Distribution of Circulating Immunoreactive Components of Parathyroid Hormone in Normal Subjects and in Patients with Primary and Secondary Hyperparathyroidism: The Role of the Kidney and of the Serum Calcium Concentration

1979 ◽  
Vol 57 (5) ◽  
pp. 435-443 ◽  
Author(s):  
M. A. Dambacher ◽  
J. A. Fischer ◽  
W. H. Hunziker ◽  
W. Born ◽  
J. Moran ◽  
...  
Keyword(s):  
Vitamin D ◽  
Renal Failure ◽  
Parathyroid Hormone ◽  
Chronic Renal Failure ◽  
Primary Hyperparathyroidism ◽  
Vitamin D Deficiency ◽  
Normal Subjects ◽  
Dependent Manner ◽  
Intact Pth ◽  
Calcium Dependent

1. The distribution of intact parathyroid hormone-(1–84) [PTH-(1–84)] and of its COOH-terminal fragments was determined in human serum by column chromatography. In addition to PTH-(1–84) (peak I), COOH-terminal fragments having molecular weights of approximately 4000–7000 (peak II) and immunoreactive components co-eluting with human PTH-(1–12) (peak III) were observed. 2. Mean concentrations of intact PTH-(1–84) and of its COOH-terminal fragments were significantly raised in chronic renal failure as compared with those of normal subjects. Mean amounts of peak II were higher in patients with chronic renal insufficiency than in nutritional vitamin D deficiency, in pseudohypoparathyroidism and in primary hyperparathyroidism, despite comparable amounts of PTH-(1–84). 3. In chronic renal failure as well as in a group of patients with vitamin D deficiency, pseudohypoparathyroidism and primary hyperparathyroidism and in controls, significant linear relations were found between the serum concentrations of calcium and log (peak II/peak I). Our findings suggest that the conversion of intact PTH-(1–84) into COOH-terminal fragments by the parathyroid glands (resulting in a raised secretion of fragments) and/or in peripheral organs may be directly related to the serum concentration of calcium. However, the degradation of the fragments may also be suppressed in a calcium-dependent manner.

scholarly journals Parathyroid hormone: what are we measuring and does it matter?

2002 ◽  
Vol 39 (3) ◽  
pp. 169-172 ◽  
Author(s):  
Aubrey Blumsohn ◽  
Amna Al Hadari
Keyword(s):  
Vitamin D ◽  
Renal Failure ◽  
Parathyroid Hormone ◽  
Chronic Renal Failure ◽  
Primary Hyperparathyroidism ◽  
Intact Parathyroid Hormone ◽  
Intact Pth ◽  
Improve Outcome ◽  
Shed Light ◽  
Improved Outcome

Immunometric assays claiming to determine intact parathyroid hormone (PTH) generally cross-react with N-truncated forms such as PTH(7-84). Laboratories need to examine the relevance of new assays with probable PTH(1-84) specificity. It is logical that assays should measure what they state they do. However, it seems unlikely that use of older 'intact' PTH assays will affect the clinical interpretation of results in primary hyperparathyroidism or vitamin D deficiency. It is plausible that appropriate application of new PTH assays could improve outcome in chronic renal failure. However, it has never been suggested that straightforward replacement of existing assays with new PTH(1-84) assays will lead to this improved outcome. A better understanding of PTH fragments and their interaction with PTH receptors may shed light on the relevance of different PTH assays. In the meantime, older technologies will continue to work well for the vast majority of patients.

scholarly journals Parathyroid hormone inhibits B cell proliferation: implications in chronic renal failure.

