Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0221002 (primary hyperparathyroidism)
 4,921 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A test was developed to diagnose various forms of hypercalciuria. A two-hour urine sample after an overnight fast and a four-hour urine sample after 1 g of calcium by mouth were tested for calcium, cyclic AMP and creatinine. The 24 patients with absorptive hypercalciuria had normocalcemia and normal fasting urinary calcium (less than 0.11 mg per milligram of urinary creatnine). Urinary calcium was high (greater than or equal to 0.2 mg per milligram of creatinine) after a calcium load. Of the 28 patients with primary hyperparathyroidism (resorptive hypercalciuria), 25 had hypercalcemia and 21 had high fasting urinary calcium. Urinary cyclic AMP, elevated in 30 per cent of fasting patients, was high (greater than 4.60 mu moles per gram of creatinine) in 82 per cent of cases after calcium load. Six patients with renal hypercalciuria had normocalcemia, high fasting urinary calcium, and high (greater than 6.86 mu moles per gram of creatinine) or high-normal fasting urinary cyclic AMP was normal. This simple test should facilitate the differentiation of various causes of hypercalciuria.
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PMID:A simple test for the diagnosis of absorptive, resorptive and renal hypercalciurias. 16 60

Responsiveness of urinary cyclic AMP and phosphate to 200 units of parathyroid extract was evaluated in 5 normal subjects, 2 patients with idiopathic hypoparathyroidism, 4 patients with pseudohypoparathyroidism and 3 patients with primary hyperparathyroidism. Among them, 3 patients with pseudohypoparathyroidism were examined prior to and during therapy with vitamin D. Two patients with primary hyperparathyroidism were examined before and after removal of adenomas. In control subjects, percent increase in cyclic AMP after parathyroid extract administration was 7265 plus or minus 3312%, and in phosphate 290 plus or minus 72%. It was found that in idiopathic hypoparathyroidism the response of cyclic AMP was in the normal range, though that of phosphate was higher than normal. In pseudohypoparathyroidism, as distinguished from what Drezner et al. called pseudohypoparathyroidism type II, the response of cyclic AMP was uniformly low, while that of phosphate was variable. Similar results were obtained during treatment with vitamin D. In primary hyperparathyroidism, the responses of both cyclic AMP and phosphate were lower than normal. After removal of adenomas, the response of phosphate became norma., but the response of cyclic AMP rose to a subnormal level in one patient, and remained low in the other. For the diagnosis of pseudohypoparathyroidism, the response in cyclic AMP was considered to be a more reliable index than that in phosphate whether the patient was being treated with vitamin D or not.
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PMID:Responsiveness of urinary cyclic AMP and phosphate to parathyroid extract in patients with parathyroid disorders. 16 73

Urinary adenosine 3' 5' - cyclic monophosphate (cyclic AMP) was assessed by a competitive protein binding method in 19 patients with primary hyperparathyroidism (PHPT) and in 15 control subjects. The mean value of 6.6 +/- S.E. 0-64 muM per 24 hours for the patients with PHPT was higher (P less than 0-001) than the mean control value of 3-2 +/- 0-24 muM per 24 hours. In all hypercalcaemic patients without renal insufficiency, urinary cyclic AMP excretion was more than 4 muM per 24 hours and decreased in the 15 patients investigated after parathyroidectomy. In a normocalcaemic hyperparathyroid patient and in three hyperparathyroid patients with renal insufficiency, urinary cyclic AMP was less than 4 muM per 24 hours.
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PMID:Urinary excretion of cyclic AMP in primary hyperparathyroidism. 16 78

Effects of parathyroidectomy on parathyroid function and calcium (Ca) metabolism were carefully evaluated in 6 patients with primary hyperparathyroidism without symptoms normally attributed to the disease and in 7 with bone disease or nephrolithiasis. Before parathyroidectomy, both groups of patients demonstrated evidence of the sequelae of parathyroid hormone (PTH) excess, since they presented one or more of the following features: low bone density by 125I-photon absorption, hypercalciuria (urinary Ca greater than 200 mg/day on an intake of 400 mg/day), negative Ca balance (absorbed Ca less than urinary Ca), elevated fasting urinary Ca greater than 0.2 mg/mg creatinine for a night-time sample after a 6-hour fast), and decreased renal function (creatinine clearance of less than 65 ml/min). Following parathyroidectomy, most of these deleterious effects were reversed commensurate with the return of immunoreactive serum PTH, serum Ca, and urinary cyclic AMP toward normal. These quantitative non-invasive techniques may be useful for the initial evaluation and follow-up of patients with asymptomatic primary hyperparathyroidism.
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PMID:Metabolic effects of parathyroidectomy in asymptomatic primary hyperparathyroidism. 17 69

