Excessive alcohol consumption leads a spectrum of liver disorders from simple steatosis (fatty liver) to severe forms of liver injury including steatohepatitis, cirrhosis, and hepatocellular carcinoma. Many proinflammatory mediators, metabolic pathways, transcriptional factors, and epigenetic factors have been identified to contribute to the development and progression of alcoholic liver disease (ALD). This chapter discusses ethanol metabolism, ALD pathogenesis, clinical diagnosis and treatment of ALD, and in more detail the advances in the pathogenesis and treatment of ALD. It also describes the neurobiology of alcohol use disorder and treatment of this disorder in patients with ALD. The preoccupation/anticipation or 'craving' stage of the addiction cycle has long been hypothesized to be a key part of the neurocircuitry that mediates relapse in humans. While reductions below harmful drinking levels is beneficial, the cornerstone in the treatment of patients with ALD remains total alcohol abstinence, as abstinence can improve outcome at all stages of liver disease.
CITATION STYLE
Gao, B., Xiang, X., Leggio, L., & Koob, G. F. (2020). Alcoholic liver disease. In The Liver: Biology and Pathobiology (pp. 682–700). wiley. https://doi.org/10.1002/9781119436812.ch53
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