RESUMEN
BACKGROUND: The pathophysiology of hepatic encephalopathy (HE) is incompletely understood. It remains elusive how the contributing factors of neuronal ammonia accumulation, cell swelling, and inflammation interact. OBJECTIVE: The objective of this study was to find the correlation between neuronal autoantibody levels and the degree of HE as first indication of immune-mediated pathogenesis. METHODS: We investigated serum autoantibody levels of representative brain proteins in patients with HE as well as in an experimental rat model with cirrhosis and HE after carbon tetrachloride exposure. They were examined in relation to presence of HE and the degree of neurological impairment evaluated by quantitative scores. RESULTS: In HE, an increase in all of the examined antibodies was observed in serum. The grade of antibody elevation correlated to the degree of encephalopathy registered by quantitative evaluation of brain dysfunction. CONCLUSION: The degree of HE parallels neuronal autoantibody elevation. In case a causal relationship could finally be established, it adds to the understanding of HE and may open a new perspective for treatment of this handicapping condition by immunosuppressive strategies.