The Effect of Cellulose Phosphate on Plasma and Urinary Magnesium at Different Levels of Parathyroid Function in Man

1976 ◽  
Vol 51 (2) ◽  
pp. 161-168 ◽  
Author(s):  
A. M. Parfitt

1. Previously published data obtained by magnesium infusion in man were found to conform to a Tm/glomerular filtration rate (GFR) model on the assumption of 80% diffusibility of plasma magnesium. The lower limit of Tm,Mg/GFR was 625 μmol/l. 2. Previously published data concerning the effect of cellulose phosphate on magnesium metabolism in normal subjects, patients with latent hypoparathyroidism and patients with primary hyperparathyroidism were found to conform to the same model, with the same lower limit for Tm,Mg/GFR for all three levels of parathyroid function. 3. The threshold for magnesium excretion is sharper with less ‘splay’ than for phosphate, but as for phosphate it is close to the normal blood concentration. 4. Because of the geometrical relationship between different methods of presentation of data, at a constant value for Tm,Mg/GFR changes in magnesium load or in GFR automatically produce changes in fractional magnesium clearance. This is the explanation for the increase in fractional magnesium clearance which occurs with diminishing renal function. 5. Renal conservation of magnesium is a passive consequence of the fall in plasma magnesium. There was no evidence of augmented tubular reabsorption of magnesium in response to magnesium deprivation in any of the three groups of subjects. 6. The tubular reabsorption of magnesium was not altered detectably by a moderate deficiency or excess of parathyroid hormone. Changes in parathyroid hormone secretion are probably not concerned in normal magnesium homeostasis.

1975 ◽  
Vol 49 (2) ◽  
pp. 83-90 ◽  
Author(s):  
A. M. Parfitt

1. The bivalent cation-binding agent, cellulose phosphate, was given for 6 days to four normal subjects and six patients with latent hypoparathyroidism (diagnosed by impaired response to EDTA infusion), all of whom were on a moderately low calcium diet. 2. In normal subjects, there was a prompt and sustained fall in urinary calcium with no change in plasma calcium, indicating increased tubular reabsorption. Plasma and urinary magnesium fell, without increase in tubular reabsorption. The urinary total hydroxyproline increased and Tm,P/ glomerular filtration rate fell after 2 days; these changes were transient and were consistent with a transient increase in parathyroid hormone secretion. 3. In the hypoparathyroid patients, urinary calcium fell more slowly and a fall in plasma calcium occurred in several subjects, the extent and duration of which corresponded with parathyroid status determined by EDTA infusion. Urinary conservation of calcium was impaired but plasma and urinary magnesium fell as in normal subjects. Urinary total hydroxyproline did not change and Tm,P/glomerular filtration rate fell more slowly than in the normal subjects. 4. The relative contributions of increased tubular reabsorption and reduced filtered load to calcium conservation in response to calcium depletion depend on the prevailing level of parathyroid function; the former is more important when parathyroid function is normal, the latter when parathyroid function is impaired. 5. In the detection of reduced parathyroid reserve, the assessment based on the plasma calcium response to cellulose phosphate agrees closely with the assessment based on the degree of recovery from EDTA-induced hypocalcaemia.


1968 ◽  
Vol 40 (4) ◽  
pp. 467-475 ◽  
Author(s):  
P. ADAMS ◽  
T. M. CHALMERS ◽  
B. L. RIGGS ◽  
J. D. JONES

SUMMARY Calcium and phosphorus metabolism were studied in 22 patients with spontaneous primary hypothyroidism. Two patients were found to have hypercalcaemia but the mean serum calcium concentration of the group was significantly less than that of control subjects. The renal tubular reabsorption of phosphate was decreased and could be increased to normal with small calcium infusions. The response to calcium deprivation and to infusions of EDTA was abnormal and suggested an impaired ability to mobilize calcium from bone. There was a significant correlation between the defect in calcium mobilization, as judged from the response to EDTA, and the renal tubular reabsorption of phosphate. In three patients serum parathyroid hormone concentrations, measured by radioimmunoassay, were in the upper part of the normal range. It is suggested that in patients with hypothyroidism the target cells in bone are less responsive to the effects of parathyroid hormone than normal; as a consequence parathyroid hormone secretion may be increased.