1990 ◽  
Vol 1 (3) ◽  
pp. 236-244
Author(s):  
J M Alexiewicz ◽  
M Klinger ◽  
T O Pitts ◽  
Z Gaciong ◽  
M Linker-Israeli ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Renal Failure ◽  
Parathyroid Hormone ◽  
Chronic Renal Failure ◽  
B Cells ◽  
B Cell ◽  
Normal Subjects ◽  
Dependent Manner ◽  
Dialysis Patients ◽  
Amino Terminal

B cell proliferation is impaired in patients with chronic renal failure, but the mechanisms underlying this defect are not known. Lymphocytes have receptors for parathyroid hormone, and it is possible that the state of secondary hyperparathyroidism of renal failure is responsible for the B cell defect. Our studies were designed to (a) examine T cell-independent B cell proliferation [3H)thymidine incorporation) induced by Staphylococcus aureus Cowan 1 after 5 days of culture, (b) evaluate the effect of parathyroid hormone on S. aureus Cowan I-induced B cell proliferation, and (c) investigate the mechanisms through which parathyroid hormone may exert its effect on B cell proliferation. Lymphocytes were obtained from 37 normal subjects and 21 dialysis patients. S. aureus Cowan I induced significant stimulation (P less than 0.01) of the proliferation of B cells from both groups, but the effect was smaller on B cells from dialysis patients (10.0 x 10(3) +/- 1.4 x 10(3) cpm) than on those from normal subjects (21.8 x 10(3) +/- 2.0 x 10(3) cpm). Both the intact molecule of parathyroid hormone (1-84 PTH) and its amino-terminal fragment (1-34 PTH) caused significant inhibition of proliferation of B cells from normal subjects in a dose-dependent manner, with the effect being significantly greater (P less than 0.01) with an equimolar concentration of 1-84 PTH than that of 1-34 PTH. Inactivation of 1-84 PTH by oxidation abolished most of its inhibitory effect on B cell proliferation.(ABSTRACT TRUNCATED AT 250 WORDS)

Clinical evaluation of two parathyroid hormone assays in the context of vitamin D supply in chronic kidney disease

2013 ◽  
Vol 154 (51) ◽  
pp. 2025-2036
Author(s):  
László Kovács ◽  
Éva Virágh ◽  
Dóra Balogh ◽  
Bernadette Kálmán ◽  
Zoltán Lőcsei ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Vitamin D ◽  
Renal Failure ◽  
Peritoneal Dialysis ◽  
Parathyroid Hormone ◽  
Chronic Renal Failure ◽  
Vitamin D Deficiency ◽  
Intact Parathyroid Hormone ◽  
Hormone Levels ◽  
The Difference

Introduction: Parathyroid hormone levels provide important information in chronic renal failure. Aim: To compare parathyroid hormone levels measured by two assays in correlation with vitamin D supply. Method: Parathyroid hormone and 25-hydroxi-vitamin-D were determined in 104 patients (31 patients with chronic renal failure without renal replacement therapy, 36 patients treated with peritoneal dialysis and 37 patients treated with hemodialysis). Results: Good correlation was found between results of the two parathyroid hormone methods, but the intact parathyroid hormone levels were higher than the biointact values. 87% and 13% of the patients had vitamin-D deficiency and insufficiency, respectively. The frequency of serious vitamin-D deficiency was higher in the peritoneal dialysis than in the hemodialysis group. Intact parathyroid hormone levels were different in dialysed patients having vitamin-D-deficiency and insufficiency, and the difference was higher for the biointact than intact values. Negative correlation was detected between biointact parathyroid hormone and 25-hydroxivitamin-D in the hemodialysis group. Conclusions: Biointact parathyroid hormone levels better reflect the vitamin D supply and bone metabolism than intact levels, especially in hemodialysed patients. Orv. Hetil., 2013, 154(51), 2025–2036.

Parathyroid Function in Primary Osteoporosis

1979 ◽  
Vol 57 (2) ◽  
pp. 167-171 ◽  
Author(s):  
R. Bouillon ◽  
P. Geusens ◽  
J. Dequeker ◽  
P. De Moor
Keyword(s):  
Vitamin D ◽  
Parathyroid Hormone ◽  
Primary Hyperparathyroidism ◽  
Vitamin D Deficiency ◽  
Normal Subjects ◽  
Primary Osteoporosis ◽  
Vitamin D Binding Protein ◽  
Parathyroid Function ◽  
25 Hydroxy Vitamin D ◽  
Nutritional Vitamin

