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- W2279367030 abstract "Alcoholic liver disease (ALD) is the most prevalent cause of advanced liver disease in Europe. ALD encompasses a large spectrum of injury, ranging from simple steatosis to frank cirrhosis. A subset of patients with ALD will develop an acute complication termed as alcoholic hepatitis (AH). The true prevalence is unknown, but histological studies of patients with ALD suggest that AH may be present in as many as 10–35% of hospitalized alcoholic patients [ 1 Christoffersen P. Nielsen K. Histological changes in human liver biopsies from chronic alcoholics. Acta Pathol Microbiol Scand A. 1972; 80: 557-565 PubMed Google Scholar , 2 Mendenhall C.L. Alcoholic hepatitis. Clin Gastroenterol. 1981; 10: 417-441 Crossref PubMed Google Scholar ]. Typical histological features of AH consist of a combination of polymorphonuclear neutrophil (PMN) infiltrate, hepatocyte ballooning and Mallory-Denk hyalin bodies. Lipocalin 2 drives neutrophilic inflammation in alcoholic liver diseaseJournal of HepatologyVol. 64Issue 4PreviewAlcohol consumption causes 3.8% of deaths worldwide and substantially contributes to a social and economic burden [1]. Alcoholic liver disease (ALD) displays a spectrum of disease phenotypes that ranges from hepatic steatosis to fibrosis and cirrhosis all of which may result in an acute hepatic inflammatory condition termed alcoholic steatohepatitis (ASH). A substantial proportion of ALD patients, especially heavy drinkers, develop ASH with a very poor prognosis [2]. Mechanistically, it has been suggested that alcohol-induced hepatocyte injury and Kupffer cell (KC) activation initiates a cytokine storm, which in turn propagates the recruitment of leukocytes, e.g. Full-Text PDF" @default.
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- W2279367030 date "2016-04-01" @default.
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- W2279367030 title "Lipocalin 2 highlights the complex role of neutrophils in alcoholic liver disease" @default.
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- W2279367030 doi "https://doi.org/10.1016/j.jhep.2016.01.020" @default.
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