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In this tutorial we will use a cerebrospinal fluid metabolic fingerprint of the hepatic encephalopathy disease described in [Weiss et al., 2016](https://europepmc.org/article/med/27520878). Hepatic encephalopathy (HE) corresponds to the neurological or neuropsychological symptoms of acute or chronic liver failure and/or portosystemic shunt. The spectrum goes from mild neuropsychological symptoms to impaired level of consciousness, often leading to coma. Even if the physiopathology is still largely unrevealed, the major role of hyperammonemia in conjunction of inflammation is [well established](https://europepmc.org/article/med/27520878). As a consequence, glutamine levels increase in the brain. However, the sole abundance of ammonemia does not scale with symptoms’ severity and it has been shown that associated inflammation, increased levels of TNF-alpha and IL-6, were much better correlated to symptoms’ severity.
In this tutorial we will use a cerebrospinal fluid metabolic fingerprint of the hepatic encephalopathy disease described in [Weiss et al., 2016](https://europepmc.org/article/med/27520878). Hepatic encephalopathy (HE) corresponds to the neurological or neuropsychological symptoms of acute or chronic liver failure and/or portosystemic shunt. The spectrum goes from mild neuropsychological symptoms to impaired level of consciousness, often leading to coma. Even if the physiopathology is still largely unrevealed, the major role of hyperammonemia in conjunction of inflammation is [well established](https://europepmc.org/article/med/27520878). As a consequence, glutamine levels increase in the brain. However, the sole abundance of ammonia does not scale with symptoms’ severity and it has been shown that associated inflammation, increased levels of TNF-alpha and IL-6, were much better correlated to symptoms’ severity.