Etiology and Causes
A decrease in phosphate levels in the body is triggered by several key factors:
- Dietary factor: deficient intake of micronutrients with food due to malnutrition.
- Renal hyperexcretion: excessive renal excretion in hyperparathyroidism, primary tubular defects, heavy metal poisoning, or cystinosis.
- Gastrointestinal losses: overdose of antacids (which bind phosphates—e.g., sodium bicarbonate, magnesium oxide, calcium carbonate, and aluminum hydroxide), malabsorption syndrome, as well as liver and biliary tract pathologies.
Pathogenesis: Where Do Phosphates Go?
An important mechanism in the development of hypophosphatemia is the redistribution of phosphates from the blood and extracellular fluid into the cells:
- Glycolysis is activated (e.g., during the development of alkalosis).
- Intracellular formation of phosphorylated carbohydrate groups increases.
- The cellular pool of organic phosphate drops, causing phosphates to rush from the blood into the cells along the concentration gradient.
Clinical Manifestations
The clinical presentation is based on severe disturbances of energy metabolism and damage to key organ systems:
- Bones and kidneys: phosphaturia develops. In children, short stature, rickets, limb deformity, and bone pain are observed; in adults, osteomalacia and osteoporosis.
- Muscles: muscle pain, hypotonia, hypokinesia, and dangerous tissue destruction (rhabdomyolysis) occur.
- Cardiovascular system: heart failure may develop.
- Nervous system and immunity: higher nervous activity suffers, neurological disorders and immunodeficiency states develop, and antioxidant defense drops.
Principles of Treatment
The management of hypophosphatemia includes two main directions:
- Elimination of the primary cause: correction of hyperparathyroidism, elimination of tubular defects, and combating conditions that stimulate glycolysis or alkalosis.
- Replacement therapy: administration of special phosphate supplements, the intake of which must be strictly monitored via blood tests.