Abstract
Hyperlacticacidemia rarely is observed in patients with cancer without shock or hypoxia. A patient with bilateral ovarian lymphoma histologically identical to the Burkitt-tumor demonstrated elevated blood lactic acid but was free of the usual causes of such an increase. The clinical course was manifested by recurrent malignant effusions accompanied by hyperlacticacidemia. Simultaneous studies of arterial blood and the malignant effusions demonstrated acidosis of the effusions (pH 7.11 - 7. 28) with lactic acid concentrations 2 to 3 fold greater (7-12 mEq/1) than blood (1. 7-3. 4 mEq/1). Similar studies on 6 control patients with effusions due to other causes failed to demonstrate comparable gradients between effusion and blood for H+ ions or lactic acid. Urea nitrogen and electrolytes did not show a gradient in the patient with lymphoma or the control patients. Viable malignant lymphoblasts from the patient''s effusions were incubated in tissue culture fluid at 37" C under aerobic and anaerobic conditions. Aerobic lactic acid production was 2.0[mu]M/min. /109 cells, or, for the patient described, 230 mM/ day. These observations suggest that lactic acid production by tumor resulted in unique biochemical gradients between effusions and blood, and was of sufficient magnitude to produce hyperlacticacidemia.

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