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Hyperphosphatemic Tumoral Calcinosis: Effects of Phosphate Depletion on Vitamin D Metabolism, and of Acute Hypocalcemia on Parathyroid Hormone Secretion and Action^*

Division of Endocrinology and Metabolism, Endocrine Research Unit, Department of Medicine, Mayo Clinic, Rochester, Minnesota 55905

Address requests for reprints to: Edward G. Lufkin, M.D., Department of Internal Medicine, Mayo Clinic, 200 First Street Southwest, Rochester, Minnesota 55905.

In hyperphosphatemic tumoral calcinosis, plasma 1,25-dihydroxyvitamin D [1,25(OH)₂D] levels are inappropriately elevated, suggesting an abnormality in vitamin D metabolism. To define this abnormality further, we measured vitamin D metabolites in two patients and four controls before and after phosphate depletion. The patients showed elevated plasma levels of 1,25(OH)₂D in the basal state. Phosphate depletion reduced serum phosphate in patients from a mean of 6.1 to 2.6 mg/dl; this was accompanied by a rise in plasma 25-hydroxyvitamin D from 33.6 to 41.9 ng/dl, and in 1,25(OH)₂D from 67.7 to 93.2 pg/ml. The absolute rise in 1,25(OH)₂D was similar to that of controls. EDTA infusion produced a normal increase of serum immunoreactive PTH levels and urinary cAMP excretion. In this form of tumoral calcinosis, 1,25(OH)₂D levels are elevated despite hyperphosphatemia, normal immunoreactive PTH, and normal serum calcium concentrations, suggesting an abnormality in the regulation of 1,25(OH)₂D synthesis or metabolism, or alternatively, another undefined stimulus for 1,25(OH)₂D synthesis. These patients appear to have concurrent abnormalities of renal tubular phosphate transport and vitamin D metabolism. (J Clin Endocrinol Metab 56:1319, 1983)

^* This work was supported in part by Grants AM-19607, AM-27440, AM-25409, and AM-26808 from the USPHS, NIH.

Received August 24, 1982.

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