate metabolism in children with idiopathic hypoparathyroidism or pseudohypoparathyroidism: effects of 1,25-dihydroxyvitamin D3. 383 46

Autosomal dominant familial hypocalciuric hypercalcemia was found in a kindred with neonatal severe primary hyperparathyroidism, previously judged to be an autosomal recessive trait. Mild hypercalcemia was documented in eight members representing three generations. Mild hypercalcemia was documented at an age as early as one week. In seven adults presumed to be heterozygotes, urinary calcium levels were in the same range as for familial hypocalciuric hypercalcemia. An additional adult member (who previously underwent parathyroidectomy for neonatal severe primary hyperparathyroidism) showed an abnormality in renal clearance of calcium and sodium characteristic of combined familial hypocalciuric hypercalcemia and surgical hypoparathyroidism. Parathyroidectomy in three hypercalcemic members did not cause normocalcemia. Unlike other kindreds with familial hypocalciuric hypercalcemia in whom hypercalcemia is consistent over time and moderate in heterozygotes, this kindred was characterized by heterozygotes showing hypercalcemia that was intermittent and mild. The consanguineous parents of the two previously described severely affected neonates were judged to be heterozygotes for familial hypocalciuric hypercalcemia. In conclusion, (1) a gene presenting as familial hypocalciuric hypercalcemia can be expressed as hypercalcemia that is intermittent and very mild in heterozygotes; (2) such a gene can cause neonatal severe primary hyperparathyroidism in homozygotes.
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PMID:Familial hypocalciuric hypercalcemia. Mild expression of the gene in heterozygotes and severe expression in homozygotes. 396 79

An adenylate cyclase bioassay for parathyroid hormone (PTH) was evaluated in peripheral sera of ten normal subjects, 15 patients with various types of hypoparathyroidism, nine patients with malignancy-associated hypercalcaemia and 60 patients with primary or secondary hyperparathyroidism. The lower limit of detectability was 150 pg/ml in terms of synthetic human PTH (1-34). PTH-like bioactivity was not detected in normal subjects, in patients with surgical hypoparathyroidism, in patients with idiopathic hypoparathyroidism or in patients with malignancy-associated hypercalcaemia. Serum from one untreated pseudohypoparathyroid patient consistently contained PTH-like bioactivity. Bioactivity was detected in sera from 50% of patients with primary or secondary hyperparathyroidism. In two patients with secondary hyperparathyroidism calcium infusions suppressed this activity within 5 min. Both in primary and in secondary hyperparathyroidism there was a significant positive correlation between levels of PTH-like bioactivity, PTH immunoreactivity and the histological severity of the disease.
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PMID:An adenylate cyclase bioassay for parathyroid hormone: some clinical experiences. 397 62

The extent and result of surgery in 39 cases of nonfamilial primary parathyroid hyperplasia followed from 2 to 20 years are reported. Thirteen patients had been subjected to subtotal parathyroidectomy leaving no gland intact, while 26 had undergone less extensive surgery leaving at least one grossly normal or near-normal gland intact without biopsy. In the former group two patients (15%) developed permanent hypoparathyroidism requiring vitamin D treatment. In the latter group there were two patients (8%) with persistent hypercalcemia, which might have been avoided with a subtotal parathyroidectomy. Judging from these results, we believe that an individualized surgical approach is justifiable in nonfamilial primary parathyroid hyperplasia. Subtotal parathyroidectomy, leaving no gland intact, is advocated as the method of choice only when all four glands are enlarged. If one or more glands are grossly normal or near normal, factors such as degree of hypercalcemia, symptoms, age, general condition, and life expectancy should be taken into consideration when the extent of the operation is decided. A more conservative operation leaving at least one grossly normal gland intact without biopsy appears to be sufficient for cure in most of these cases and minimizes the risk for development of permanent hypoparathyroidism.
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PMID:Surgical strategy in nonfamilial primary parathyroid hyperplasia: long-term follow-up of thirty-nine cases. 399 79

334 patients were operated on for PHPT during the years 1956-79. A follow-up study of the material was performed during the years 1980-82 and it included 289 patients. The material was divided into single adenoma (SA) and multiglandular disease (MGD) cases. The initial diagnosis of SA given by the primary operation was later changed in 12 patients (4%) by reoperations performed for persistent or recurrent hypercalcaemia; the follow-up study changed the diagnosis in four patients. The proportion of MGD in the follow-up material was 15.2%. Reoperations were performed in 4% in the SA group and in 29% in the MGD group. The primary results concerning the serum calcium level were good in both SA and MGD groups, but, at the follow-up study 1.6% of the patients in the SA group and 41% of the patients in the MGD group were hypercalcaemic (serum calcium over 2.65 mmol/l). The hypercalcaemia at the follow-up study was, however, slight in general (mean 2.75 +/- 0.09 mmol/l). In the whole material, permanent hypoparathyroidism occurred in 1.2%, permanent unilateral vocal cord paralysis in 0.9% and permanent bilateral vocal cord paralysis in 0.6%. Operative mortality was 0.9%. The "conservative" strategy used in the whole material gave good results in SA patients but considerably worse results in MGD patients. Accordingly, MGD patients should be operated more "radically".
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PMID:Observations on 334 patients operated on for primary hyperparathyroidism. 402 77