1. Parathyroid hormone and 25-hydroxy-vitamin D concentrations were measured in patients with severe primary osteoporosis and the results were compared with those found in normal subjects and in patients with primary hyperparathyroidism of vitamin D deficiency. 2. The parathyroid hormone concentrations in 19 patients with primary osteoporosis were within the normal range, both in the basal state (215 ± 85 ng/l, mean ± sd) and during a maximal stimulation (460 ±154 ng/l) induced by the infusion of disodium EDTA (70 mg/kg body weight). Increased serum concentrations of parathyroid hormone were found in patients with primary hyperparathyroidism (821 ± 323 ng/l, n = 33) and nutritional vitamin D deficiency (565 ± 144 ng/l, n = 11). 3. Serum 25-hydroxy-vitamin D concentrations (16·8 ± 7·7 μg/l) were found to be normal in patients with primary osteoporosis. Slightly (9·1 ± 2·1 μg/l) or markedly lower (2·2 ± 1·1 μg/l) 25-hydroxy-vitamin D concentrations were found respectively in patients with primary hyperparathyroidism and secondary hyperparathyroidism due to vitamin D deficiency. The serum concentration of the vitamin D-binding protein was normal in all groups. 4. A clearcut separation was therefore obtained between osteoporotic subjects (normal parathyroid hormone and normal 25-hydroxy-vitamin D concentrations) and patients with either primary hyperparathyroidism (increased parathyroid hormone and normal 25-hydroxy-vitamin D) or vitamin D deficiency (high parathyroid hormone and very low 25-hydroxy-vitamin D).

scholarly journals PREVALENCE OF VITAMIN D DEFICIENCY IN DIFFERENT GROUPS OF CHRONIC RENAL FAILURE PATIENTS

2015 ◽  
Vol 21 (3) ◽  
pp. 887-890 ◽  
Author(s):  
Bistra T. Galunska ◽  
◽  
Daniela I. Gerova ◽  
Dobrin N. Paskalev ◽  
Rositza Y. Zorcheva ◽  
...  
Keyword(s):  
Vitamin D ◽  
Renal Failure ◽  
Chronic Renal Failure ◽  
Vitamin D Deficiency

Parathyrin radioimmunoassay: diagnostic utility of antisera produced against carboxyl-terminal fragments of the hormone from the human.

1978 ◽  
Vol 24 (3) ◽  
pp. 451-454 ◽  
Author(s):  
F P Di Bella ◽  
J M Kehrwald ◽  
K Laakso ◽  
L Zitzner
Keyword(s):  
Renal Failure ◽  
Parathyroid Hormone ◽  
Chronic Renal Failure ◽  
Guinea Pigs ◽  
Normal Subjects ◽  
Terminal Region ◽  
Diagnostic Utility ◽  
Human Origin ◽  
Widespread Availability ◽  
Carboxyl Terminal

Abstract Antisera directed toward the carboxyl-terminal region of human parathyrin (parathyroid hormone), for use in daignostically applicable radioimmunoassays of the hormone in serum, are scarce, largely because of the lack of suitable immunogens of human origin. We produced four antisera in goats and guinea pigs by immunization with recently discovered carboxyl-terminal fragments of human parathyrin extracted from parathyroid tumors. Here, we report results of radioimmunoassays of nearly 200 normal and pathological sera with one of these antisera; we observed almost complete differentiation between concentrations of parathyrin in serum of healthy normal subjects and patients with primary, secondary (due to chronic renal failure), or "ectopic" hyperparathyroidism (due to nonparathyroid cancer). The availability of a new immunogen should now make possible the deliberate production of large quantities of diagnostically applicable parathyrin antisera directed toward the carboxyl-terminal region of human parathyrin. This should, in turn, lead to more widespread availability of this useful radioimmunoassay.

