Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020437 (hypercalcemia)
 10,293 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A sensitive and simplified radioreceptor assay for 1, 25-dihydroxyvitamin D (1, 25-(OH)2D) in human plasma was described and applied to preliminary clinical studies. Tritium-labeled 1, 25-(OH)2D3 was produced by incubating chick kidney homogenate with tritium labeled 25-hydroxyvitamin D3 (25-OHD3). A cytosol receptor was obtained from rachitic chick intestine (Kd=5.3 X 10(-11) M). Lipids in 5 ml of heparinized human plasma were extracted with dichloromethane, and 1, 25-(OH)2D was isolated by a Sephadex LH-20 column followed by high pressure liquid column chromatography. Recovery of 1, 25-(OH)2D3 after the plasma extraction and chromatography ranged from 58 to 100%. The assay was sensitive to 5 pg/tube. Diluted plasma from a patient on a high dose of 1 alpha-OHD3 showed a dilution curve parallel to the standard curve. The cytosol receptor showed a cross reactivity to various vitamin D3 metabolites physiologically present in the circulation and it was thought to be essential to eliminate other vitamin D3 metabolites 1,25-(OH)2D from plasma samples by high pressure liquid chromatography. Plasma concentrations of 1, 25-(OH)2D were, in the case of most normal subjects, distributed from 7 to 33 pg/ml and the range of distribution became greater in relation to age, indicating that plasma values should be matched to age. Whereas markedly high values of 1, 25-(OH)2D in plasma were found in some cases of primary hyperparathyroidism with prominent bone resorption, relatively low values were seen in some patients with chronic renal failure, senile osteoporosis, osteomalacia and hypercalcemia due to bone metastasis.
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PMID:Competitive protein binding assay for 1,25-dihydroxy-vitamin D in human plasma. 74 68

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

Calcium enters the pancreatic juice from two sources, one fraction associated with enzyme protein and another small fraction presumably by diffusion. The calcium concentration in pancreatic juice is lower than in plasma. It decreases with high flow rates and increases asymptotically to plasma concentration with low rates. In chronic pancreatitis calcium concentration is raised in the secretin-stimulated juice. After pancreozymin in moderate chronic pancreatitis it is low but in severe stages of the disease it is high signalling total dissociation from the entrance of enzyme protein, which is very low in these cases. Hypercalcemia stimulates enzyme secretion in the pancreas, hypocalcemia inhibits it. Calcium is essential for intracellular processes associated with secretion, the exact place in the sequence of "stimulus-secretion-coupling" still being unknown. Calcitonin as one of the hormones which regulates calcium homeostasis, inhibits secretion of enzymes but not of fluid and bicarbonate. The action of the parathyroid hormone on the exocrine pancreas is unknown. In primary hyperparathyroidism with chronic hypercalcemia acute and chronic pancreatitis occur 10 to 20 times more frequently than in the general population. In acute pancreatitis of whatever origin hypocalcemia is atypical feature of the disease indicating bad prognosis. The mechanism of its development is still unclear. In chronic pancreatitis the forming of calcified stones in the ducts is typical in cases associated with alcoholism, with protein malnutrition and with primary hyperparathyroidism. But it occurs also in cases with unknown etiology signalling a more general pathophysiological phenomenon. The calcium salts form a precipitate on protein plugs in the juice, which have been observed even in early stages of the disease in the small and larger ducts of the gland.
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PMID:The role of calcium in pancreatic secretion and disease. 77 77

Tthe findings of 150 patients with proven primary hyperparathyroidism are reported. The purpose of the analysis was to find differences between the various clinical manifestations of the disease. Furthermore the occurrence of acute hyperparathyroid crisis in our series as well as in the literature are described. 65.8% of the patients were females, 34.2% were males. The leading symptom in 98 patients (group I) were kidney stones and in 23 patients (group II) cystic bone disease. Both manifestations of the disease occurred in only 7 patients (group III) and no symptoms related to the kidneys or to the bones occurred in 24 patients (group IV). Because of the difference of the clinical manifestations the additional data were analyzed for each group separately and compared with each other. There was no difference in the mean serum calcium levels for all four groups, however, patients of group I were on the average younger, the duration of the disease was longer and the weight of the parathyroid adenoma was lower compared to the other three groups. Data are presented regarding calcium excretion, phosphate clearance and tubular reabsorption of phosphate for each group. At operation single or multiple adenoma formation was present in 133 patients, whereas diffuse hyperplasia was found in 17 and carcinoma in 2 other patients. 46 of the adenomas were found in atypical anatomical localisation. This observation is responsible for the many unsuccessful or second explorations of the neck. The weight of the adenomas varied between 0.1 and 23.5 g. The most difficult diagnosis was that of diffuse hyperplasia. The success of the surgical intervention was usually established in over 80% of the cases within 24 to 48 hours after the operation with a significant fall of serum calcium. There is still no definite explanation for the variability of the clinical manifestations of primary hyperparathyroidism. Parathyroid hormone determinations on larger numbers of patients are not yet published. The assumption, that different hormones or peptide fragments are responsible for the different action on bone and kidney is discussed. In our series of 152 patients acute hyperparathyroid crisis occurred eight times. Our findings are compared to the other well documented cases in the literature. Main symptoms were nausea, vomiting abdominal pain and different states of cerebral dysfunction. Most of the patients had calcium levels over 16 mg/100 ml. Partial renal insufficiency with elevated blood urea and phosphate retention was found in ov er 50% of the cases. Overall mortality of all cases with acute parathyroid crisis is 52.5%. The pathogenesis of acute hyperparathyroidism and the implications of high calcium levels are discussed. According to our own experience hypercalcemia can be controlled with an intensive therapeutic program and emergency operation for acute parathyroid crisis is no longer necessary.
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PMID:[Primary hyperparathyroidism. An analysis of 152 patients with special references to acute life threatening complications (acute hyperparathyroidism)]. 79 28

