Abstract
Changes in intestinal microbiome and barrier function are critical in the development of alcohol-related liver disease (ALD). Here, we determined the effects of a one-week alcohol withdrawal on parameters of intestinal barrier function in heavy drinkers with ALD in comparison to healthy non-drinkers (controls). In serum samples of 17 controls (m = 10/f = 7) and 37 age-matched ALD patients (m = 26/f = 11) undergoing a one-week alcohol withdrawal, markers of liver health and intestinal barrier function were assessed. Liver damage, e.g., fibrosis and hepatic steatosis, were assessed using FibroScan. Before alcohol withdrawal, markers of liver damage, lipopolysaccharide binding protein (LBP) and overall TLR4/TLR2 ligands in serum were significantly higher in ALD patients than in controls, whereas intestinal fatty acid binding protein (I-FABP) and zonulin protein concentrations in serum were lower. All parameters, with the exception of LBP, were significantly improved after alcohol withdrawal; however, not to the level of controls. Our data suggest that one-week of abstinence improves markers of intestinal barrier function and liver health in ALD patients.
Highlights
Age and gender distribution were similar between Alcohol-related liver disease (ALD) patients (n = 37) and controls (n = 17) whereas BMI of ALD patients was significantly higher compared to healthy controls (Table 1)
Liver stiffness was elevated in ALD patients and was significantly lower after withdrawal while fibrosis stages were mostly unchanged
Activities of ALT, AST, and γ-GT in serum were significantly higher in ALD patients than in controls before alcohol withdrawal (Table 1)
Summary
Despite intense public campaigns informing of the risks of high and especially chronic alcohol ingestion, alcohol consumption is still among the leading causes of liver damage in many countries world-wide [1]. Alcohol-related liver disease (ALD) comprises a spectrum of conditions ranging from simple steatosis to alcoholic hepatitis and even advanced fibrosis, as well as cirrhosis [2]. Intense research efforts have been undertaken to delineate molecular mechanisms underlying the development of ALD; mechanisms are still not fully understood and therapies primarily focus on abstinence being afflicted with high relapse rate. It has been shown that the development of ALD is associated with changes of intestinal microbiota composition in the upper parts of the small intestine and elevated bacterial endotoxin levels (for overview see [4]), further suggesting that ALD may be a disease evolving from the direct effects of ethanol metabolism in the liver, e.g., the increase in the ratio of NADH + H+ to NAD+ and induction of CYP2E1
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