The syndrome of phosphorus depletion became widely recognized following the description by Lotz et al1 of hypophosphatemia in patients undergoing prolonged therapy with antacids. Since their description, others have reported similar cases of hypophosphatemia due to therapy with antacids in patients with uremia,2,3 in patients receiving intravenous hyperalimentation without phosphorus supplementation,4-6 and in the debilitated and starved patient.7 The clinical and laboratory findings in these patients included confusion, weakness, anorexia, malaise, paresthesias,1-3,6,7 electroencephalographic and electromyographic changes,3 altered hemoglobin-oxygen affinity,2,4,5 changes in the concentrations of erythrocyte organic phosphates and glycolytic intermediates,2,4,5,7 and, more recently, hemolytic anemia with rigid red blood cells (RBC).7 Metabolic studies in a severely hypophosphatemic patient are presented herein to support the concept that a generalized inhibition of glycolysis and glycogenolysis with subsequent depletion of energy stores may underly the manifestations of severe hypophosphatemia.
A 47-year-old chronic
Klock JC, Williams HE, Mentzer WC. Hemolytic Anemia and Somatic Cell Dysfunction in Severe Hypophosphatemia. Arch Intern Med. 1974;134(2):360–364. doi:10.1001/archinte.1974.00320200170025
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