Inflammation and Hepatic Encephalopathy

Abstract

Hepatic Encephalopathy (HE) is a life-threatening and complicated neuropsychiatric syndrome which is associated with the presence of porto-systemic shunting, and/or with acute and chronic liver injury. Ammonia plays a central and incontrovertible role in pathogenesis of HE, however, a full-bodied evidence base is present indicating the major role played by inflammation in exacerbating the HE caused neurological effects. Research progressed showcasing the diverse face of HE and characterized the key roles of inflammation, infection, and oxidative stress along with other possible parameters. Inflammation is a very common and significant biological process which functions by generating a plethora of molecules, acting in response to tissue alterations. Such response is a result of tissues trying to maintain and restore their integrity and alter back the homeostasis by inducing various repair mechanisms. Regulation of these processes is essential to ensure the equilibrium and to avoid uncontrolled amplification of the response which might lead to disease progression further down the spectrum.