Severe alcoholic hepatitis: why do we know a lot, but can do so little?

Abstract

Severe alcoholic hepatitis (SAH) is characterized by high both immediate and long - term mortality, caused by these patients ’ a special form of liver failure development which is acute on the background of chronic one (acute-on-chronic liver failure). Steatosis, oxidative stress, increased permeability of the intestinal wall, the formation of toxic metabolites and the cytokine cascade are considered to be the main pathogenetic elements of the SAH. The course of SAH is accompanied by the so-called liver-associated immunodeficiency, which is associated with a high risk of fatal infectious complications, causing up to А of all deaths. This variant of immunodeficiency is characterized by hyperactivation of some elements of the immune system along with suppression of the activity of others. Despite advances in the study of pathogenesis, today the only therapeutic agent affecting the survival of patients with SAH are corticosteroids. A significant improvement in prognosis in the absence of response to corticosteroid therapy can only be achieved by performing an urgent liver transplant. Currently, several new treatment options for patients with SAH are being developed. We believe that selective influence on key immunopathological processes deserves special attention.