Abstract
Alcohol use disorder is associated with a wide array of hepatic pathologies ranging from steatosis to alcoholic-related cirrhosis (AC), alcoholic hepatitis (AH), or hepatocellular carcinoma (HCC). Biomarkers are categorized into two main categories: biomarkers associated with alcohol consumption and biomarkers of alcoholic liver disease (ALD). No ideal biomarker has been identified to quantify the degree of hepatocyte death or severity of AH, even though numerous biomarkers have been associated with AH. This review provides information of some of the novel and latest biomarkers that are being investigated and have shown a substantial association with the degree and severity of liver injury and inflammation. Importantly, they can be measured noninvasively. In this manuscript, we consolidate the present understanding and prospects of these biomarkers; and their application in assessing the severity and progression of the alcoholic liver disease (ALD). We also review current and upcoming management options for AH.
Highlights
Alcohol consumption has a major role in the development of alcoholic liver disease (ALD) in the United States [1]
The phenotypical manifestation of ALD consists of steatosis, steatohepatitis, alcoholic cirrhosis (AC), alcoholic hepatitis (AH) and hepatocellular carcinoma (HCC) depending on the chronic and heavy nature of alcohol intake [3,4,5,6]
In one study [41], soluble CD163 (sCD163) levels were 30% higher in AH when compared alcoholic cirrhosis and 10 times higher when compared to a healthy control group
Summary
Alcohol consumption has a major role in the development of alcoholic liver disease (ALD) in the United States [1]. Several biomarkers have been identified and have been linked as a possible therapeutic target to reduce inflammatory pathways in the liver [10]. This has led to the classification of biomarkers based on both alcohol consumption as well as ALD. Established markers of liver damage (AST and ALT) are highly nonspecific [11], and are affected by a wide array of pathologies. This creates a gap in understanding and characterization of AH as well, which has been historically classified using surrogate biomarkers. We have provided review of the current and upcoming therapeutic options for AH
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