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Vitamin D deficiency is associated with several alterations in mineral metabolism [1]. Initially, the development of secondary hyperparathyroidism maintains normal circulating 1,25-dihydroxyvitamin D (1,25-vitamin D) and serum calcium values, but both these values decrease in advanced vitamin D deficiency. Serum phosphorus values usually decrease because of secondary hyperparathyroidism, but rarely are serum phosphorus values high [1]. The rare variant of hyperphosphatemia with vitamin D deficiency has been attributed to an acquired pseudohypoparathyroidism type II resulting from hypocalcemia and/or receptor desensitization from chronically elevated parathyroid hormone (PTH) values [1, 2].  The paradigm for phosphate regulation changed dramatically with the discovery of bone-derived hormone fibroblast growth factor 23 (FGF23), which allows bone to interact with other organ systems involved in the regulation of mineral homeostasis. FGF23 inhibits production of 1, 25-vitamin D, renal phosphate reabsorption and secretion of PTH [3]. In turn, 1,25-vitamin D and phosphate stimulate FGF23 production. We present a case of intermittent hyperphosphatemia associated with severe vitamin D deficiency in which 25-hydroxyvitamin D (25-vitamin D) and 1,25-vitamin D were markedly decreased in the absence of impaired renal function. In contrast to previous reports of pseudohypoparathyroidism with severe vitamin D deficiency, hypocalcemia was absent and the PTH value was normal. We hypothesize that an abnormal FGF23 response may have played a role in the hyperphosphatemia observed in this patient.

An unusual case of hyperphosphatemia in a vitamin D-deficient patient with tuberculosis