Hepatic Encephalopathy as a Gliopathy

Abstract

Hepatic encephalopathy (HE) is defined as a wide spectrum of neuropsychiatric abnormalities caused by liver dysfunction (acute or chronic) and/or portal-systemic shunting. The histopathologic hallmark of HE is astrocyte swelling following acute liver failure (ALF) or the presence of the so-called Alzheimer type 2 astrocytosis under chronic liver disease. HE can be classified according to the undelaying cause into three types: type A as an essential component of acute liver failure, type B as a consequence of porto-systemic shunts in the absence of liver dysfunction, and type C in patients with liver cirrhosis and porto-systemic bypass. While ammonia, manganese, proinflammatory cytokines, and other precipitating factors play a role in the pathogenesis of HE, the exact mechanisms leading to the development of HE are not fully elucidated. This chapter provides a brief overview of HE with a focus on the mechanisms of AT2A.