Die Serumkonzenztrationen von S-100B bei Leberzirrhose und transjugulärem intrahepatischen portosytemischen Stent-Shunt in Abhängigkeit von der minimalen hepatischen Enzephalopathie der Leber- und der Nierenfunktion

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Portal-sytemic encephalopathy is prototypical among neuropsychiatric disorders that fall under the term of Hepatic Encephalopathies. Ammonia toxicity is central to the pathophysiology of portal-systemic encephalopathy, and neuronal ammonia toxicity is modulated by activated astrocytes. The calcium-binding astroglial key protein S100B is released in response to glial activation, and measurements in serum have only recently become possible. Serum S100B was determined by an ultrasensitive ELISA in patients (n=34) with liver cirrhosis and transjugular intrahepatic stent-shunt. Minimal hepatic encephalopathy and overt portal-sytemic encephalopathy were determined by age-adjusted psychometric tests and clinical staging respectively. Serum S100B was specifically elevated in the presence of minimal or early portal-systemic encephalopathy. S100B levels elevated above a reference value (S100B < 110 pg/ml). Serum S100B seems to be a promising biochemical surrogate marker for mild cognitive impairments due to portal-systemic encephalopathy. At the same time, the influence of Serum S100B through changes in the liver and the renal function are taken into account.

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