Resolvin D1 values in patients with alcohol-associated liver disease

Resolvin D1 (RvD1), a specialized pro-resolving lipid mediator, has been associated with liver injury in experimental models of alcohol-associated liver disease (ALD). This study aimed to evaluate the relationship between serum RvD1 levels and clinical phenotypes of ALD.

This case-control study included 82 patients with ALD and 48 healthy controls (HCs). The ALD patients were categorized into three subgroups: alcohol-associated steatotic liver (ASL), alcohol-associated hepatitis (AH), and alcohol-associated cirrhosis (AC). Serum RvD1 levels were measured using the enzyme-linked immunosorbent assay (ELISA) test. The Fibrosis-4 (Fib-4) index was used to assess liver fibrosis in all participants. For the AH and AC groups, the Model for End-stage Liver Disease Sodium (MELD-Na) scores were calculated. Child-Pugh classification was applied to the AC patients and Maddrey's Discriminant Function was applied to the AH patients. An esophagogastroduodenoscopy was performed in the AH and AC patients to evaluate portal hypertension.

The serum RvD1 levels were significantly lower in the AH and AC groups compared to the ASL and HC groups (p < 0.001), with no significant difference between the AH and AC groups or between the ASL groups and the HC group. In the AC group, patients with ascites and/or esophageal/gastric varices had lower serum RvD1 levels compared to those without (p = 0.013 and p = 0.004, respectively). Additionally, the serum RvD1 levels decreased with advancing Child-Pugh class (p = 0.004). The serum RvD1 levels were inversely correlated with the Fib-4 scores, the MELD-Na and Child-Pugh scores in both the AC group (p < 0.05 for all).

Serum RvD1 levels are associated with the severity of ALD and may represent a promising non-invasive biomarker. However, due to the absence of an external validation cohort, these findings should be interpreted as exploratory. Further validation in independent populations is warranted to confirm the clinical utility of RvD1 in ALD.