Abstract
Hypophosphatemia is frequently observed in a variety of disease states including ketoacidosis, chronic alcoholism, malabsorption, severe burns, hyperparathyroidism, renal tubular defects, and re-feeding after starvation (1, 2). Since phosphate is a ubiquitous anion involved in such diverse functions as maintaining the structural integrity of the cell membrane, regulating a variety of intracellular enzymes, energy storage in the form of ATP, and regulating tissue delivery of oxygen through 2,3-DPG levels (2), it is not surprising that the clinical syndromes associated with phosphate depletion are equally diverse. Pathophysiologic disturbances associated with hypophosphatemia include hemolytic anemia, rhabdomyoly-sis, myopathy, impaired cardiac output, CNS abnormalities (encephalopathy, seizures), abnormal liver function tests, and platelet and leukocyte dysfunction (1, 2).
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© 1982 Plenum Press, New York
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Simonson, D., DeFronzo, R.A. (1982). Hypophosphatemia and Glucose Intolerance. In: Massry, S.G., Letteri, J.M., Ritz, E. (eds) Regulation of Phosphate and Mineral Metabolism. Advances in Experimental Medicine and Biology, vol 151. Springer, Boston, MA. https://doi.org/10.1007/978-1-4684-4259-5_28
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DOI: https://doi.org/10.1007/978-1-4684-4259-5_28
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