Decrease of serum calcium concentration and lost influence of calcium on parathyroid hormone release in a patient with primary hyperparathyroidism after treatment with diphosphonates

1993 ◽  
Vol 53 (5) ◽  
pp. 301-303
Author(s):  
Harold Kotzmann ◽  
Peter Bernecker ◽  
Thomas Svoboda ◽  
Bruno Niederle ◽  
Anton Luger
Keyword(s):  
Parathyroid Hormone ◽  
Primary Hyperparathyroidism ◽  
Serum Calcium ◽  
Calcium Concentration ◽  
Hormone Release ◽  
Serum Calcium Concentration ◽  
Parathyroid Hormone Release

scholarly journals Persistent Hypercalcemia After Parathyroidectomy in an Adolescent and Effect of Treatment With Cinacalcet HCl

2006 ◽  
Vol 52 (12) ◽  
pp. 2286-2293 ◽  
Author(s):  
Lorin M Henrich ◽  
Alan D Rogol ◽  
Pierre D’Amour ◽  
Michael A Levine ◽  
John B Hanks ◽  
...  
Keyword(s):  
Parathyroid Hormone ◽  
Primary Hyperparathyroidism ◽  
Serum Calcium ◽  
Calcium Concentration ◽  
Case Conference ◽  
Serum Calcium Concentration ◽  
Pharmacodynamic Profile ◽  
Laboratory Results ◽  
Calcium Phosphorus ◽  
Effect Of Treatment

Abstract Background: Hyperparathyroidism is uncommon in adolescence and is more likely to persist after parathyroidectomy than in adults. Cinacalcet HCl is a new calcimimetic that has been used successfully for the treatment of primary and secondary hyperparathyroidism in adults, but its use in adolescents has not been reported. Case: A 16 year-old male presented with hypercalcemia that had persisted for 1.5 years after parathyroidectomy for primary hyperparathyroidism. Parathyroid hormone (PTH) concentrations were nonsupressed despite a mean (SD) serum calcium concentration of 2.82 (0.06) mmol/L. Treatment with cinacalcet HCl was initiated and a pharmacodynamic profile was obtained for serum calcium, phosphorus, and PTH. Cinacalcet HCl normalized serum calcium. The changes in PTH were assay dependent. Issues: We use this case conference to review the evaluation of hypercalcemia in adolescents, examine the changes in relevant laboratory results during treatment with cinacalcet HCl, and discuss differences among assays for PTH. Conclusions: Interpretation of PTH results in patients treated with cinacalcet HCl requires consideration of the pharmacodynamic effects of the drug and the nature of the PTH assay.

Dynamics of parathyroid hormone release and serum calcium regulation after surgery for primary hyperparathyroidism

1992 ◽  
Vol 16 (4) ◽  
pp. 625-631 ◽  
Author(s):  
Wilhelm Graf ◽  
Jonas Rastad ◽  
Göran Åkerström ◽  
Leif Wide ◽  
Sverker Ljunghall
Keyword(s):  
Parathyroid Hormone ◽  
Primary Hyperparathyroidism ◽  
Serum Calcium ◽  
Calcium Regulation ◽  
Hormone Release ◽  
Parathyroid Hormone Release

BIOASSAY OF PARATHYROID HORMONE IN RATS BY DETERMINATION OF PLASMA CALCIUM, URINARY 32P EXCRETION AND SERUM ALKALINE PHOSPHATASE

1966 ◽  
Vol 35 (3) ◽  
pp. 229-238 ◽  
Author(s):  
R. J. TREACHER
Keyword(s):  
Alkaline Phosphatase ◽  
Parathyroid Hormone ◽  
Serum Calcium ◽  
Calcium Concentration ◽  
Serum Alkaline Phosphatase ◽  
Plasma Calcium ◽  
Significant Alteration ◽  
Good Precision ◽  
Serum Calcium Concentration

SUMMARY Methods for assay of parathyroid hormone based on an increase in serum calcium concentration, urinary 32P excretion and serum alkaline phosphatase elevation in parathyroidectomized rats have been compared and modifications introduced to improve sensitivity, precision, speed and ease of manipulation. Both the serum calcium and urinary 32P assay gave good precision (mean λ = 0·23 and 0·29, respectively) but by the serum calcium method less than 10 USP units of parathyroid hormone could not be detected, whereas the phosphaturic assay detects as little as 0·5 USP unit. Both assays are simple to perform and each requires only 2 days to complete. They can be combined in a single design using the same animals. Assays based on serum alkaline phosphatase levels in parathyroidectomized rats were not successful since it was impossible to produce a significant alteration in serum alkaline phosphatase by the administration of parathyroid hormone.

Clinical and Molecular Genetics of Primary Hyperparathyroidism

2020 ◽  
Vol 52 (08) ◽  
pp. 578-587
Author(s):  
William F. Simonds
Keyword(s):  
Parathyroid Hormone ◽  
Primary Hyperparathyroidism ◽  
Tumor Suppressor Genes ◽  
Calcium Concentration ◽  
Systemic Circulation ◽  
Parathyroid Glands ◽  
Serum Calcium Concentration ◽  
Parathyroid Neoplasia ◽  
Excessive Secretion ◽  
Tumor Dna

AbstractCalcium homeostasis is maintained by the actions of the parathyroid glands, which release parathyroid hormone into the systemic circulation as necessary to maintain the serum calcium concentration within a tight physiologic range. Excessive secretion of parathyroid hormone from one or more neoplastic parathyroid glands, however, causes the metabolic disease primary hyperparathyroidism (HPT) typically associated with hypercalcemia. Although the majority of cases of HPT are sporadic, it can present in the context of a familial syndrome. Mutations in the tumor suppressor genes discovered by the study of such families are now recognized to be pathogenic for many sporadic parathyroid tumors. Inherited and somatic mutations of proto-oncogenes causing parathyroid neoplasia are also known. Future investigation of somatic changes in parathyroid tumor DNA and the study of kindreds with HPT yet lacking germline mutation in the set of genes known to predispose to HPT represent two avenues likely to unmask additional novel genes relevant to parathyroid neoplasia.