1. Normal subjects showed a highly reproducible, rapid increase in plasma adenosine 3':5'-cyclic monophosphate (cyclic AMP) after an intravenous injection of 200 MRC units of highly purified bovine parathyroid hormone. 2. No significant increase in plasma cyclic AMP was observed after administration of bovine parathyroid hormone to patients with severe chronic renal failure. 3. Even when renal function was not impaired, some patients with primary hyperparathyroidism, who had high concentrations of endogenous parathyroid hormone, showed resistance to bovine parathyroid hormone and when this was injected intravenously it caused only a small increase in plasma cyclic AMP. This resistance was reversible since there was marked improvement in the response after parathyroidectomy, when endogenous parathyroid hormone concentration had fallen. 4. It was possible to reproduce this resistance to the hormone by intravenous infusion of bovine parathyroid hormone into normal subjects. When the hormone (1000 MRC units) was infused over 2 h, after an initial increase there was a progressive decline in plasma cyclic AMP concentration and a fall in urinary cyclic AMP excretion. The response to a standard test stimulus (200 MRC units of bovine parathyroid hormone given as a rapid intravenous injection) was examined at intervals after 1000 units of bovine parathyroid hormone had been infused. Initially, the response was severely impaired; at 4 h, partial recovery had occurred and, 24 h after the infusion, recovery of the response was complete. The resistance was therefore reversible. Infusion of the amino-terminal peptide, fragment 1-34, gave the same effect as infusion of intact hormone. Region-specific assays for the hormone were used to show that the concentration of immuno-assayable hormone remained high during the infusions. 5. The mechanism of this reversible resistance to parathyroid hormone remains to be elucidated; it seems unlikely that circulating hormone fragments could account for the prolonged impairment in the responsiveness to the intact hormone. It is possible that alteration in the formation, intracellular degradation or, perhaps, release of cyclic AMP from the cells, is the cause. Changes in the characteristics of the hormone receptor sites might also explain the phenomenon.
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PMID:Reversible resistance to the renal action of parathyroid hormone in man. 18 Nov 94

Daily urinary cyclic AMP (AMPcU) has been compared to pth plasma level and to bone resorption parameters in 44 cases of metabolic bone disease. In 14 cases of primary hyperparathyroidism, AMPcU was always increased likewise in 4 cases of osteomalacia with secondary hyperparathyroidism. On the whole series of cases a significant correlation has been found (1) between PTH plasma level and AMPcU and (2) between bone resporption surfaces and AMPcU. Conversely, no correlation between PTH and periosteocytic lacunae size, nor between AMPcU and periosteocytic lacunae has been found.
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PMID:[Relation between urinary cyclic AMP, PTH and histomorphometric resorption parameter. A study of 44 human iliac crest bone biopsies]. 18 20

To test the hypothesis that lithium is a general inhibitor of hormone-activated adenylate cyclase, we infuse parathyroid hormone (PTH) into human subjects prior to and during lithium carbonate administration. PTH infusion caused a significant increase in urinary cyclic AMP and urinary phosphate excretion. There was no significant difference in these responses in the lithium compared to the control period. In four patients with primary hyperparathyroidism, lithium had no significant effect on serum calcium or phosphate or on tubular reabsorption of phosphate. The data do not substantiate the hypothesis that lithium (at therapeutic concentrations) is a general inhibitor of hormonally-activated adenylate cyclase, nor do they support its potential clinical utility in primary hyperparthyroidism.
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PMID:Lithium does not inhibit the parathyroid hormone-mediated rise in urinary cyclic AMP and phosphate in humans. 18 15