The concentration of calcium in the pancreatic juice is lower than in plasma. Two calcium fractions occur in the juice, the one associated with the enzyme protein and the other entering the juice via diffusion. In chronic pancreatitis the calcium concentration of the juice is increased in post-secretin periods. Hypercalcemia stimulates enzyme secretion and elevates calcium concentration in the juice. Hypocalcemia inhibits secretion of enzymes and fluid. Calcium is an important mediator substance for the secretion of pancreatic hydrolases at the intracellular level. In primary hyperparathyroidism with chronic hypercalcemia the prevalence of acute and chronic pancreatitis is 10--12 times higher than in normal population. In chronic pancreatitis caused by alcoholism, primary hyperparathyroidism, and chronic protein deficiency without alcoholism calcifying duct stones are seen in the pancreas in high frequency.
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PMID:[Calcium, pancreatic secretion and pancreatitis (author's transl)]. 82 62

Data were reviewed on 26 patients suffering from primary hyperparathyroidism (PHPT). The diagnosis of PHPT is increasing in frequency, due to greater awareness and better methods of detection. Delay in recognition has gradually decreased, thus permitting earlier treatment. No single test or any combination of tests can be considered satisfactorily pathognomonic of PHPT. Hypercalcemia is the most satisfactory finding suggestive of PHPT. Cervical exploration should be an integral part of the diagnostic work-up. Removal of a distinct adenoma is adequate therapy if the other parathyroid glands are normal. Subtotal parathyroidectomy should be performed only in cases of hyperplasia of all parathyroid glands.
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PMID:Surgery in primary hyperparathyroidism. 83 57

The first case of primary hyperparathyroidism associated with renal cell carcinoma, nasopharynx carcinoma and thyroid carcinoma is reported. Selective venous sampling with radioimmunoassays for parathyroid hormone was helpful in the differentiation of primary hyperparathyroidism from hypercalcemia associated with malignancy.
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PMID:Primary hyperparathyroidism with triple cancers consisting of renal cell carcinoma, nasopharynx carcinoma and thyroid carcinoma. 83 5

A hypercalcemia syndrom in the case of a 63 year old female patient is reported on, who simultaneously suffered from hyperthyroidism and suspected primary hyperparathyroidism. During autopsy an ectopic (ventral mediastinum) parathyroid adenoma and a gall bladder carcinoma were discovered. Each of these three diseases can induce hypercalcemia by themselves.
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PMID:[Syndrom of hypercalcemia in a case of hyperthyroidism, primary hyperparathyroidism and cancer of the gall-bladder (author's transl)]. 85 80

Analysis of a series of 200 surgically treated cases of primary hyperparathyroidism was carried out in an effort to identify not only the changing clinical patterns and improved diagnostic methods but also to assess the long term results of our conventional operative methods in light of recent reports of a high incidence of diffuse hyperplasia and a high recurrence rate when surgery is restricted to removal of the adenoma. As reported by others the "chemical diagnosis" of primary hyperparathyroidism, the clinical setting in which unsuspected hypercalcemia is demonstrated on routine blood analysis, accounts for the majority of diagnoses today. Impending or actual "parathyroid crisis" has been observed with alarming frequency. The use of the thiazide challenge test provides a useful diagnostic aid in many instances. The incidence of diffuse hyperplasia was 6% in this series while an adenoma was present in 88%. No instance of recurrence was observed in either the cases of adenomas or diffuse hyperplasia.
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PMID:The surgical treatment of primary hyperparathyroidism: a 20 year experience. 85 73

Patients with breast cancer and bone destruction were found to have a pattern of calcium metabolism which was broadly similar to that found in other malignancies, but different from that in primary hyperparathyroidism. Thus, they tended to have reduced absorption of calcium from the intestine, elevated endogenous faecal calcium and normal or reduced urinary cyclic AMP excretion. Since prostaglandin synthetase inhibitors have been shown to inhibit breast cancer-induced osteolysis in vitro we have attempted to reduce bone destruction and serum calcium in patients with hypercalcaemia complicating breast cancer using these agents. High doses failed to reduce the serum calcium or the urinary hydroxyproline: creatinine ratio in ten patients with skeletal metastases, four of whom had hypercalcaemia.
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PMID:Calcium metabolism in breast cancer. 87 Sep 1


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