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Alcoholic hepatitis (AH) covers a spectrum of disease severities from subclinical liver inflammation to acute liver failure. Among the histological features of alcoholic liver disease (ALD), AH is associated with the highest risk of fibrosis progression, leading to development of cirrhosis in 40% of cases. Patients hospitalised for severe forms of AH show 1-month mortality rates of 40–50%.1 Patients with AH form a heterogeneous population, in severity, and probably in disease pathogenesis. This diverse clinical picture might be caused by various factors including host factors, immunity and as recently suggested, intestinal microbiota (IM).2
Patients with ALD present with an altered IM, a condition that is commonly called ‘dysbiosis’, and an increased intestinal permeability, even at an early stage of alcoholic liver injury; this leads to elevated endotoxin levels, with the highest levels in patients with cirrhosis.3 It has been shown that gut microbiota play an important role in experimental ALD. Mice treated with certain antibiotics are resistant to experimental ALD4 and alcohol-induced liver injury was largely blocked in mice lacking CD14 or TLR4 receptors.5 Administration of certain probiotics such as Lactobacillus rhamnosus GG to alcohol-fed mice improves the GI barrier and liver disease.6 Mutlu et al investigated the mucosa-associated colonic microbiome in subjects with and without …
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