Phosphorus administration in patients with profound hypophosphatemia

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].