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A Detailed Evaluation of Oral Phosphate Therapy in Selected Patients With Primary Hyperparathyroidism^*

Departments of Internal Medicine, Radiology, and Pediatrics, Yale University, New Haven, Connecticut 06510; Research and Medical Services, Veterans Administration Medical Center, Houston, Texas 77211; and the National Animal Disease Center, Ames, Iowa 50010

Address requests for reprints to: Arthur E. Broadus, M.D., Ph.D., Department of Internal Medicine, Yale University School of Medicine, Box 3333, 2088 LMP, New Haven, Connecticut 06510.

Recent studies have emphasized the pathophysiological importance of circulating 1,25-dihydroxyvitamin D [1,25-(OH)₂D] in the pathogenesis of hypercalciuria and renal stone formation in primary hyperparathyroidism. Reasoning that phosphate administration might be capable of reducing the plasma concentration of 1,25-(OH)₂D in patients with a prominent l,25-(OH)₂D-mediated absorptive component to their disease, 10 carefully selected patients were treated with oral phosphate (1500 mg elemental phosphorus daily) for 1 yr.

Phosphate treatment significantly reduced circulating 1,25-(OH)₂D levels (84 to 56 pg/ml), the calciuric response to an oral calcium tolerance test (0.30 to 0.21 mg calcium/dl GF), and calcium excretion on an unrestricted calcium diet (438-269 mg/day), in essence reversing the absorptive pattern of abnormalities observed before treatment. This response, however, was accompanied by an increase in biochemical hyperparathyroidism, as assessed by circulating immunoreactive PTH and nephrogenous cAMP excretion.

In patients with biochemical evidence of an increase in bone resorption before therapy, histomorphometric, radiographic, and biochemical data revealed a trend toward a reduction in bone turnover during phosphorus therapy, with an apparent maintenance of coupled bone resorption and bone formation. This trend, however, was of marginal statistical significance in the patient group as a whole.

It is concluded 1) that phosphate therapy represents a viable medical alternative in selected patients with primary hyperparathyroidism, 2) that the net response in treated patients is multifaceted and complex, and 3) that the efficacy of phosphate therapy will ultimately depend upon its long term effects on skeletal homeostasis. (J Clin Endocrinol Metab 56: 953 1983)

^* This work was supported in part by NIH Grants RR-125 and AM-20570, the General Clinical Research Center, Yale-New Haven Hospital, and the V.A.

Received August 12, 1982.

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