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

We studied long-term morbidity after parathyroid surgery for primary hyperparathyroidism in 100 patients and compared it with the long-term morbidity of medical follow-up from the literature. The surgical treatment of primary hyperparathyroidism was associated with negative results of neck explorations, persistent hypercalcemia, recurrent hypercalcemia, permanent hypoparathyroidism, or recurrent laryngeal nerve damage in 13 (19%) of 68 patients followed up for five years postoperatively. A review of medical follow-up as reported in the literature showed progression of disease in 8% to 22% of patients followed up for five to ten years. There was no convincing evidence that mild primary hyperparathyroidism resulted in progressive osteoporosis or renal failure. Furthermore, no significant improvement in hypertension, peptic ulcer disease, or renal function followed successful parathyroid surgery. Unless future studies demonstrate progressive osteoporosis or renal damage in untreated, mild primary hyperparathyroidism, medical follow-up is a reasonable alternative to surgery in the compliant patient over 50 years of age.
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PMID:Primary hyperparathyroidism. A review of the long-term surgical and nonsurgical morbidities as a basis for a rational approach to treatment. 270 30

Eighty-three patients undergoing reoperations for hyperparathyroidism were studied. Preoperative diagnosis was reviewed, and localization was employed in selected patients. Cervical reexploration was carried out in a systematic manner, and mediastinotomy was required in 11 patients. Sixty patients had had previous parathyroid exploration. Missed adenomas were found in 34, of which 28 were single and 6 were double adenomas. Fourteen single adenomas were in normal locations and 14 were in ectopic locations. Seventeen patients had hyperplasia; 6 were wrongly diagnosed as adenoma, 3 had inadequate excision, 2 had supernumerary glands, and 6 had remnant hypertrophy. Three patients had recurrent carcinoma. Two had wrong diagnoses and 4 had uncertain diagnoses. Reoperation eliminated hypercalcemia in 71 patients (85.5%). Eight patients developed permanent hypoparathyroidism, and 1 had a permanent recurrent nerve palsy. Reoperative parathyroid surgery can be minimized with thorough initial cervical exploration, correct pathologic interpretation, and adequate parathyroid resection.
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PMID:Strategy in reoperative surgery for hyperparathyroidism. 273 Mar 18

The "N-tact" immunoradiometric assay (IRMA) from INCSTAR for parathyrin (PTH) in serum involves a 125I-labeled affinity-purified antiserum to PTH 1-34 and an affinity-purified antiserum to PTH 39-84, the latter bound to a polystyrene bead. The mean detection limit, determined in six consecutive assays, was 4 ng/L. The within-batch CV was less than 7% in the range 15 to 2135 ng/L. The between-batch CV was 11.7% and 5.3% at 30 and 371 ng/L, respectively. Serum PTH in 14 proven cases of primary hyperparathyroidism was 49-808 (median 111) ng/L, undetectable (less than 5 ng/L) in 10 cases of primary hypoparathyroidism and in 10 cases of hypercalcemia associated with malignancy, compared with 7-39 ng/L in 45 normal subjects. PTH was 9 to 19 ng/L in four patients with familial benign hypercalcemia. In 39 patients with renal failure, apparent concentrations were 14 to 857 (median 133) ng/L, but sera from these patients pre-diluted with zero standard did not parallel dilutions of the standard, PTH 1-84. PTH concentrations were not significantly decreased in blood or serum kept at 20 degrees C for up to 6 h. After successful removal of a parathyroid adenoma, the mean half-time for disappearance of PTH in vivo in five hyperparathyroid patients was 3.3 min.
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PMID:Performance and diagnostic application of a two-site immunoradiometric assay for parathyrin in serum. 277 25

The synthetic amino-terminal fragment of PTH, PTH-(1-34), was recently released for clinical testing of PTH responsiveness. We measured the urinary cAMP and phosphaturic responses to infusion of PTH-(1-34) [3U/kg BW (200 U maximum), iv in 10 min] in patients with pseudohypoparathyroidism and idiopathic hypoparathyroidism, as well as normal subjects. The protocol used data from 5 30-min urine collections and 4 blood samples. Based on the results in 7 patients with pseudohypoparathyroidism (hypocalcemia with increased serum immunoreactive PTH concentrations), 2 patients with suspected pseudohypoparathyroidism, 9 patients with surgical hypoparathyroidism, and 10 normal subjects, this testing protocol differentiated well among these conditions. The patients with pseudohypoparathyroidism had blunted cAMP and phosphaturic responses to PTH-(1-34) administration compared to those of either normal or hypoparathyroid subjects. Induced hypercalcemia failed to restore a normal cAMP response to PTH-(1-34) infusion in 2 patients with pseudohypoparathyroidism. Calculation of the cAMP response to PTH-(1-34) as nanomoles per dL glomerular filtrate during the first 30 min after infusion provided better differentiation among groups than other parameters of cAMP metabolism. Calculating the phosphaturic response as the percent fall in tubular maximum for phosphate reabsorption during the first hour after infusion gave the best degree of statistical separation among groups. We conclude that this new diagnostic agent is effective for the study of renal responsiveness to PTH, and that the protocol described here reliably differentiates patients with pseudohypoparathyroidism from those with hypocalcemia due to other causes.
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PMID:Synthetic human parathyroid hormone-(1-34) for the study of pseudohypoparathyroidism. 284 29