1984 ◽  
Vol 247 (5) ◽  
pp. E675-E680 ◽  
Author(s):  
L. Magliola ◽  
L. R. Forte

Previous studies have suggested that prolactin (PRL) may affect calcium (Ca) homeostasis by an action on vitamin D metabolism. In this study, the effects of PRL on parathyroid hormone (PTH) secretion were investigated in dispersed bovine parathyroid cells (PTC). PRL (0.013-1.3 microM) caused concentration-dependent increases in PTH secretion. PRL-stimulated PTH release was apparent as early as 1 h and was progressive thereafter for up to 3 h. PRL enhanced PTH release over a wide range of ambient Ca concentrations (0.5-2.0 microM). Ovine and rat PRL were more effective than bovine PRL in stimulating PTH secretion. This effect was apparently specific for PRL because neither ovine nor bovine growth hormone stimulated PTH secretion. PRL-stimulated PTH release was not mediated through the beta-adrenergic or dopaminergic receptor systems of PTC and was not associated with increased adenosine 3',5'-cyclic monophosphate (cAMP) levels. This study demonstrated a direct effect of PRL to stimulate PTH secretion in vitro. Although these data do not provide evidence for an effect of PRL in vivo, we suggest a mechanism by which PRL may influence parathyroid function and Ca homeostasis in the bovine species.


1997 ◽  
Vol 8 (4) ◽  
pp. 627-631
Author(s):  
K A Graham ◽  
N A Hoenich ◽  
M Tarbit ◽  
M K Ward ◽  
T H Goodship

Correction of acidosis in hemodialysis patients increases the sensitivity of the parathyroid glands to calcium. In this study, the parathyroid response to the correction of acidosis in eight hemodialysis patients was determined by performing dynamic assessment of parathyroid function before and after the correction of acidosis. The parathyroid response to intravenous calcitriol before and after the correction of acidosis was also assessed. After optimal correction of acidosis, there were no significant changes in blood pH, ionized calcium, phosphate, or alkaline phosphatase values, but the level of venous total CO2 increased significantly. Parathyroid hormone/ionized calcium curves were displaced downward after correction of acidosis, but not after the administration of intravenous calcitriol. The correction of metabolic acidosis in hemodialysis patients with secondary hyperparathyroidism can suppress parathyroid hormone secretion by increasing the sensitivity of the parathyroid glands to ionized calcium.


1985 ◽  
Vol 68 (3) ◽  
pp. 321-326 ◽  
Author(s):  
M. S. Seshadri ◽  
Y. L. Chan ◽  
M. R. Wilkinson ◽  
R. S. Mason ◽  
S. Posen

1. An adenylate cyclase bioassay for parathyroid hormone (PTH) was evaluated in peripheral sera of ten normal subjects, 15 patients with various types of hypoparathyroidism, nine patients with malignancy-associated hypercalcaemia and 60 patients with primary or secondary hyperparathyroidism. The lower limit of detectability was 150 pg/ml in terms of synthetic human PTH (1-34). 2. PTH-like bioactivity was not detected in normal subjects, in patients with surgical hypoparathyroidism, in patients with idiopathic hypoparathyroidism or in patients with malignancy-associated hypercalcaemia. Serum from one untreated pseudohypoparathyroid patient consistently contained PTH-like bioactivity. 3. Bioactivity was detected in sera from 50% of patients with primary or secondary hyperparathyroidism. In two patients with secondary hyperparathyroidism calcium infusions suppressed this activity within 5 min. 4. Both in primary and in secondary hyperparathyroidism there was a significant positive correlation between levels of PTH-like bioactivity, PTH immunoreactivity and the histological severity of the disease.