Effect of chronic renal failure and parathyroid hormone on phospholipid content of brain synaptosomes

1989 ◽  
Vol 256 (4) ◽  
pp. F705-F710
Author(s):  
A. Islam ◽  
M. Smogorzewski ◽  
S. G. Massry
Keyword(s):  
Central Nervous System ◽  
Renal Failure ◽  
Nervous System ◽  
Parathyroid Hormone ◽  
Chronic Renal Failure ◽  
Cholesterol Content ◽  
Phospholipid Content ◽  
Intact Pth ◽  
Central Nervous System Dysfunction ◽  
Brain Synaptosomes

The effects of 21 days of chronic renal failure (CRF) with and without excess parathyroid hormone (PTH) and those of 21 days administration of intact PTH on phospholipids and cholesterol contents of rat brain synaptosomes were examined. CRF and PTH treatment were associated with a significant (P less than 0.01-0.02) reduction in the synaptosomal contents of total phospholipids, phosphatidylinositol (PI), phosphatidylserine (PS), and phosphatidylethanolamine (PE). Parathyroidectomy (PTX) prior to the induction of CRF prevented the decrements in the synaptosomal contents of total phospholipids, PI, PS, and PE. The synaptosomal contents of these phospholipids in CRF-PTX rats were not different from those in normal rats despite CRF. There were no significant changes in the cholesterol content of the synaptosomes in the various experimental groups of animals. The data show that CRF affects synaptosomal metabolism of total phospholipids, PI, PS, and PE, and these derangements are due to the state of secondary hyperparathyroidism of renal failure. The decrements in the content of PI, PS, and PE could be, at least in part, responsible for the previously reported abnormalities in the neurotransmitter functions of brain synaptosomes in CRF and could underlie some of the abnormalities in central nervous system dysfunction in uremia.

Association between vitamin D receptor Fokl polymorphism and serum parathyroid hormone level in patients with chronic renal failure

2005 ◽  
Vol 28 (4) ◽  
pp. 117-121 ◽  
Author(s):  
E. Vigo Gago ◽  
C. Cadarso-Suárez ◽  
R. Perez-Fernandez ◽  
R. Romero Burgos ◽  
J. Devesa Mugica ◽  
...  
Keyword(s):  
Vitamin D ◽  
Renal Failure ◽  
Parathyroid Hormone ◽  
Chronic Renal Failure ◽  
Vitamin D Receptor ◽  
Hormone Level ◽  
Parathyroid Hormone Level ◽  
Serum Parathyroid Hormone

scholarly journals A Survey of Diagnoses in Patients with a Low Intact Parathyroid Hormone Concentration

1993 ◽  
Vol 30 (3) ◽  
pp. 252-255 ◽  
Author(s):  
E M C Manning ◽  
W D Fraser
Keyword(s):  
Renal Failure ◽  
Parathyroid Hormone ◽  
Chronic Renal Failure ◽  
Paget’S Disease ◽  
Blood Sampling ◽  
Intact Parathyroid Hormone ◽  
Hormone Concentration ◽  
Intact Pth ◽  
Common Diagnosis ◽  
Wide Range

Intact parathyroid hormone (PTH) was analysed in 1107 samples over a 13 month period. Of these, 181 samples (16%) gave results of ≤ 1 pmol/L and the case notes of 169 of these 181 patients were examined. Eighty-two patients (48%) were hypercalcaemic at the time of the PTH assay. As expected, the most common diagnosis in this group was hypercalcaemia of malignancy but surprisingly this accounted for only 42 of the hypercalcaemic patients; an unexpectedly high proportion (20 patients) had chronic renal failure with hypercalcaemia due to excessive treatment with 1α-hydroxycholecalciferol; eight patients had transient unexplained hypercalcaemia and the remaining 12 patients were hypercalcaemic for a variety of causes including immobilization, bendrofluazide treatment and Paget's disease. Fifty-nine patients (35%) were normocalcaemic: 26 had osteoporosis, 10 had chronic renal failure and the remainder had a wide range of diagnoses. It is possible that the low intact PTH result in a proportion of the normocalcaemic group was caused by ingestion of calcium tablets prior to blood sampling for PTH. Twenty-eight patients (17%) were hypocalcaemic: 24 of these had hypoparathyroidism, two had chronic renal failure and two had transient unexplained hypocalcaemia.

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