Reoperation for persistent or recurrent primary hyperparathyroidism immediately connotes a complex clinical management problem. Successful cure of hypercalcemia is less frequent whereas complications are more common compared to initial explorations. Of 212 patients operated on at the Mayo Clinic from 1978 through 1986, 189 (89%) were cured. Sporadic disease, multiple endocrine neoplasia, and familial hyperparathyroidism were found in 183 (87%), 20 (9%), and 9 (4%) patients, respectively. Prior to the most recent reoperation, these patients had undergone from one to five operations. Preoperative localization examinations were performed in 192 patients (91%). Cervical high-resolution, real-time ultrasonography, computed tomography, and thallium-technetium scintigraphy had sensitivity rates of 87%, 56%, and 71%, respectively. When the tumor was localized preoperatively, the operative time and cost were significantly reduced compared to nonlocalized tumors. Cervical reexploration only was required in 154 (72%), combined cervical and mediastinal exploration occurred in 46 (22%), and mediastinal exploration only was performed in 12 (6%). There was no perioperative mortality; permanent hypoparathyroidism developed in 33 patients (16%), and six patients (2.9%) suffered permanent unilateral vocal cord paralysis. Anatomically, the most frequent site to find a missed parathyroid adenoma was in the normal location. The large majority of these glands were removed through a cervical incision although, on occasion, they were retracted from the anterior superior mediastinum or the low tracheoesophageal space. These data confirm that reoperative parathyroid surgery can be performed safely, with a rather high degree of success, but too-frequently results in a lifetime morbidity of hypoparathyroidism.
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PMID:Reoperative parathyroid surgery. 290 May 81

The abnormalities of calcium-phosphorum metabolism observed in hyperthyroidism (tendency to hypercalcaemia with subsequent functional hypoparathyroidism, increase in serum alkaline phosphatase and in hydroxyprolinuria) essentially result from excessive mobilization of bone calcium and phosphates by the thyroid hormones themselves. Histomorphometric studies have shown that the skeletal repercussions of hyperthyroidism are almost constant. There is, in particular, excessive bone remodelling due to increased bone-forming and bone-resorbing cellular activities. However, since bone resorption is quantitatively more stimulated than bone formation, the physiological bone loss is accelerated and is only partly repaired by re-establishment of the normal thyroid function.
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PMID:[Phospho-calcium and bone metabolism in hyperthyroidism in adults]. 293 96

Calcium ion is one of the factors which modulate erythrocyte deformability. It is known that calciotropic hormones such as calcitonin (CT) and parathyroid hormone (PTH) exert hypocalcemizing and hypercalcemizing effects, respectively. Their action is mediated, at the level of their target cells, through adenylcyclase activation with the production of cyclic 3,5-adenosinmonophosphate (cAMP). Modifications of transmembrane calcium fluxes have been described and were attributed to these hormones. Erythrocyte deformability has been evaluated by Dormandy method of red blood cell filtration in hypocalcemic patients affected by hypoparathyroidism, in patients with hypercalcemia due to malignancy or primary hyperparathyroidism and in normal age- and sex-matched subjects. Erythrocyte filtration values resulted to be significantly increased with respect to normal values in hypercalcemic patients and at the lower limits of normality in hypocalcemic subjects. Subsequently, acute studies were performed in normal volunteers in whom venous infusions of synthetic salmon calcitonin determined a significant reduction of erythrocyte filtration values, whereas venous infusions of the 1-34 synthetic human PTH fragment induced a significant increase in filtration values of red blood cells. An infusion of a cAMP analogue, dibutyryl-cAMP, determined a slight reduction of erythrocyte filtration values. The calciotropic hormones influence erythrocyte deformability through mechanisms that are yet to be clarified.
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PMID:[Calcitonin, parathyroid hormones, calcium ion, cyclic 3,5-adenosine monophosphate (cAMP) and erythrocyte deformability]. 299 4

