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MicroRNA in alcoholic hepatitis: implications for pathophysiology and treatment
  1. Felix Stickel1,
  2. Laurent Dubuquoy2
  1. 1 Department of Gastroenterology and Hepatology, University Hospital of Zurich, Zurich, Switzerland
  2. 2 LIRIC—Lille Inflammation Research International Center—U995, Univ. Lille, Inserm, CHU Lille, Lille, France
  1. Correspondence to Professor Felix Stickel, Department of Gastroenterology and Hepatology, University Hospital of Zurich, Rämistrasse 100, Zurich CH-8091, Switzerland; felix.stickel{at}usz.ch, felix.stickel{at}hirslanden.ch

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Alcoholic hepatitis alcoholic hepatitis (AH) represents a necroinflammatory complication of alcoholic liver disease, which affects a relatively small but considerable fraction of heavy drinkers with various degrees of underlying alcoholic liver damage. The true incidence of alcoholic hepatitis (AH) is unclear, but is found in around 20% of those with available liver histology, and estimated in approximately 10%–35% of alcoholics hospitalised for decompensating liver disease.1 Severe alcoholic hepatitis (AH) severe alcoholic hepatitis (sAH) has a grave prognosis with a 1-month mortality rate of up to 50%, a figure assessed for patients with a discriminant function score of ≥32 in the initial treatment trial by Maddrey and coworkers.2 Since that time, advances in intensive care medicine, response-guided treatment of selected patients with corticosteroids and improved management of infectious complications contributed to a slightly better outcome of patients with severe alcoholic hepatitis (sAH).3 Although randomised clinical trials have explored several options, effective medical treatments that improve the underlying inflammatory process are still restricted to corticosteroids to which only 50% of patients with severe alcoholic hepatitis (sAH) respond adequately.

The pathogenesis of severe alcoholic hepatitis (sAH) involves cytokine-mediated necroinflammation of the liver parenchyma, consecutive hepatocyte damage and cholestasis in the context of a systemic inflammatory response syndrome. Yet, the entire pathophysiology is still only incompletely understood and likely encompasses hitherto unknown mechanisms that could be crucial and potentially exploitable for therapeutic intervention. Hence, studies that pursue novel hypotheses to explore new therapeutic targets are of particular interest. Among the manifold potential mechanisms is that of microRNAs (miRNA) in human diseases, including liver diseases. miRNAs are highly conserved small non-coding RNA molecules that is composed of 18–25 nucleotides involved in epigenetic regulation of numerous target genes either at the posttranscriptional level or transcriptionally via targeting promoter …

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