Effect of Pyridoxine-2-Oxoglutarate Administration in Patients with Advanced Cirrhosis : Control of Ammonia Pyruvate and Lactate High Plasma Concentrations

Abstract

The treatment of cirrhotic patients with impending coma is often limited, being the pathogenesis of hepatic encephalopathy barely known. The currently most employed therapeutic measures are directed towards reducing hyperammonemia, although a causative relation between elevated ammonia concentrations in plasma or CSF and the encephalopathy has not been firmly established¹. Cirrhotic liver has a lowered ability to clear ammonia, therefore it is necessary to inhibit ammonia production or to enhance its extra-hepatic utilization. Oxoglutaric acid, an intermediate of the trycarboxilic acid cycle (TAC), has been used in order to reduce high ammonia concentrations because it can be aminated to form glutamic acid in extrahepatic tissues^2,3. Administration of oxoglutaric acid in pharmacological doses could affect other metabolites as well as ammonia, however there are no studies evaluating such effects in cirrhotic patients. Since changes in the amino acid pattern or in the concentrations of some products of glucose oxidization could be involved in the pathogenesis of the hepatic encephalopathy, we studied the effect of both acute and chronic administration of oxoglutaric acid on ammonia, amino acids, glucose, lactic and pyruvic acids in cirrhotic patients with hyperammonemia.