Radioimmunoassay of parathyroid hormone (parathyrin) in monkey and man.

1977 ◽  
Vol 23 (11) ◽  
pp. 1989-1994 ◽  
Author(s):  
G K Hargis ◽  
G A Williams ◽  
W A Reynolds ◽  
W Kawahara ◽  
B Jackson ◽  
...  
Keyword(s):  
Tissue Culture ◽  
Parathyroid Hormone ◽  
Rhesus Monkey ◽  
Serum Calcium ◽  
Calcium Concentration ◽  
Culture Media ◽  
Parathyroid Tissue ◽  
Serum Calcium Concentration ◽  
Tissue Culture Media

Abstract A radioimmunoassay for rhesus monkey and human immunoreactive parathyrin was developed in which a selected anti-bovine parathyrin antiserum, radioiodinated purified bovine parathyrin tracer, and human parathyroid tissue-culture media standards were used. The resulting data indicate that (a) the method is sensitive, specific, accurate and reproducible; (b) it is valid for both the rhesus monkey and the human; (c) the serum immunoreactive parathyrin concentration of the monkey is essentially the same as that in man; (d) monkey immunoreactive parathyrin responds to changes in serum calcium concentration similarly to that in man; and (e) the rhesus monkey is therefore a suitable species in which to study parathyroid physiology, from which conclusions can be applied to the human.

Effects of acute metabolic acidosis on parathyroid hormone action and calcium mobilization

1976 ◽  
Vol 230 (1) ◽  
pp. 127-131 ◽  
Author(s):  
N Beck ◽  
SK Webster
Keyword(s):  
Parathyroid Hormone ◽  
Metabolic Acidosis ◽  
Serum Calcium ◽  
Calcium Concentration ◽  
Tubular Reabsorption ◽  
Calcium Mobilization ◽  
Measurable Effect ◽  
Bilateral Nephrectomy ◽  
Serum Calcium Concentration ◽  
Acute Metabolic Acidosis

Mechanisms through which metabolic acidosis increases calcium mobilization have been investigated in thyroparathyroidectomized rats with induction of acute metabolic acidosis by infusing NH4C1 intravenously. Acute metabolic acidosis directly raised serum calcium concentration and augmented the effect of parathyroid hormone (PTH) to raise serum calcium concentration. The same effects of metabolic acidosis were observed in rats with surgically removed intestines and bilateral nephrectomy, suggesting that acute metabolic acidosis directly increases calcium mobilization from bone and augments the effect of PTH to mobilize calcium from bone. In the kidney, acidosis directly inhibited the tubular reabsorption of calcium, but augmented the effect of PTH to increase tubular reabsorption of calcium. Acidosis had no measurable effect on calcitonin action.

Relationship between external and cytoplasmic calcium concentrations, parathyroid hormone release and weight of parathyroid glands in human hyperparathyroidism

1988 ◽  
Vol 116 (3) ◽  
pp. 457-464 ◽  
Author(s):  
C. Wallfelt ◽  
E. Gylfe ◽  
R. Larsson ◽  
S. Ljunghall ◽  
J. Rastad ◽  
...  
Keyword(s):  
Parathyroid Hormone ◽  
Calcium Concentration ◽  
Hormone Release ◽  
Cytoplasmic Calcium ◽  
Serum Concentrations ◽  
Maximal Inhibition ◽  
Adult Cattle ◽  
Calcium Effects ◽  
The Individual ◽  
Parathyroid Hormone Release

ABSTRACT Parathyroid hormone (PTH) release and cytoplasmic calcium concentrations were investigated at ambient calcium concentrations of 0·5–3·0 mmol/l in dispersed parathyroid cells from 44 hypercalcaemic patients with primary or uraemic hyperparathyroidism (HPT). In comparison with parathyroid cells from adult cattle, release of PTH by human preparations was reduced and values of the ambient calcium concentration causing half-maximal inhibition of PTH release (median effective dose, ED50) were significantly increased. Half-maximal inhibition of PTH release was obtained with concentrations of cytoplasmic calcium almost identical to the concentrations of ionized calcium in the plasma of the individual patients. Cytoplasmic concentrations of calcium in the parathyroid cells were inversely related to release of PTH. Concentrations of cytoplasmic calcium were significantly lower in human than in bovine cells and the ED50 for ambient calcium increase on cytoplasmic calcium was raised to the same extent as the ED50 for ambient calcium inhibition of PTH release in human compared with bovine cells. The magnitude of the increased ED50 for ambient calcium inhibition of PTH release and increase of cytoplasmic calcium concentration was similar in adenomas and sporadic as well as hereditary primary hyperplasias, but the secretion was the least aberrant in uraemic hyperplasias, although they had by far the largest glandular mass. Serum concentrations of total calcium before surgery correlated with the ED50 for ambient calcium effects of PTH release and cytoplasmic calcium, but not with glandular weight. These findings demonstrate a universally abnormal regulation of cytoplasmic calcium in HPT and its importance for PTH release, and that disturbance of cytoplasmic calcium rather than the increased glandular mass contributes to the hypercalcaemia in adenomatous and hyperplastic HPT. J. Endocr. (1988) 116, 457–464

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