Urinary excretion of cyclic adenosine 3',5'-monophosphate (3',5'-AMP) was tested in normal subjects and patients with pseudohypoparathyroidism, idiopathic hypoparathyroidism, surgical hypoparathyroidism, and pseudopseudohypoparathyroidism under basal conditions and after a 15 min infusion of purified parathyroid hormone. Basal excretion of the nucleotide was less than normal in the patients with hypocalcemic disorders and greater than normal in pseudopseudohypoparathyroidism. Parathyroid hormone caused a marked increase in excretion of 3',5'-AMP in all subjects except those with pseudohypoparathyroidism; nine patients with this disorder did not respond to the hormone and four showed a markedly deficient response. Radioimmunoassay showed that parathyroid hormone circulated in increased amounts in plasma from patients with pseudohypoparathyroidism and became undetectable when serum calcium was increased above 12 mg/100 ml. Suppression of parathyroid hormone secretion by induction of hypercalcemia did not alter the deficient response to exogenous hormone. The results indicate that: (a) parathyroid hormone circulates in abnormally high concentrations in pseudohypoparathyroidism and secretion of the hormone responds normally to physiological control by calcium; (b) testing urinary excretion of 3',5'-AMP in response to infusion of purified parathyroid hormone appears to be an accurate and sensitive index for establishing the diagnosis of pseudohypoparathyroidism; and (c) the metabolic defect of the disorder can be accounted for by a lack of or defective form of parathyroid hormone-sensitive adenyl cyclase in bone and kidney.
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PMID:Pseudohypoparathyroidism: defective excretion of 3',5'-AMP in response to parathyroid hormone. 430 2

A procedure for bioassaying parathyroid hormone-like activity in human urine has been developed. 24-hr urine samples were concentrated with dry Sephadex G-25 and bioassayed in the young thyroparathyrocauterized mouse by the measurement of whole blood calcium. Recovery of biological activity and radioiodinated beef parathyroid hormone was over 80%. Normal subjects usually excreted less than 30 U (USP) of activity per day while 18 patients with proven primary hyperparathyroidism excreted a mean of 182 U/day (USP). The activity was not found in 7 patients with hypoparathyroidism or in 5 patients with carcinoma of the breast, but was present in 9 patients with uremia and in 5 with carcinoma of the lung and hypercalcemia.
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PMID:A study of urinary excretion of parathyroid hormone in man. 565 89

Hypercalcaemia developed in 21 patients due to vitamin-D poisoning; 2 were poisoned twice and 2 were poisoned three times. All patients had taken milligram doses of vitamin D, which for 5 patients was inappropriate. For the other 16 patients (mainly with hypoparathyroidism) milligram doses of vitamin D were appropriate; the patients were poisoned either early in therapy, trying to correct the plasma-calcium too quickly, or, later, because of failure to follow up patients properly. 2 patients died as a result of their intoxication. Constant vigilance is essential when patients are taking large doses of vitamin D.
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PMID:Vitamin-D poisoning: survey of causes in 21 patients with hypercalcaemia. 610 86

Between September 1975 and June 1980, 27 patients with primary hyperparathyroidism caused by multiple-gland disease underwent reoperative parathyroid surgery at the National Cancer Institute. In an effort to minimize persistence and recurrence we adopted a strategy of attempting total parathyroidectomy. Immediate autotransplantation was not performed, but rather tissue was assessed in vitro for suppressibility and was cryopreserved. Patients with prolonged postoperative hypoparathyroidism underwent autotransplantation with cryopreserved tissue. Of 26 surviving patients, 23 (88%) were cured of hypercalcemia. Although 13 had hypoparathyroidism at the time of discharge, 4 of these 13 no longer required calcium or vitamin D within 1 year. At follow-up 17 were normocalcemic without medication (14 without and 3 with autografts). Thirteen patients had four or five glands removed. Two of these remain hypercalcemic, and at follow-up nine were normocalcemic without medication (seven without and two with autografts). Patients with multiple-gland disease, even those undergoing total parathyroidectomy, remain at risk for persistent or recurrent hypercalcemia. Such patients do no inevitably acquire hypoparathyroidism, and normocalcemia in patients undergoing immediate autotransplantation need not be attributed to the autograft. Selective, deferred autotransplantation with cryopreserved tissue prevents confusion regarding the source of postoperative hypercalcemia should it occur, minimizes the risk of graft-dependent hypercalcemia by restricting autotransplantation to those truly in need of additional tissue, and can effectively manage hypoparathyroidism.
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PMID:Reoperative parathyroid surgery for primary hyperparathyroidism caused by multiple-gland disease: total parathyroidectomy and autotransplantation with cryopreserved tissue. 612 56


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