Excretion of urocanic acid following oral histidine in heart failure.

et al., 1952). In liver disease or folic acid deficiency, abnormal quantities ofthe metabolites, urocanic acid and formiminoglutamic acid (Figlu), appear in the urine following an oral dose of the amino acid L-histidine (Luhby, Cooperman, and Teller, 1959; Spray and Witts, 1959; Kohn, Mollin, and Rosenbach, 1961; Carter, Schaffner, and Heller, 1960; Bennett and Chanarin, 1962; Merritt et al., 1962). In mammalian liver, the major pathway of histidine metabolism is its degradative conversion via urocanic acid to glutamic acid (Fig. 1). The abnormal excretion of Figlu in heart failure (Grasbeck, Bjorksten, and Nyberg, 1961) was confirmed by one of us (Rose, 1964), and in addition excess urocanic acid was noted. It therefore appeared that the hepatic congestion of heart failure resulted in defective histidine metabolism, and it was decided to study this in more detail. We have therefore estimated the excretion of urocanic acid following an oral dose of histidine in patients with congestive cardiac failure due to