1975 ◽  
Vol 49 (2) ◽  
pp. 91-98 ◽  
Author(s):  
A. M. Parfitt

1. The bivalent cation-binding agent, cellulose phosphate, together with a low calcium diet was given for 6 days to nine patients with primary hyperparathyroidism subsequently verified at surgery. 2. Urinary calcium fell promptly by 8·4 mmol/24 h, and by 70%, and reached amounts below 4·0 mmol/24 h in five of the nine patients. The magnitude of fall may have been related to increased synthesis of vitamin D by the skin in a sub-tropical environment. Plasma magnesium fell steadily and urinary magnesium fell by 80%. 3. The plasma calcium showed two types of response. In five patients there was no significant change because a reduction in calcium load was offset by a further increase in the already high tubular reabsorption of calcium. In the remaining four patients, the tubular reabsorption of calcium was at a higher level initially and failed to increase further on the experimental regime, with a corresponding fall in plasma calcium. 4. The hypercalcaemia of primary hyperparathyroidism can be explained by increased gastrointestinal absorption and increased renal tubular reabsorption of calcium; net bone resorption makes only a small contribution but an additional factor dependent on the blood-bone equilibrium is not ruled out. 5. Comparison with other published data suggests that the fall in urinary calcium in response to a calcium-depleting regimen is prevented by concurrent depletion of inorganic phosphate and may be enhanced by concurrent depletion of magnesium. 6. Persistence of hypercalcaemia combined with an increase in tubular reabsorption of calcium in response to cellulose phosphate may be of diagnostic value in suspected primary hyperparathyroidism. 7. Cellulose phosphate may be of value in stone prevention in patients with primary hyperparathyroidism who are unsuitable for surgical treatment.


1979 ◽  
Vol 57 (2) ◽  
pp. 167-171 ◽  
Author(s):  
R. Bouillon ◽  
P. Geusens ◽  
J. Dequeker ◽  
P. De Moor

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).


1990 ◽  
Vol 70 (4) ◽  
pp. 951-956 ◽  
Author(s):  
JACK F. TOHME ◽  
JOHN P. BILEZIKIAN ◽  
THOMAS L. CLEMENS ◽  
SHONNI J. SILVERBERG ◽  
ELIZABETH SHANE ◽  
...  

1982 ◽  
Vol 242 (1) ◽  
pp. R141-R150
Author(s):  
A. Jung ◽  
G. P. Mayer ◽  
J. G. Hurst ◽  
R. Neer ◽  
J. T. Potts

A model for parathyroid gland response to differing calcium and magnesium concentrations is proposed based on direct determinations of parathyroid hormone (PTH) secretion rate. A proportional control seems adequate for physiological variations of calcium and magnesium levels. At extreme hypocalcemia, nonlinearities are observed: a model involving the depletion of a storage compartment is proposed, the size of which is calculated. PTH distribution was studied in another group of animals; sampling was made from the saphenous artery and the thoracic duct. Concentrations of plasma and lymph-intact PTH and carboxy-terminal fragments were determined by means of two different radioimmunoassays. The analysis of the results leads to the formulation of a five-compartment model, which shows that the metabolism of intact PTH is only partly due to the formation of carboxy-terminal fragments, most being directly secreted or catabolized. Linking these models for secretion and distribution of PTH, simulation studies were undertaken and compared with published data. This model is then discussed in comparison with previous work concerning other polypeptide hormones.


1968 ◽  
Vol 42 (4) ◽  
pp. 529-534 ◽  
Author(s):  
R. M. BUCKLE ◽  
A. D. CARE ◽  
C. W. COOPER ◽  
H. J. GITELMAN

SUMMARY The influence of plasma magnesium concentration on parathyroid gland function has been evaluated by perfusion at a constant rate of an isolated parathyroid gland in five goats and one sheep with whole blood of varying magnesium content. The concentration of magnesium in fresh whole blood was adjusted either by dialysis or by the addition of magnesium chloride before the perfusion. In each experiment, the concentration of calcium was maintained constant or was slightly altered to oppose the possible influence of magnesium on the rate of release of parathyroid hormone. Parathyroid hormone concentration in parathyroid venous plasma was estimated by a specific radioimmunoassay. In each experimental animal we observed that the concentration of parathyroid hormone in the effluent plasma diminished when the concentration of magnesium was raised or increased when the concentration of magnesium was lowered. These observations demonstrate a specific influence of magnesium on the rate of release of parathyroid hormone.


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