The causes of hypophosphatemia include decreased intestinal absorption (vitamin D deficiency, phosphorus-binding antacids, malabsorption); urinary losses (hyperparathyroidism, hyperglycemic states, X-linked hypophosphatemic rickets, oncogenic osteomalacia, alcoholism, or certain toxins); and shifts of phosphorus from extracellular to intracellular compartments (administration of insulin in diabetic ketoacidosis or by hyperalimentation or refeeding in a malnourished pt). In syndromes of severe primary renal phosphate wasting (X-linked hypophosphatemic rickets, autosomal dominant hypophosphatemic rickets, oncogenic osteomalacia), the phosphatonin hormone FGF23 (fibroblast growth factor 23) plays a key pathogenetic role.
Treatment: Hypophosphatemia Mild hypophosphatemia can be replaced orally with milk, carbonated beverages, or Neutra-Phos or K-Phos (up to 2 g/d in divided doses). For severe hypophosphatemia (0.75 mmol/L; [<2.0 mg/dL]), IV phosphate may be administered at initial doses of 0.2-0.8 mmol/kg of elemental phosphorus over 6 h. The total body phosphate depletion cannot be predicted from the serum phosphate level; careful monitoring of therapy is therefore required. Hypocalcemia should be corrected first, and the dose reduced 50% in hypercalcemia. Serum calcium and phosphate levels should be measured every 6-12 h; a serum calcium × phosphate product of >50 must be avoided. |
Section 13. Endocrinology and Metabolism