The influence of severe hypophosphatemia (≤1.0 mg/dl) on vitamin D metabolism was prospectively determined in 11 patients before and after intravenous phosphorus administration. Evidence of liver dysfunction was present in ten patients. The mean (±SE) plasma 25 hydroxycholecalciferol [25(OH)D] was significantly decreased before phosphorus therapy when compared to control subjects (9.4 ± 1.3 vs. 17.8 ± 1.3 ng/ml, P < 0.001). With phosphorus administration, serum phosphorus increased from 0.59 ± 0.07 to 2.58 ± 0.09 mg/dl while 1.25 dihydroxycholecalciferol [1,25(OH)2D] decreased from 34.6 ± 4.3 o 14.3 ± 2.9 pg/ml (P < 0.001). Plasma 25(OH)D, plasma immunoreactive PTH (both amino and carboxyterminal) and serum calcium did not change after phosphorus administration, suggsting that phosphorus alone was responsible for the change in plasma 1,25(OH)2D concentration. An inverse correlation was found between serum phosphorus and plasma 1,25(OH)2D (r = -0.62, P < 0.005). In addition, a direct correlation was observed between plasma 25(OH)D and 1,25(OH)2D both before (r = 0.66, P < 0.005) and after (r = 0.74, P < 0.005) phosphorus administration. Thus, the decrease in 1,25(OH)2D levels with phosphorus therapy suggests a role of serum phosphate in the regulation of this sterol, and hypophosphatemia or phosphorus depletion may change the relationship of substrate [25(OH)D] to product [1,25(OH)2D].
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