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Reduced Red Cell Glycolysis, 2,3-Diphosphoglycerate and Adenosine Triphosphate Concentration, and Increased Hemoglobin-Oxygen Affinity Caused by Hypophosphatemia

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Presented 8 December 1970 at the Annual Meeting of the American Society of Hematology, San Juan, P.R.

Supported by grants HE06241-09, HE5500, AM13947-01, RR44, and General Research Support Grant, U.S. Public Health Service, Washington, D.C.; grant DA49-193-MD-2656, U.S. Army Medical Research and Development Command, Washington, D.C.; and the U.S. Atomic Energy Commission at the University of Rochester Atomic Energy Project, Rochester, N.Y.

Dr. Lichtman is a Scholar of the Leukemia Society of America; Dr. Cohen is a recipient of a Research Career Development Award K3, HE17, 885, U.S. Public Health Service.

This paper has been assigned Publication No. UR-49-1341.

▸Requests for reprints should be addressed to Marshall A. Lichtman, M.D., Department of Medicine, University of Rochester Medical Center, 260 Crittenden Blvd., Rochester, N.Y. 14620

Rochester, New York

Ann Intern Med. 1971;74(4):562-568. doi:10.7326/0003-4819-74-4-562
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A marked reduction in red cell glucose utilization, lactate production, and 2,3-diphosphoglycerate and adenosine triphosphate concentration occurred in a patient with intractable diarrhea during a period of hypophosphatemia induced by parenteral nutrition with hypertonic glucose and protein hydrolysate. During the period of hypophosphatemia the patient's hemoglobin had an increased affinity for oxygen. Restoration of plasma phosphate to normal in vivo or in vitro corrected the metabolic abnormalities of the patient's erythrocytes. During normophosphatemia hemoglobin-oxygen affinity was decreased in keeping with the increase in red cell organic phosphates associated with anemia. Therefore, severe hypophosphatemia in man can produce significant limitations on red cell metabolism, resulting in a curtailment of glycolysis, reduction of organic phosphates, and an inefficient relationship between hemoglobin and oxygen. Tissue oxygen delivery could be impaired under such circumstances. Furthermore, adenosine triphosphate levels can reach concentrations that threaten the survival of the red cell. These observations also provide support for the critical role of extracellular inorganic phosphate concentration in the maintenance and modulation of red cell metabolism in vivo.





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