Phosphorus imbalance refers to conditions in which the element phosphorus is present in the body at too high a level (hyperphosphatemia) or too low a level (hypophosphatemia).
Almost all of the phosphorus in the body occurs as phosphate (phosphorus combined with four oxygen atoms), and most of the body's phosphate (85%) is located in the skeletal system, where it combines with calcium to give bones their hardness. The remaining amount (15%) exists in the cells of the body, where it plays an important role in the formation of key nucleic acids, such as DNA, and in the process by which the body turns food into energy (metabolism). The body regulates phosphate levels in the blood through the controlled release of parathyroid hormone (PTH) from the parathyroid gland and calcitonin from the thyroid gland. PTH keeps phosphate levels from becoming too high by stimulating the excretion of phosphate in urine and causing the release of calcium from bones (phosphate blood levels are inversely proportional to calcium blood levels). Calcitonin keeps phosphate blood levels in check by moving phosphates out of the blood and into the bone matrix to form a mineral salt with calcium.
Most phosphorus imbalances develop gradually and are the result of other conditions or disorders, such as malnutrition, poor kidney function, or a malfunctioning gland.
Hypophosphatemia (low blood phosphate) has various causes. Hyperparathyroidism, a condition in which the parathyroid gland produces too much PTH, is one primary cause. Poor kidney function, in which the renal tubules do not adequately reabsorb phosphorus, can result in hypophosphatemia, as can overuse of diuretics, such as theophylline, and antacids containing aluminum hydroxide. Problems involving the intestinal absorption of phosphate, such as chronic diarrhea or a deficiency of vitamin D (needed by the intestines to properly absorb phosphates) can cause the condition. Malnutrition due to chronic alcoholism can result in an inadequate intake of phosphorus. Recovery from conditions such as diabetic ketoacidosis or severe burns can provoke hypophosphatemia, since the body must use larger-than-normal amounts of phosphate. Respiratory alkylosis, brought on by hyperventilation, can also result in temporary hypophosphatemia.
Symptoms generally occur only when phosphate levels have decreased profoundly. They include muscle weakness, tingling sensations, tremors, and bone weakness. Hypophosphatemia may also result in confusion and memory loss, seizures, and coma.
Hyperphosphatemia (high blood phosphate) also has various causes. It is most often caused by a decline in the normal excretion of phosphate in urine as a result of kidney failure or impaired function. Hypoparathyroidism, a condition in which the parathyroid gland does not produce enough PTH, or pseudoparathyroidism, a condition in which the kidneys lose their ability to respond to PTH, can also contribute to decreased phosphate excretion. Hyperphosphatemia can also result from the overuse of laxatives or enemas that contain phosphate. Hypocalcemia (abnormally low blood calcium) can cause phosphate blood levels to increase abnormally. A side-effect of hyperphosphatemia is the formation of calcium-phosphate crystals in the blood and soft tissue.
Hyperphosphatemia is generally asymptomatic; however, it can occur in conjunction with hypocalcemia, the symptoms of which are numbness and tingling in the extemities, muscle cramps and spasms, depression, memory loss, and convulsions. When calcium-phosphate crystals build up in the blood vessels, they can cause arteriosclerosis, which can lead to heart attacks or strokes. When the crystals build up in the skin, they can cause severe itching.
Disorders of phosphate metabolism are assessed by measuring serum or plasma levels of phosphate and calcium. Hypophosphatemia is diagnosed if the blood phosphate level is less than 2.5 milligrams per deciliter of blood. Hyperphosphatemia is diagnosed if the blood phosphate level is above 4.5 milligrams per deciliter of blood. Appropriate tests are also used to determine if the underlying cause of the imbalance, including assessments of kidney function, dietary intake, and appropriate hormone levels.
Treatment of phosphorus imbalances focuses on correcting the underlying cause of the imbalance and restoring equilibrium. Treating the underlying condition may involve surgical removal of the parathyroid gland in the case of hypophosphatemia caused by hyperparathyroidism; initiating hormone therapy in cases of hyperphosphatemia caused by hypoparathyroidism; ceasing intake of drugs or medications that contribute to phosphorus imbalance; or instigating measures to restore proper kidney function.
Restoring phosphorus equilibrium in cases of mild hypophosphatemia may include drinking a prescribed solution that is rich in phosphorus; however, since this solution can cause diarrhea, many doctors recommend that patients drink 1 qt (0.9 L) of skim milk per day instead, since milk and other diary products are significant sources of phosphate. Other phosphate-rich foods include green, leafy vegetables; peas and beans; nuts; chocolate; beef liver; turkey; and some cola drinks. Severe hypophosphatemia may be treated with the administration of an intravenous solution containing phosphate.
Restoring phosphorus equilibrium in cases of mild hyperphosphatemia involves restricting intake of phosphorus-rich foods and taking a calcium-based antacid that binds to the phosphate and blocks its absorption in the intestines. In cases of severe hyperphosphatemia, an intravenous infusion of calcium gluconate may be administered. Dialysis may also be required in severe cases to help remove excess phosphate from the blood.
Phosphorus imbalances caused by hormonal disorders or other genetically determined conditions cannot be prevented. Hypophosphatemia resulting from poor dietary intake can be prevented by eating foods rich in phosphates, and hypophosphatemia caused by overuse of
Bales, C. W., and M. K. Drezner. "Divalent Ion Homeostasis: Calcium and Phosphorus Metabolism." In Textbook of Internal Medicine, ed. W. N. Kelley. New York: J. B. Lippincott Co., 1992.
Knochel, J. P. "Disorders of Phosphorus Metabolism." In Harrison's Principles of Internal Medicine, ed. Anthony S. Fauci, et al. New York: McGraw-Hill, 1997.
Barcia, J. P., C. F. Strife, and C. B. Langman. "Infantile Hypophosphatemia: Treatment Options to Control Hypercalcemia, Hypercalciuria, and Chronic Bone Demineralization." Journal of Pediatrics 130 (1997): 825-828.
Tom Brody, PhD