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)

Estrogens decrease serum total and ionized calcium (Ca) concentrations in postmenopausal women with or without primary hyperparathyroidism, but cause little or no increase in serum PTH suggesting a modification of the relationship between the two. In order to define this relationship, we studied the effect of conjugated estrogens on total and ionized serum Ca and serum PTH concentrations in five normal postmenopausal women, before and after 3, 11, and 23 weeks of therapy. Dynamic tests of parathyroid gland function, based on 2-h iv infusions of CaCl2 and NaEDTA, were performed at each time. Total and ionized serum Ca and carboxylterminal PTH were measured every 15 min during the infusions, and parathyroid function was evaluated by a nonlinear 4-parameter mathematical model. Estrogen therapy caused decreases in serum total [2.36 +/- 0.04 (SD) mmol/L, baseline vs. 2.19 +/- 0.05 mmol/L, 23 weeks, P less than 0.005) and ionized calcium (1.27 +/- 0.01 mmol/L, baseline vs. 1.21 +/- 0.02 mmol/L, 23 weeks, P less than 0.005]; the decreases were evident at 3 weeks and persisted for the duration of the study. Serum PTH concentrations did not change (8.94 +/- 1.84 pmol/L, baseline vs. 8.98 +/- 2.38 pmol/L, 23 weeks). Three parameters of the parathyroid function, the maximal response to hypocalcemic stimulation, the nonsuppressible fraction of circulating PTH, and the slope of PTH on calcium at the set point were not affected by estrogen treatment. The fourth parameter, the set point of PTH stimulation by serum total calcium (2.16 +/- 0.04 mmol/L, baseline vs. 1.97 +/- 0.07 mmol/L, 23 weeks, P less than 0.0166) or by serum ionized Ca (1.19 +/- 0.04 mmol/L, baseline vs. 1.12 +/- 0.03 mmol/L, 23 weeks, P less than 0.01), was decreased by estrogen treatment. This was evident at the earliest time point studied and persisted thereafter. The decrease in ionized Ca set point only explained 40% of the decrease in total calcium set point, the remaining 60% being related to hemodilution of plasma protein during therapy. We conclude that estrogen replacement can influence parathyroid function in postmenopausal women by resetting the set point of PTH stimulation by ionized Ca. This in turn could contribute to the estrogen-induced changes in their Ca balance.
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PMID:Estrogen replacement decreases the set point of parathyroid hormone stimulation by calcium in normal postmenopausal women. 292 12

We compared the clinical performance of a carboxyl-terminal radioimmunoassay for human parathyroid hormone (iPTH), using either a dynamic reference interval (95% confidence limits of serum iPTH concentrations observed in 11 normal individuals during intravenous infusions of Na2EDTA and CaCl2) or a gaussian (2 SD) reference interval derived from 233 normocalcemic individuals. The 2 SD ranges were 3.5 to 9.8 pmol/L for serum iPTH and 2.19 to 2.53 mmol/L for total calcium. The iPTH dynamic interval was lower for calcium concentrations greater than 2.50 mmol/L; it was higher, wider, and continued to increase for calcium values less than or equal to 2.25 mmol/L. Use of the dynamic reference interval increased the clinical sensitivity of our assay from 81% and 61% to 100%, respectively, in primary hyperparathyroidism (n = 47) and hypoparathyroidism (n = 18). Test specificity was maintained at 100% in hypocalcemic disorders but fell to 93% (62/67) in hypercalcemic disorders. Overall, use of the dynamic reference interval improved the assay performance.
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PMID:Clinical performance of a parathyrin immunoassay with dynamically determined reference values. 305 63

Radioimmunoassay for parathyroid hormone (PTH) in equids was performed on blood samples from healthy equids and equids with hypercalcemia and hypophosphatemia. The assay was validated for equine carboxy-terminal PTH. Manipulation of serum ionized Ca in healthy equids by infusing Na2 EDTA and CaCl2 produced an expected increase and decrease, respectively, in measurable immunoreactive PTH. Intra-assay and interassay coefficients of variation were 2.6% and 11.7%, respectively. The range of PTH valves for healthy mature horse mares and geldings maintained on pasture was less than 0.27 ng/ml to 0.92 ng/ml and for horse colts fed grain was 0.61 to 1.25 ng/ml. Serum PTH values were measured on 2 equine patients with hypercalcemia, 1 pony with primary hyperparathyroidism and 1 horse with pseudohyperparathyroidism. Both patients had increased serum PTH values.
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PMID:Radioimmunoassay for parathyroid hormone in equids. 359 56

