Assay of Parathyroid Hormone in Human Serum and its Uses

1976 ◽  
Vol 13 (1-6) ◽  
pp. 549-554 ◽  
Author(s):  
J. S. Woodhead ◽  
D. A. Walker
Keyword(s):  
Differential Diagnosis ◽  
Parathyroid Hormone ◽  
Human Serum ◽  
No Value ◽  
Clinical Application ◽  
Calcium Metabolism ◽  
Clinical Problem ◽  
Plasma Calcium ◽  
Biochemical Data ◽  
Health And Disease

The assay of parathyroid hormone has contributed greatly to our understanding of calcium metabolism in health and disease. The most important clinical application of the assay is in the differential diagnosis of hypercalcaemia, which is an increasing clinical problem. PTH assays are of little or no value in the absence of other biochemical data, especially accurate determinations of plasma calcium and phosphate.

scholarly journals Rapid activation of the medullary bone osteoclast cell surface by parathyroid hormone.

1978 ◽  
Vol 76 (3) ◽  
pp. 615-618 ◽  
Author(s):  
S C Miller
Keyword(s):  
Electron Microscope ◽  
Parathyroid Hormone ◽  
Calcium Metabolism ◽  
De Novo ◽  
Plasma Calcium ◽  
Medullary Bone ◽  
Transmission Electron ◽  
Egg Shell ◽  
Rapid Activation

Quantitative transmission electron microscope methods were used to determine the response of functionally inactive avian medullary bone osteoclasts to parathyroid hormone (PTH). Egg-lying Japanese quail were used during a period of the egg cycle when medullary bone was not being resorbed for egg shell calcification and when medullary bone osteoclasts were functionally inactive. Ruffled borders adjacent to bone surfaces were rarely, if ever, found on these cells. 20 min after the administration of PTH, over 70% of the osteoclast profiles had ruffled borders adjacent to bone surfaces. These ruffled borders were bounded by filamentous-rich "clear zones" and resembled ruffled borders found on functionally active cells. There was also a marked increase in plasma calcium levels after PTH administration. This study demonstrates that PTH stimulates the de novo generation of ruffled borders on osteoclasts in vivo and suggests that osteoclasts may be involved in the acute regulation of calcium metabolism by exogenous PTH.

PARATHYROID HORMONE SECRETION IN DISORDERS OF CALCIUM METABOLISM STUDIED BY MEANS OF EDTA

1974 ◽  
Vol 75 (2) ◽  
pp. 286-296 ◽  
Author(s):  
J. H. Lockefeer ◽  
W. H. L. Hackeng ◽  
J. C. Birkenhäger
Keyword(s):  
Parathyroid Hormone ◽  
Primary Hyperparathyroidism ◽  
Calcium Metabolism ◽  
Hormone Secretion ◽  
Parathyroid Tissue ◽  
Small Mass ◽  
Idiopathic Hypercalciuria ◽  
List Type ◽  
Immunoreactive Parathyroid Hormone ◽  
Pth Level

ABSTRACT In 22 of 28 cases of primary hyperparathyroidism (PHP) the rise in the serum immunoreactive parathyroid hormone (IRPTH or PTH) level observed in response to lowering of the serum calcium by EDTA, exceeded that obtained in 8 control subjects. In 5 of these 22 patients who were studied again after parathyroidectomy the supranormal response was abolished. Fifteen of these 22 hyper-responsive PHP patients had basal IRPTH levels not exceeding the highest level in the controls and that of other groups of patients investigated (idiopathic hypercalciuria, non-parathyroid hypercalcaemia, operated PHP). Fourteen of the 22 hyper-reactive patients with PHP did not show hypocalcaemia during the infusion of EDTA. The extent of the release of PTH elicited by EDTA in cases of PHP does not as yet allow a prediction of the amount of pathological parathyroid tissue present, although all the PHP patients showing a normal release of PTH had a relatively small mass of parathyroid tissue (up to about 1 g) subsequently removed. In 9 cases of nephrolithiasis (8 of whom had idiopathic hypercalciuria) and in 7 cases of non-parathyroid hypercalcaemia, a normal PTH release was found.

