Alcohol-Related Histopathology

Alcoholic liver disease (ALD) has been recognized for centuries, but the growing epidemic of non-alcoholic fatty liver disease (NAFLD) makes it clear that ALD is a subset of the general class of fatty liver diseases. The histopathological findings of both ALD and NAFLD overlap significantly, and this is an important topic to which we will return at the end of this essay. ALD has three categories of histopathological changes: steatosis, steatohepatitis, and steatofibrosis1,2 (Table 1). All these changes begin and are usually most prominent in the centrilobular region of the hepatic lobule. The centrilobular hepatocytes are enzymatically prepared to metabolize alcohol through, for example, cytosolic alcohol dehydrogenase and the induction of cytochrome p450 enzymes.2 Such pathways produce the fatty acids accumulating in steatotic hepatocytes and create the toxic metabolites causing inflammation, hepatocyte injury, and fibrosis. Of course the features described here may often be seen in autopsy and explant specimens because of the role of alcohol in death or the need for transplantation. However, they are most important in the biopsy setting. The publication ‘‘EASL Clinical Practical Guidelines: Management of Alcoholic Liver Disease’’ points to the lack of consensus regarding the role of liver biopsy in the assessment of ALD but suggests the following principles3 : • Percutaneous biopsy may be performed in most patients, but transjugular biopsy is recommended for patients with a low platelet count and/or a prolonged prothrombin time.

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