PTH radioimmunoassay today represents an unreplaceable tool in the diagnosis of primary hyperparathyroidism. However, the diagnostic importance of its dosage on selective venous samples is still discussed. Herein, we report our experience of 47 patients operated on for primary hyperparathyroidism. The catheterization of neck veins was performed according to Doppman and co-workers. The PTH assay was carried out with COOH- and NH2-specific antisera. (In 5 cases an inhibition test with CaCl2 infusion was practiced during selective catheterization to preoperatively discriminate between adenoma and hyperplasia.) In 8 cases loading tests with EDTA and in 6 cases with CaCl2 were also performed in association with peripheral venous sampling, in an attempt to improve its sensibility. The 47 cases operated upon showed the following results: the peripheral PTH values were significantly raised in 60% of the cases; the selective PTH dosage with COOH-specific antiserum showed a parathyroid hyperfunction in 100% of the surgically confirmed cases, whereas with the NH2-specific antiserum an increased PTH rate was found only in 84%. A right preoperative localization was obtained in 73%. The value of loading tests is more difficult to evaluate and is discussed in detail.
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PMID:PTH radioimmunoassay and loading tests in the diagnosis of patients with primary hyperparathyroidism. 680 Jul 98

The secretion of intact parathyroid hormone (PTH) was investigated in 11 patients operated on for parathyroid adenoma at 1 year after surgery and compared with that of seven healthy individuals and five patients operated on because of clinical and biochemical signs of primary hyperparathyroidism with equivocal diagnosis after surgery. The investigation was performed by infusing Na2EDTA and CaCl2 at constant rates. No significant difference was found in the suppressibility of PTH secretion by calcium. The set point (the calcium concentration required for half-maximal inhibition of PTH secretion) was slightly lower in patients (1.20 +/- 0.02 mmol/l) compared with healthy subjects (1.23 +/- 0.03 mmol/l; P < 0.05). During the hypocalcemic EDTA infusion, the secretion of PTH was higher in controls compared with patients (P < 0.01). By comparing the data from the infusion tests in patients operated on for parathyroid adenomas with the data obtained from the patients with equivocal diagnosis after parathyroid surgery, a good probability for the diagnosis could be obtained.
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PMID:Postoperative studies on parathyroid hormone secretion in patients operated on for primary hyperparathyroidism. 830 65

Calcium infusion in normal men decreases immunoreactive PTH (iPTH). Intact iPTH (I) shows the greatest decline, and there is a greater decrease in carboxyl-terminal iPTH (C) than in midcarboxyl-terminal iPTH (M); thus, C/I, M/I, and M/C ratios are increased. To verify whether this adaptive mechanism to hypercalcemia was present in patients with primary hyperparathyroidism (PHP), we measured total serum calcium (Ca), I, C, and M as well as C/I, M/I, and M/C ratios in 32 normocalcemic normal subjects (NN), in the same normal subjects made hypercalcemic (HN), in 31 patients with PHP, and in 12 patients with nonparathyroid hypercalcemia (NPHN). Eight patients with PHP and the 32 NN were submitted to CaCl2 and Na2 EDTA infusions to evaluate their parathyroid function. Ca was lower (P < 0.005) in NN (2.21 +/- 0.06 mmol/L) than in PHP (2.80 +/- 0.25 mmol/L) or NPHN (2.83 +/- 0.20 mmol/L). The HN Ca value (2.80 +/- 0.18 mmol/L) was similar to those in PHP and NPHN subjects. C, M, and I were increased in PHP compared to the other groups (P < 0.005). PHP had C/I and M/I ratios of 2.03 +/- 0.72 and 9.04 +/- 7.69, values similar to NN (2.29 +/- 0.55 and 8.70 +/- 3.0), but lower than HN (5.36 +/- 2.48 and 25.93 +/- 13.86; P < 0.005) and NPHN (11.91 +/- 13.06 and 18.69 +/- 10.81; P < 0.005). NPHN also had a lower M/C ratio than HN (2.76 +/- 2.02 vs. 4.99 +/- 1.81; P < 0.05). PHP and NN could increase their C/I ratio to the same maximum (4.71 +/- 1.26 vs. 5.70 +/- 2.94), but PHP did so at a much higher set-point (2.67 +/- 0.19 vs. 2.24 +/- 0.10 mmol/L; P < 0.005). PHP also had higher set-points for M/I, and M/C ratios even if they failed to increase the ratios to the high values in NN [M/I 11.6 +/- 6.4 vs. 29.3 +/- 18.3 (P < 0.005); M/C, 2.16 +/- 1.20 vs. 5.0 +/- 1.93 (P < 0.005)]. Thus, carboxyl-terminal fragments are not secreted preferentially in PHP as they are in other hypercalcemic conditions. This relates to a higher set-point for the regulation of C/I and M/I ratios, permitting the secretion of more intact hormone relative to C or M fragments. The lower M/C ratio in NPHN and in PHP made more hypercalcemic compared to HN suggests a lower production or a higher clearance of midcarboxyl-terminal fragments in chronic hypercalcemia.
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PMID:Carboxyl-terminal fragments of parathyroid hormone are not secreted preferentially in primary hyperparathyroidism as they are in other hypercalcemic conditions. 834 45