Metabolic and therapeutic studies of a patient with acute leukemia and severe lactic acidosis of prolonged duration

Abstract

A young man with acute nonlymphocytic leukemia had severe lactic acidosis for 11 months from the time of diagnosis until shortly before death except for a period of 3 weeks during which his leukemia was in complete remission. Severe respiratory alkalosis followed that brief remission. The clearance rate of neither fructose nor lactate from the blood was abnormal, but the clearance of blood glucose was accelerated. These data suggest that elevated blood lactate levels resulted from an overproduction of lactate from glucose. In vitro peripheral blood leukocyte incubation failed to demonstrate increased lactate production by these cells. However, the severity of acidosis correlated with peripheral white cell counts and with the percentage of blast forms in bone marrow aspirates obtained serially throughout the patient's course. These studies suggest that marrow leukemic cells or leukemic cells infiltrating parenchymal organs such as the liver may be responsible for the excess production of lactate. Despite arterial lactate concentrations as great as 42 meq/liter, the patient was ambulatory and felt well when given enough alkali to maintain a near normal arterial pH. When the requirement for sodium bicarbonate reached 2,400 meq/day intravenously, oral sodium and potassium acetate therapy was better tolerated and found to be at least equally as effective. Such therapy allows the patient to be mobile and represents an advance in the therapy of lactic acidosis in the conscious patient.