A disorder of phosphorus metabolism caused by a lower than normal concentration of phosphate in the circulating blood. Also known as hypophosphatemia. Manifestations include hemolysis, lethargy, weakness, and convulsions. Causes include fasting, prolonged use of aluminum hydroxide, magnesium hydroxide or aluminum carbonate binding agents, glycolysis and alkalosis, hyperthyroidism, vitamin D deficiency, certain renal tubular diseases (e.g., Fanconi’s syndrome), alcoholism and anti-vitamin D rickets (familial hypophosphatemia). Treatment may include intravenous rehydration and phosphate supplementation, as well as treatment for the cause. Etiology of hypophosphatemia: The general diet contains adequate phosphate. However, hypophosphatemia can occur in the following situations: fasting, especially in patients undergoing intravenous hypernutrition, as glucose increases cellular uptake of phosphate, leading to hypophosphatemia. Prolonged administration of binding agents such as aluminum hydroxide, magnesium hydroxide, or aluminum carbonate, which inhibit the intestinal lumenal absorption of phosphate. Glycolysis and alkalosis, which can rapidly deplete intracellular phosphate concentrations, increase cellular uptake of phosphate, resulting in hypophosphatemia. After insulin therapy in patients with diabetic acidosis, glycolysis increases and phosphate moves intracellularly. Hyperparathyroidism with increased secretion of parathyroid hormone, which increases urinary phosphate excretion. Vitamin D deficiency, which reduces intestinal luminal phosphate absorption. Certain renal tubular diseases, such as Fanconi’s syndrome, when urinary phosphate excretion is significantly increased. Alcoholism, which causes hypophosphatemia due to reduced diet, increased glycolysis, and treatment of gastritis with antacid binding agents. Anti-vitamin D rickets (familial hypophosphatemia), a sex-linked dominant disorder with impaired proximal tubular phosphorus reabsorption and poor intestinal calcium absorption.