Serum level changes of endogenous and postheparin diamine oxidase (histaminase) in clinical and experimental hepatitis.

In patients suffering from acute viral hepatitis (n = 12) an about 50 per cent decrease of serum diamine oxidase (DAO, histaminase, E.C.N. 1.4.3.6) was detected as compared to a healthy control group (n = 24). Normally, the intravenous injection of heparin is promptly followed by a marked rise of plasma DAO. In viral hepatitis, however, after application of heparin (200 IU/kg b.w., i.v.) the enzyme release from the visceral organs into the plasma was markedly decreased. There was an inverse correlation between the serum glutamic pyruvic transaminase (SGPT) and the postheparin enzyme. Normalization of SGPT occurred before the normalization of post-heparin diamine oxidase (PHD). In galactosamine "hepatitis" of rats (800 mg Gal-N/kg b.w., i.p.), in contrary to human viral hepatitis plasma DAO increased about 5-fold after heparin application. This increased PHD in plasma of Gal-N rats was correlated to enhanced animal's endogenous plasma DAO activity (r=0.685, p less then 0.0005, n = 54). The cause of these enzyme activity changes and its possible pathophysiological meaning are still unknown. It is concluded from these experiments that in Gal-N "hepatitis" of rats plasmatic DAO level changes are mediated by endogenous heparin, released from disrupted mast cells. Increased basal DAO levels correspond to the enhanced release after heparin application, both possibly induced by less stable binding of the enzyme to the cells of the small intestine in inflammation. Both, decreased endogenous and post-heparin DAO levels in human hepatitis would correspond to a depletion of the enzyme containing organs.