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Alcoholic Hepatitis: A Review.

Alcoholic liver disease (ALD) represents a spectrum of injury, ranging from simple steatosis to alcoholic hepatitis to cirrhosis. Regular alcohol use results in fatty changes in the liver which can develop into inflammation, fibrosis and ultimately cirrhosis with continued, excessive drinking. Alcoh...

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Published in:Alcohol & Alcoholism. Supplement Vol. 54; no. 4; pp. 408 - 417
Main Authors: Hosseini, Nooshin, Shor, Julia, Szabo, Gyongyi
Format: algorithm pictorial review tables/charts Journal Article
Published: Oxford University Press / USA Jul2019
Online Access:View this record in EBSCOhost
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        13586173
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      jtl: Alcohol & Alcoholism. Supplement
      issn: 13586173
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    pubinfo:
      dt: Jul2019
      vid: 54
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      pub: Oxford University Press / USA
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        10.1093/alcalc/agz036
        138251628
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      tig:
        atl: Alcoholic Hepatitis: A Review.
      aug:
        au:
          Hosseini, Nooshin
          Shor, Julia
          Szabo, Gyongyi
        affil: University of Massachusetts, Gastroenterology, University of Massachusetts Medical School
      sug:
        subj:
          Hepatitis, Alcoholic Pathology
          Hepatitis, Alcoholic Mortality
          Hepatitis, Alcoholic Drug Therapy
          Inflammation Risk Factors
          Fibrosis Risk Factors
          Liver Cirrhosis, Alcoholic Risk Factors
          Binge Drinking Risk Factors
          Morbidity
          Treatment Outcomes
          Reactive Oxygen Species
          Macrophages
          Neutrophils
          Liver Pathology
          Cytokines Metabolism
          Prednisolone Therapeutic Use
      ab: Alcoholic liver disease (ALD) represents a spectrum of injury, ranging from simple steatosis to alcoholic hepatitis to cirrhosis. Regular alcohol use results in fatty changes in the liver which can develop into inflammation, fibrosis and ultimately cirrhosis with continued, excessive drinking. Alcoholic hepatitis (AH) is an acute hepatic inflammation associated with significant morbidity and mortality that can occur in patients with steatosis or underlying cirrhosis. The pathogenesis of ALD is multifactorial and in addition to genetic factors, alcohol-induced hepatocyte damage, reactive oxygen species, gut-derived microbial components result in steatosis and inflammatory cell (macrophage and neutrophil leukocyte) recruitment and activation in the liver. Continued alcohol and pro-inflammatory cytokines induce stellate cell activation and result in progressive fibrosis. Other than cessation of alcohol use, medical therapy of AH is limited to prednisolone in a subset of patients. Given the high mortality of AH and the progressive nature of ALD, there is a major need for new therapeutic intervention for this underserved patient population.
      pubtype: Academic Journal
      doctype:
        algorithm
        pictorial
        review
        tables/charts
        Journal Article
      ougenre: Article
    language: English
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