P78 Patients with alcohol related liver disease have high levels of oxidative stress

Abstract

<h3>Background and Aims</h3> Chronic alcohol use generates reactive oxygen species (ROS) through the CYP2E1 pathway and contributes to the pathogenesis of alcohol-related liver disease (ALD). However, the understanding of the role of ROS in alcoholic hepatitis (AH) is lacking. We aimed to measure oxidative stress in well-defined cohort of ALD and AH patients and compare with healthy subjects using a well-validated and reproducible assay. <h3>Method</h3> Patients from University Hospitals Plymouth with AH (new jaundice, coagulopathy, heavy alcohol use, discriminant function [DF]&gt;32); ALD (ongoing alcohol use, no new jaundice, cirrhosis) and healthy volunteers (HV) were recruited. Model for end stage liver disease (MELD) and DF scores were used to evaluate liver disease severity. Thiobarbituric acid reactive substrate (TBARS) assay kit was used to measure levels of malondialdehyde (MDA)-TBA adduct, a naturally occurring product of lipid peroxidation. <h3>Results</h3> 22 subjects were recruited: 10 AH (6 males; median MELD 12; DF 45.6); 5 ALD (2 males; median MELD 18) and 7 HVs (3 males). MDA was significantly higher in AH vs HVs (median 36.1μM vs 14.8μM; p&lt;0.01) and in ALD vs HVs (median 28.6μM vs 14.8μM; p = 0.03) but similar between AH and ALD patients. In AH patients, there was no strong correlation between MDA levels with MELD or DF (r=0.14 and 0.57, respectively; both p&gt;0.05) (figure 1). <h3>Conclusion</h3> Oxidative stress as measured by lipid peroxidation is increased in patients with ALD and AH when compared to HVs.