Dipropylacetate and aminoaciduria

Dipropylacetate (DPA) is an anticonvulsant, which has been successfully used in the treatment of several types of epilepsy. The mode of action has not yet been definitely elucidated, although evidence of influence on gamma aminobutyric acid (GABA) turnover in brain has been presented. Several recent reports of the occurrence of hyperglycinemia in association with DPA-treatment indicate that this agent also influences other areas of amino acid metabolism. In the present study of 10 patients receiving DPA for epilepsy, high concentrations of glycine in plasma and CSF were observed, whereas the levels of all other amino acids remained virtually unchanged. The effect of DPA on urinary excretion of amino acids seems to be of considerable significance as marked elevation of urine concentrations of alanine, asparagine, cystine, glycine, histidine, isoleucine and leucine, phenylalanine and tyrosine were observed. This secondary hyperglycinemia could be due to suppression of glycine conjugation reactions, whereas DPA or its metabolites might interfere with tubular reabsorption of various amino acids, thereby causing hyperaminoaciduria.