Disorders of phosphorus metabolism caused by lower than normal concentrations of phosphate in circulating blood, also known as hypophosphatemia, manifesting as hemolysis, lethargy, weakness and convulsions. Causes include fasting, prolonged use of aluminum hydroxide, magnesium hydroxide or aluminum carbonate and other binding agents, glycolysis and alkalosis, hyperthyroidism, vitamin D deficiency, certain renal tubular diseases (such as Fanconi’s syndrome), alcoholism and anti-vitamin D rickets (familial hypophosphatemia). Pathogenesis: The general diet contains adequate phosphate. However, hypophosphatemia can occur in the following situations: 1, fasting, especially in patients undergoing intravenous hypernutrition, because glucose can increase cellular uptake of phosphate, resulting in hypophosphatemia. 2, long-term administration of aluminum hydroxide, magnesium hydroxide or aluminum carbonate a binding agent to inhibit the intestinal lumen absorption of phosphate. 3, glycolysis and alkalosis, can rapidly deplete the concentration of intracellular phosphate, increasing the cellular uptake of phosphate, thus causing hypophosphatemia. After insulin therapy in patients with diabetic acidosis, glycolysis increases and phosphate moves intracellularly. 4, hyperparathyroidism, increased secretion of parathyroid hormone, so that urinary phosphate excretion increased. 5, vitamin D deficiency, reducing the absorption of phosphate in the intestinal lumen. 6, certain renal tubular diseases, such as Fanconi’s syndrome, when urinary phosphate excretion increased significantly. 7, alcoholism, due to reduced diet, increased glycolysis and treatment of gastritis with antacid binding agents, causing hypophosphatemia. 8, anti-vitamin D rickets (familial hypophosphatemia), a sex-linked dominant disorder, proximal tubular phosphorus reabsorption disorder, intestinal calcium absorption is also poor.