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Query: UMLS:C0221002 (primary hyperparathyroidism)
 4,921 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In a recent series of 110 cases of primary hyperparathyroidism, estimations of plasma immuno-parathormone (PTH) were carried out in fifty two patients. This estimation proved reliable, making possible the confirmation of the diagnosis. In the absence of renal insufficiency, there was a highly positive relationship between PTH levels and plasma calcium. The relationship between PTH and the weight of the parathyroid tumour was less significant. For technical reasons, this long and difficult estimation cannot be used on a routine basis. However, it is most useful in cases in which other laboratory findings are not typical.
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PMID:[The estimation of parathormone in primary hyperparathyroidism (author's transl)]. 66 96

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

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

In normocalciuric and in hypercalciuric renal stone formers tubular calcium reabsorption (TRCa) was studied before and during an intravenous calcium infusion. In addition two patients with proven primary hyperparathyroidism (pHPT) were studied. TRCa was decreased in hypercalciuric stone formers whereas an increase was noted both in pHPT and in normocalciuric subjects. It is concluded that normocalciuric nephrolithiasis may be a manifestation of mild and/or early pHPT.
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PMID:[Normocalcemic nephrolithiasis and primary hyperparathyroidism]. 70 Oct 62

Glucose-induced insulin secretion was studied in ten patients with primary hyperparathyroidism and two with idiopathic hypoparathyroidism both before and after treatment. In each individual, insulin secretion during an intravenous glucose tolerance test was greater when the plasma calcium was higher. No consistent change in insulin secretion with plasma calcium concentration was observed during an oral glucose tolerance test. These findings could be explained by the suggestion that insulin secretion provoked by orally administered glucose is enhanced by gut hormones which may stimulate insulin secretion by a mechanism independent of extracellular calcium.
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PMID:Glucose-induced insulin secretion in patients with parathyroid disorders. 70 99

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

Here we report a highly sensitive and convenient ligand binding assay for the determination of 1,25(OH)2D3 in small volumes of human plasma. This method involves: (1) extraction of vitamin D3 and its metabolites using methanol-methylene chloride with separation of phases by centrifugation; (2) gel chromatography and high pressure liquid chromatography for the quantitative isolation of 1,25-(OH)2D3; and (3) a sensitive ligand binding assay for 1,25-(OH)2D3 employing cytosol receptor from the intestinal mucosa of rachitic chicks. Using modified rachitogenic chick diets allows early (less than 4 wks) harvesting of active receptor for 1,25-(OH)2D3 in high yield. The method includes a rapid and effective procedure for stable and long-term storage of the active cytosol receptor. A convenient dextran-charcoal means is used for the separation of receptor bound from free 1,25-(OH)2D3 resulting in the achievement of a lower (less than 5%) background (i.e., nonspecific binding) than reported for other 1,25-(OH)2D3 assays. Analysis of this receptor shows it to be a saturable, single class of binding sites with a dissociation constant (Kd) of approximately 3.7 x 10-11. The final recovery of 1,25-(OH)2D3 following extraction and chromatography is 80 +/- 3% and triplicate determinations can be made on a 3 ml plasma sample. The ligand binding assay routinely detects less than or equal to 5pg of 1,25-(OH)2D3 per assay tube and the inter- and intraassay variation, based on repeated determinations of 1,25-(OH)2D3 in pooled normal human plasma, is less than 5%. Preliminary studies indicate that our methodology will permit measurement of plasma 1,25-(OH)2D3 levels in all normal subjects and in pathophysiologic states where 1,25-(OH)2D3 levels may be below or above normal values. 1,25-(OH)2D3 values (pg/ml +/- SEM) in human plasma obtained from both normals and patients with various untreated calcium homeostatic disorders were: normals = 33.5 +/- 1.8; end-stage chronic renal failure = 5.1 +/- 1.2; primary hypoparathyroidism = 18.3 +/- 2.8; primary hyperparathyroidism = 61.4 +/- 7.1; and hyperthyroidism with associated hypercalcemia = 42.1 +/- 8.4.
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PMID:An improved method for the measurement of 1,25-(OH)2D3 in human plasma. 75 33

In hypercalcemic patients with primary hyperparathyroidism who were fasted over a prolonged period, alcohol ingestion induced a significant fall in glucose whereas insulin remained unchanged. The hypercalcemic patients thereby differed from normocalcemic subjects, who showed a significant decline in both glucose and insulin when alcohol was ingested after a prolonged period of fasting. An increased uptake of calcium into the beta-cells appears to have been a prerequisite for the occurrence of an unchanged insulin secretion during alcohol hypoglycemia in hypercalcemic patients, since a calcium-blocking agent, verapamil, infused intravenously during and after alcohol ingestion, brought about a normalization of the insulin response to alcohol hypoglycemia in such patients.
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PMID:Effect of verapamil on insulin response to alcohol hypoglycemia in patients with primary hyperparathyroidism. 75 47


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