Effect of Cellulose Phosphate and Dietary Calcium Restriction in Primary Hyperparathyroidism

Abstract

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.

Primary hyperparathyroidism: evaluated by 47Calcium kinetics, calcium balance and serum bone‐Gla‐protein

“…The enhanced urinary excretion of calcium in PHP is therefore mainly caused by the increased net absorption of calcium and to a much lesser extent by the perhaps slighly increased mobilization of bone mineral. This is in agreement with the findings that the urinary excretion of calcium in PHP is positively related to serum levels of 1,25-dihydroxyvitamin D [24], and that the urinary excretion of calcium decreases about 30% during treatment with sodium cellulose phosphate, which binds intestinal calcium [25]. In the present study the dermal calcium loss was found increased.…”

“…The increase in intestinal calcium absorption was only moderate in the present patient group. Furthermore, the hypercalcemia in PHP is not significantly influenced by dietary calcium restriction or treatment with sodium cellulose phosphate [25]. Glucocorticoids, which reduce vitamin D mediated intestinal calcium absorption has no effect on the hypercalcaemia in PHP [26].…”

Effect of Vitamin D Nutrition on Parathyroid Adenoma Weight: Pathogenetic and Clinical Implications*

“…In a patient from whom surgery is withheld for any reason, limiting dietary intake of vitamin D and Ca are often advised in the hope of minimizing the hypercalcemia. Restricting dietary calcium intake can lead to a substantial fall in urinary calcium excretion but to only a trivial fall in plasma calcium, accompanied by increased bone resorption (34), and an increased risk of developing osteitis fibrosa (1,8). Patients with primary hyperparathyroidism need at least as much vitamin D as normal subjects and possibly more, especially because, for a variety of reasons, vitamin D deficiency is becoming more common again (33).…”