Evaluation of intact serum parathyroid hormone (PTH 1-84) in the diagnosis of disorders of calcium metabolism

1988 ◽  
Vol 117 (4_Suppl) ◽  
pp. S64-S65
Author(s):  
K. KRUSE ◽  
U. KRACHT ◽  
K. WOHLFART ◽  
U. KRUSE
Keyword(s):  
Parathyroid Hormone ◽  
Calcium Metabolism ◽  
Serum Parathyroid Hormone

A radioimmunoassay for human parathyroid hormone utilizing a goat anti-bovine PTH serum

1981 ◽  
Vol 96 (2) ◽  
pp. 215-221 ◽  
Author(s):  
L. E. Mallette
Keyword(s):  
Parathyroid Hormone ◽  
Primary Hyperparathyroidism ◽  
Secondary Hyperparathyroidism ◽  
Human Serum ◽  
Central Region ◽  
Antigenic Site ◽  
Human Parathyroid Hormone ◽  
Domestic Goat ◽  
Standard Serum ◽  
Dilution Curves

Abstract. An antiserum (NG-1) against bovine PTH (bPTH) generated in the domestic goat was characterized for use in the radioimmunoassay of PTH in human serum. When a carboxyterminal fragment of bPTH is used as radioligand, this antiserum detects only an antigenic site in the central region of the hPTH molecule. The synthetic hormone fragment, hPTH-(44-68), will displace 93% of the tracer, after which the addition of intact hPTH causes no further displacement. The assay does not detect the synthetic aminoterminal 1-34 fragment of the bovine or human hormones, nor the carboxyterminal fragment of the human hormone, hPTh-(53-84). Standard curves with bPTH-(1-84) and partially purified hPTH are not parallel, so that hPTH is used as standard. Serum from subjects with uraemia or primary hyperparathyroidism gives dilution curves parallel to that with the hPTH standard. The assay with NG-1 has been applied to the diagnosis of primary and secondary hyperparathyroidism, used to monitor the disappearance of PTH after parathyroidectomy, and for measurement of PTH in selective venous samples.

scholarly journals Familial Hypocalciuric Hypercalcaemia (FHH): A Case Report

2018 ◽  
Vol 3 (09) ◽  
Author(s):  
Tivya Kulasegaran ◽  
Pranav Kumar
Keyword(s):  
Differential Diagnosis ◽  
Case Report ◽  
Parathyroid Hormone ◽  
Autosomal Dominant ◽  
Genetic Test ◽  
Calcium Sensor ◽  
Clearance Ratio ◽  
Autosomal Dominant Disorder ◽  
Casr Gene ◽  
Inactivating Mutation

Familial hypocalciuric hypercalcaemia (FHH) is a rare genetic autosomal dominant disorder, with 3 variants described. An inactivating mutation in the calcium sensor receptor (CASR) gene causes the subtype 1, which represents 65% of the cases. Inactivation of Ca-sensing receptors (CaSR) can also lead to hypercalcemia associated with increased parathyroid hormone (PTH) secretion.[1] It is characterised by causes mild asymptomatic hypercalcemia[2] and hypocalciuria with normal or elevated PTH. FHH is generally asymptomatic and treatment is not needed. Differential diagnosis with primary hyperparathyroidism (PHPT) is crucial and based on calcium-creatinine clearance ratio (CCCR), which, when under 0.02 points to the diagnosis of FHH.[3] Genetic test is necessary for confirmation.[4]

scholarly journals Neonatal hypocalcemic Seizures: About a 41-Day-Old Infant

2020 ◽  
pp. 9-14
Author(s):  
A. Radi ◽  
O. Bakkali ◽  
M. Kmari ◽  
A. Ourrai ◽  
A. Hassani ◽  
...  
Keyword(s):  
Vitamin D ◽  
Differential Diagnosis ◽  
Parathyroid Hormone ◽  
Infant Formula ◽  
Calcium Gluconate ◽  
Hypovitaminosis D ◽  
Vitamin D Supplementation ◽  
Neonatal Seizures ◽  
Common Cause ◽  
Neonatal Hypocalcemia

Neonatal crises have several etiologies. Hypovitaminosis D and hypocalcemia are the most common cause of childhood seizures, but their frequency has been reduced due to vitamin D supplementation and infant formula. Most hypocalcemic crises have an underlying endocrinological origin rather than a deficit in intake. We describe the case of a 41-day-old infant admitted for neonatal seizures for hypocalcemia. Although symptoms and concentrations of calcium and parathyroid hormone (PTH) levels favored isolated congenital hyperparathyroidism after eliminating other differential diagnoses. The course of the disease was favorable with intravenous (IV) calcium gluconate 10%, then orally alfacalcidol and vitd2. The case is presented with a brief review of the pathophysiology, differential diagnosis and treatment of neonatal hypocalcemia.

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