Abstract

Hepatic Encephalopathy (HE) is one of the major complications of acute or chronic liver failure. Its neurological and mental symptoms range from subtle behavioral abnormalities to deep coma and death. In addition, a subclinical HE state, named minimal HE (mHE) is a very frequent misdiagnosed complication. Although the etiology of hepatic encephalopathy is not fully elucidated, hyperammonemia plays a key role in its development. In liver diseases, its reduced detoxifying capability results in increased blood and brain ammonia concentrations. Under this condition, ammonia is neurotoxic to both neuronal and astrocyte cells in the CNS. Hyperammonemia is also an essential promotor of neuroinflammation increasing proinflammatory cytokines such as IL-1β and IL-6. It is known that even without morphological liver alterations, there are changes in the pro-inflammatory cytokines release and increase in the BBB permeability among other alterations. The aim of this review is to approach the neuroinflammatory aspects of minimal hepatic encephalopathy, where there are no clear manifestations of the disease.

Keywords: Minimal hepatic encephalopathy; Hyperammonemia; Neuroinflammation; Liver disease; Microglia; Astrocyte; AM404