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.

Patient SummaryÌý A 47-year-old chronic