The diagnosis of primary hyperparathyroidism (PHP) depends increasingly on laboratory tests, since the majority of patients are elderly people without typical symptoms. A mean plasma calcium level close to the upper normal limit serves to diagnose hypercalcemia. To rule out malignant disease, the most common cause of hypercalcemia, measurement of plasma PTH is the most appropriate test. Determination of blood phosphorus, chloride, and alkaline phosphatase, and of urinary calcium and phosphorus, contribute to the investigation of the metabolic effects of the given disease but are not very useful for causal diagnosis. Urinary and nephrogenous cyclic AMP reflect PTH secretion but can be elevated in paraneoplastic hypercalcemia. Diagnosis of subtle forms of PHP by dynamic tests is largely of scientific interest, since they do not necessarily need treatment. The diagnosis of hypoparathyroidism is primarily clinical. PTH measurements rarely distinguish normal from low values. In severe hypocalcemia of non-parathyroid origin, plasma PTH is elevated (except in hypomagnesemia). In borderline cases, measurement of urinary cyclic AMP or of plasma PTH after attempted stimulation by EDTA infusion is helpful, especially in distinguishing between subtle hypoparathyroidism and tetany induced by hyperventilation.
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PMID:[Diagnostic tests in parathyroid diseases]. 300 36

1,25-Dihydroxyvitamin D (1,25-(OH)2D) plays a crucial role in the maintenance of blood calcium and phosphorus levels and in normal skeletal mineralization. The concentration of this metabolite in the blood is, by necessity, tightly regulated. The most important stimuli for renal 1,25-(OH)2D synthesis include parathyroid hormone (PTH), its second messenger cyclic adenosine monophosphate (cAMP) and phosphate deprivation. Hypocalcemia and calcitonin, initially thought to act via stimulation of PTH release, have now been shown to directly stimulate 1-hydroxylation. Estrogens also increase 1,25-(OH)2D production, probably by upregulating renal PTH receptors. Inhibitors of the renal 25-(OH)D 1 alpha-hydroxylase include 1,25-(OH)2D itself, hypercalcemia, and phosphate loading. The PTH-vitamin D axis as modulated by the serum ionized calcium level controls adaptation to alterations in dietary calcium and sodium intake and to changes in skeletal turnover based on the level of physical activity. Although normally the renal production of 1,25-(OH)2D is tightly regulated and changes little in response to vitamin D challenge, there are certain conditions in which 1,25-(OH)2D appears to be substrate-dependent. These include hypoparathyroidism, hyperparathyroidism, vitamin D deficiency, sarcoidosis and the anephric state, conditions in which PTH is not well-modulated by alterations in serum ionized calcium or in which extrarenal synthesis of 1,25-(OH)2D occurs. In several disorders, including absorptive hypercalciuria, pseudohypoparathyroidism, hypophosphatemic rickets, and tumoral calcinosis, the regulation of the renal 1 alpha-hydroxylase appears to be altered.
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PMID:Normal and abnormal regulation of 1,25-(OH)2D synthesis. 306 16

Mediastinal exploration by sternotomy was carried out 36 times in 35 patients with evidence of hyperparathyroidism amongst a group of 1,461 operations for hyperparathyroidism between 1962 and 1987. The exploration was indicated 30 times as re-operation for hyperparathyroidism persistent after one or more negative cervicotomy procedures or recurrent, and 6 times from the outset, (5 in a context of acute hypercalcemia). Exploration was positive 20 times (16 adenomas, 2 hyperplasias, 2 metastases of a parathyroid carcinoma), but negative 16 times (3 diagnostic errors, 6 cervical lesions discovered subsequently, 7 explorations totally negative). The site of mediastinal parathyroid lesions is usually intrathymic (13 cases) but may sometimes (3 cases) be in the middle mediastinum. Pre-operative investigation to identify the site of a possible mediastinal lesion, in re-operation surgery, remains unreliable, the best investigation in this series being thoracic CT scan with 63% true positives. Thallium-Technetium subtraction isotope scan, carried out once with a good result, should now have a place amongst investigations. The principal post-operative complication is hypoparathyroidism which can be prevented by cryopreservation of a fragment of the lesion for possible subsequent reimplantation. Mediastinal exploration is rarely indicated in hyperparathyroid surgery and should be undertaken only after meticulous cervical exploration.
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PMID:[Mediastinal exploration by sternotomy in surgery of hyperparathyroidism. 36 cases]. 306 94


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