Urinary cyclic AMP (UcAMP) appropriate for the serum calcium concentration was determined in normal subjects during the base-line state and during alteration in their serum calcium concentrations by saline and calcium infusions. This was compared to the UcAMP in 76 patients with hypercalcemia and 5 patients with hypocalcemia. In 54 of 56 patients with primary hyperparathyroidism, the UcAMP was inappropriately high for their serum calcium concentration, the 2 exceptions having renal failure. In four patients with vitamin D intoxication, sarcoidosis, milkalkali syndrome, and thiazide-induced hypercalcemia and in five patients with hypocalcemia due to hypoparathyroidism, the UcAMP was appropriately low for their serum calcium concentration. In 16 patients with nonparathyroid neoplasms, 10 had UcAMP levels that were inappropriately high suggesting ectopic parathyroid hormone (PTH)-mediated hypercalcemia and 6 had UcAMP levels that were appropriately low suggesting that their hypercalcemia was due to osteolytic factors other than PTH. Correlations between UcAMP, serum calcium concentration, and carboxyl-terminal immunoreactive PTH suggest that random UcAMP is a sensitive accurate reflection of circulating biologically active PTH. If there is adequate renal function (serum creatinine concentration less than 2.0 mg/dl), a random UcAMP expressed as mumol/g creatinine and analyzed as a function of the serum calcium concentration completely separates patients with PTH and non-PTH-mediated hypercalcemia.
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PMID:Urinary cyclic AMP analyzed as a function of the serum calcium and parathyroid hormone in the idfferential diagnosis of hypercalcemia. 18 21

Urinary cyclic AMP excretion per 24 h or per g creatinine in primary hyperparathyroidism (1 degrees HPT) has been evaluated by several authors with conflicting results. In 50 patients with 1 degrees HPT, 25 patients with secondary (2 degrees) HPT and 35 healthy control persons we determined urinary cyclic AMP per 24 h or per g creatinine. These parameters did not satisfactorily discriminate patients from controls, especially when glomerular filtration rate (GFR) as determined by creatinine clearance was reduced. Since urinary cyclic AMP is derived from plasma by glomerular filtration and from kidney by tubular production-the amount of tubules is reflected by GFR-the cyclic nucleotide was related to GFR. In controls urinary cyclic AMP correlated better with GFR than with creatinine excretion. Additionally, in 45 of 50 patients with 1 degrees HPT and in all with 2 degrees HPT, urinary cyclic AMP/GFR was raised. In 1 degrees HPT serum levels of parathyroid hormone correlated closer with urinary cyclic AMP/GFR than with urinary cyclic AMP/g creatinine. The ratio cyclic AMP/GFR decreased to normal or subnormal values after removal of adenomatous or hyperplastic glands in 1 degrees HPT and during infusion of calcium in 2 degrees HPT. In 50 patients with renal lithiasis caused by diseases other than 1 degrees HPT (anatomical variations, pyelonephritis, immobilization after tetraplegia) the ratio cyclic AMP/GFR was not raised. Urinary cyclic AMP/GFR, therefore, reflects parathyroid hormone excess more reliably than cyclic AMP/g creatinine.
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PMID:Hyperparathyoidism: influence of glomerular filtration rate on urinary excretion of cyclic AMP. 19 82

This study demonstrates that appreciable changes in serum parathyroid hormone and urinary cyclic AMP occur during experimentally induced hyper- and hypocalcemia in almost all patients with primary hyperparathyroidism regardless of histology. A single patient with tertiary hyperparathyroidism also demonstrated a significant elevation of serum parathyroid hormone and urinary cyclic AMP in response to EDTA induced reduction in ionized calcium. Thus, total autonomy of hormone secretion was not present in the great majority of the patients with a parathyroid adenoma, parathyroid hyperplasia, or the single patient with tertiary hyperparathyroidism. Therefore, preoperative evaluation of the rsponse of urinary cyclic AMP and serum parapthyroid hormone to EDTA or calcium infusion will not distinguish parathyroid adenomas from hyperplasia on the basis of total autonomy of hormone secretion. If a difference in secretory control is present between parathyroid adenomas and parathyroid hyperplasia, it is more subtle than total autonomy for adenomas and nonautonomy for hyperplasia.
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PMID:Nonautonomy of parathyroid hormone and urinary cyclic AMP in primary hyperparathyroidism. 19 97


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