Only limited quantities of phosphate are stored within cells, and most tissues depend upon ECF Pi for their metabolic phosphate. When ECF Pi levels are low, cellular dysfunction follows. At a whole organism level, the effects of hypophosphatemia include anorexia, anemia, muscle weakness, bone pain, rickets and osteomalacia, general debility, increased susceptibility to infection, paresthesias, ataxia, confusion, and even death (Lotz et al., 1968). The muscle weakness, which involves especially proximal muscle groups when prolonged or severe, can lead to muscle fiber degeneration. The skeleton will exhibit either rickets in children or osteomalacia in adults. In both, the disorder consists of a failure to mineralize forming growth plate cartilage or bone matrix, together with impairment of chondroblast and osteoblast function (Lotz et al., 1968). These severe manifestations are usually confined to situations in which ECF Pi falls below ~0.3 mmol/liter (0.9 mg/dl).

Phosphorus is so ubiquitous in various foods that near total starvation is required to produce dietary phosphorus deficiency. However, movement of sugar into cells pulls Pi into the cells as well. Refeeding of energy-depleted individuals, either orally or parenterally, without adequate attention to supplying Pi, can precipitate extreme, even fatal, hypophosphatemia (Bushe, 1986; Dale et al., 1986; Knochel, 1977, 1985; Ritz, 1982; Silvis and Paragas, 1972; Stein et al., 1966; Travis et al., 1971; Young et al., 1985). Such outcomes can occur on recovery from alcoholic bouts, from diabetic ketoacidosis, and on refeeding with calorie-rich sources without paying attention to phosphorus needs. Also, aluminum-containing antacids, by binding diet phosphorus in the gut, can, when consumed in high doses, produce hypophosphatemia in their own right, as well as aggravate phosphate deficiency related to other problems (Lotz et al., 1968).

In full-term infants, severe hypophosphatemia from purely dietary causes is virtually unknown. It is likely to occur only in situations of poorly managed parenteral nutrition (in which intakes of phosphate are inadequate), with inappropriate administration of fluid and electrolyte therapy (which causes excessive renal phosphorus loss), or with rapid refeeding after prolonged dietary restriction (Koo and Tsang, 1997; Weinsier and Krumdieck, 1981). In the case of severely malnourished infants, especially with accompanying severe diarrhea, hypophosphatemia has been reported with an associated hypokalemia and hypotonia (Freiman et al., 1982).



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