Hypophosphatemia

Introduction Phosphorus metabolism disorder caused by lower than normal phosphate concentration in circulating blood. Also known as hypophosphatemia. The table is currently hemolysis, burnout, weakness and convulsions. The cause is fasting, long-term use of aluminum hydroxide, magnesium hydroxide or aluminum carbonate and other binding agents, glycolysis and alkalosis, hyperthyroidism, vitamin D deficiency, certain tubular diseases (such as Fanconi syndrome) ), alcoholism and anti-vitamin D rickets (familial hypophosphatemia). Treatment can be intravenous rehydration and phosphate supplementation, while treating the cause.

Cause

The general diet contains sufficient phosphate. However, hypophosphatemia can occur in the following situations: Fasting, especially in patients with high intravenous nutrition, glucose can increase the uptake of phosphate by cells, leading to hypophosphatemia. Long-term use of a combination of aluminum hydroxide, magnesium hydroxide or aluminum carbonate to inhibit the intestinal absorption of phosphate. Glycolysis and alkalosis can rapidly deplete the concentration of intracellular phosphate and increase the uptake of phosphate by cells, causing hypophosphatemia. After insulin treatment in patients with diabetic acidosis, glycolysis increases and phosphate also moves into the cells. Hyperparathyroidism, increased secretion of parathyroid hormone, increased urinary phosphate excretion. Vitamin D deficiency reduces the absorption of phosphate in the intestine. Some tubular diseases, such as Fanconi's syndrome, have a marked increase in urinary phosphate excretion. Alcoholism, caused by reduced diet, increased glycolysis, and treatment of gastritis with an acid-resistant binder, causes hypophosphatemia. Anti-vitamin D rickets (familial hypophosphatemia), sexually linked dominant genetic disease, near-curved small tube phosphorus reabsorption, intestinal calcium absorption is also poor.

The most common cause of hypophosphatemia is alkalosis (respiratory and metabolic). Usually hypophosphatemia can be identified by the following procedure: urinary phosphate is determined after the cause of alkalosis is ruled out. If urinary phosphate excretion increases, plasma calcium is measured. Increased plasma calcium, consider primary hyperparathyroidism, ectopic parathyroid gland, malignant tumor; if the plasma calcium is normal or reduced, consider secondary hyperparathyroidism, rickets or osteomalacia, Fan Ke Nissl's syndrome, low phosphate blood rickets. Urinary phosphate excretion is reduced, and dietary phosphate reduction, antacid therapy, and insulin therapy should be considered.

an examination

Related inspection

Blood routine blood phospholipid (PL)

The most common cause of hypophosphatemia is alkalosis (respiratory and metabolic). Usually hypophosphatemia can be identified by the following procedure: urinary phosphate is determined after the cause of alkalosis is ruled out. If urinary phosphate excretion increases, plasma calcium is measured. Increased plasma calcium, consider primary hyperparathyroidism, ectopic parathyroid gland, malignant tumor; if the plasma calcium is normal or reduced, consider secondary hyperparathyroidism, rickets or osteomalacia, Fan Ke Nissl's syndrome, low phosphate blood rickets. Urinary phosphate excretion is reduced, and dietary phosphate reduction, antacid therapy, and insulin therapy should be considered.

Differential diagnosis

Symptoms of hypophosphatemia are: central nervous system symptoms such as paresthesia, dysarthria, hyperreflexia, tremors, ataxia, and coma. Since red blood cell 2,3-diphosphoglycerate is reduced, the life span of red blood cells is shortened, and spherical red blood cell disease and hemolysis can be expressed. Weak, weak muscles, muscle pain, and even paralysis. Bone pain (due to osteomalacia), a false fracture can be seen on the X-ray film. Leukocyte phagocytosis is dysfunctional and prone to infection. Platelet dysfunction, decreased platelet aggregation ability.

1, the identification of vitamin D deficiency rickets

The identification of this disease and vitamin D deficiency rickets is based on the following characteristics:

(1) The intake of vitamin D has exceeded the general requirement and there is still a skeletal change in active rickets.

(2) There is still activity of active rickets after 2 to 3 years old.

(3) Intramuscular injection of 400,000 to 600,000 U of vitamin D, the blood phosphorus increased in a few days for children with general D deficiency rickets, and the long bone X-ray showed improvement in 2 weeks, but the patients did not have these changes.

(4) Hypophosphatemia is common among family members and is a feature of low phosphorus anti-D rickets.

2. Identification with hypocalcemia and anti-vitamin D rickets

The disease should also be differentiated from hypocalcemia and anti-vitamin D rickets. The latter, also known as vitamin D dependent rickets, is less common because the kidney lacks 1-hydroxylase and cannot synthesize 1,25-(OH)2D3. The onset time is often accompanied by muscle weakness from several months after birth, and early hand and foot sputum can occur. Blood calcium is reduced, blood phosphorus is normal or slightly lower, blood chlorine is increased, and amino acid urine can occur. Although it is treated with conventional dose of vitamin D, it still shows signs of rickets on X-ray long bone tablets. To increase the amount of vitamin D to 10,000 U / d or dihydrotachysterol (DHT) 0.2 ~ 0.5 mg / d to see the effect. Healed with 0.25 to 2 g of 1,25-(OH)2D3. This disease is generally autosomal recessive.

3. Other

In addition, the disease must be differentiated from Fanconi syndrome and renal tubular acidosis.

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