Sodium Cellulose Phosphate: Mechanism of Action and Effect on Mineral Metabolism

Pak, Charles Y.C.

doi:10.1002/j.1552-4604.1973.tb00064.x

Cited by 18 publications

(15 citation statements)

References 19 publications

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“…Those patients in whom the plasmacalcium did not change (group a) behaved in a manner closely similar to the normal subjects, in that the reduction in load was exactly compensated by an increase in tubular reabsorption (Parfitt, 1975); these reciprocal changes were both of much greater magnitude in the hyperparathyroid patients than in the normal subjects. On the other hand, in those patients who showed a fall in plasma calcium on the experimental regime (group b), the fall in load was not balanced by any increase in tubular reabsorption, a response found also by Pak (1973) in one patient with sarcoidosis and hypercalcaemia. This suggests that failure to augment tubular reabsorption of calcium was the main reason for the fall in calcium in group (b).…”

Section: Discussionmentioning

confidence: 78%

Effect of Cellulose Phosphate and Dietary Calcium Restriction in Primary Hyperparathyroidism

Parfitt

1975

Clinical Science

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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 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.

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Section: Discussionmentioning

confidence: 78%

Effect of Cellulose Phosphate and Dietary Calcium Restriction in Primary Hyperparathyroidism

Parfitt

1975

Clinical Science

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“…The mode of action of this compound differs fundamentally from that of soluble orthophosphates (20,21). At the dose utilized in this study, 5 g three times a day orally, cellulose phosphate has been shown to reduce intestinal calcium absorption by as much as 165 mg/day (20). Among patients with absorptive hypercalciuria, cellulose phosphate decreased urinary calcium by 120-230 mg/day to the normal range (less than 200 mg/day).…”

Section: Discussionmentioning

confidence: 89%

“…Cellulose phosphate is a nonabsorbable ion-exchange resin, which, when given orally, "binds" calcium and inhibits its absorption from the intestinal tract (20). The mode of action of this compound differs fundamentally from that of soluble orthophosphates (20,21). At the dose utilized in this study, 5 g three times a day orally, cellulose phosphate has been shown to reduce intestinal calcium absorption by as much as 165 mg/day (20).…”

Section: Discussionmentioning

confidence: 92%

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The Hypercalciurias CAUSES, PARATHYROID FUNCTIONS, AND DIAGNOSTIC CRITERIA

Pak¹,

Oata²,

Lawrence³

et al. 1974

J. Clin. Invest.

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497

137

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A B S T R A C T The causes for the hypercalciuria and diagnostic criteria for the various forms of hypercalciuria were sought in 56 patients with hypercalcemia or nephrolithiasis (Ca stones), by a careful assessment of parathyroid function and calcium metabolism. A study protocol for the evaluation of hypercalciuria, based on a constant liquid synthetic diet, was developed. In 26 cases of primary hyperparathyroidism, characteristic features were: hypercalcemia, high urinary cyclic AMP (cAMP, 8.58+3.63 SD gmol/g creatinine; normal, 4.02±0.70 umol/g creatinine), high immunoreactive serum parathyroid hormone (PTH), hypercalciuria, the urinary Ca exceeding absorbed Ca from intestinal tract (CaA), high fasting urinary Ca (0.2 mg/mg creatinine or greater), and low bone density by 'I photon absorption. The results suggest that hypercalciuria is partly secondary to an excessive skeletal resorption (resorptive hypercalciuria). The 22 cases with renal stones had normocalcemia, hypercalciuria, intestinal hyperabsorption of calcium, normal or low serum PTH and urinary cAMP, normal fasting urinary Ca, and normal bone density. Since their CaA exceeded urinary Ca, the hypercalciuria probably resulted from an intestinal hyperabsorption of Ca (absorptive hypercalciuria). The primacy of intestinal Ca hyperabsorption was confirmed by responses to Ca load and deprivation under a metabolic dietary regimen. During a Ca load of 1,700 mg/day, there was an exaggerated increase in the renal excretion.of Ca and a suppression of cAMP excretion. The urinary Ca of 453±+154 SD mg/day was significantly higher than the control group's 211+42 mg/ day. The urinary cAMP of 2.26±0.56 umol/g creatinine was significantly lower than in the control group. In contrast, when the intestinal absorption of calcium was limited by cellulose phosphate, the hvpercalciuria was kc'ceiz(l for plblicatifn 9 July 1073 and in rezxsed form 11 September 1973. corrected and the suppressed renal excretion of cAMP returned towards normal. Two cases with renal stones had normocalcemia, hypercalciuria, and high urinary cAMP or serum PTH. Since CaA was less than urinary Ca, the hypercalciuria may have been secondary to an impaired renal tubular reabsorption of Ca (renal hypercalciuria). Six cases with renal stones had normal values of serum Ca, urinary Ca, urinary cAMP, and serum PTH (normocalciuric nephrolithiasis). Their CaA exceeded urinal Ca, and fasting urinary Ca and bone density were normal. The results support the proposed mechanisms for the hypercalciuria and provide reliable diagnostic criteria for the various forms of hypercalciuria.

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“…The drug action may be localized to the specific step in the stone-forming process (table I). For example, sodium cellulose phosphate inhibits nucleation of brushite and calcium oxalate in urine by reducing the state of saturation with respect to these calcium salts [7,14]. Thiazide [15,28] and orthophosphate [13,22] inhibit nucleation and growth of the nidus by reducing the state of saturation and stimulating the renal excretion of in hibitors (such as pyrophosphate).…”

Section: Mechanism Of Drug Actionmentioning

confidence: 99%