Abstract
Background: The association between markers of inflammation (interleukin (IL)-6 and IL-10), monocyte activation (sCD163 and sCD14), and microbial translocation (lipopolysaccharide (LPS) and LPS binding protein) and liver fibrosis in patients with alcohol use disorder (AUD) and no overt liver disease is not well established. Methods: We studied patients admitted for treatment of AUD at two hospitals in Barcelona. Advanced liver fibrosis (ALF) was defined as FIB-4 > 3.25. Results: A total of 353 participants (76.3% male) were included and 94 (26.5%) had ALF. In adjusted correlation analyses, sCD163, sCD14, IL-6, IL-10, and LPS binding protein levels directly correlated with FIB-4 values (adjusted correlation coefficients 0.214, 0.452, 0.317, 0.204, and 0.171, respectively). However, LPS levels were inversely associated with FIB-4 (−0.283). All plasma marker levels in the highest quartile, except LPS, were associated with ALF (sCD163, sCD14, IL-6, IL-10, and LPS binding protein: adjusted odds ratio (aOR) 11.49 (95% confidence interval 6.42–20.56), 1.87 (1.11–3.16), 2.99 (1.79–5.01), 1.84 (1.11–3.16), and 2.13 (1.30–3.50), respectively). Conversely, LPS levels in the lowest quartile were associated with ALF (aOR 2.58 (1.48–4.58), p < 0.01). Conclusion: In AUD patients, plasma levels of the markers of inflammation, monocyte activation, and microbial translocation are associated with ALF.
Highlights
IntroductionAlcohol use promotes microbial translocation due to changes in the microbiome and increased intestinal permeability, leading to systemic inflammation, monocyte activation, and progression of liver disease [2]
Alcohol-related liver disease is the most frequent alcohol-related chronic medical problem and alcohol use is a major culprit of the global increase in liver-related deaths [1].Alcohol use promotes microbial translocation due to changes in the microbiome and increased intestinal permeability, leading to systemic inflammation, monocyte activation, and progression of liver disease [2]
Each row represents a different model. a Adjusted for sex, alcohol intake, and HCV infection. In this series of AUD patients with no decompensated liver disease admitted for hospital treatment of the disorder, plasma marker levels consistent with increased monocyte activation and increased systemic inflammation were associated with the presence of advanced liver fibrosis (ALF), as were higher LPS binding protein (LBP) levels
Summary
Alcohol use promotes microbial translocation due to changes in the microbiome and increased intestinal permeability, leading to systemic inflammation, monocyte activation, and progression of liver disease [2]. The early diagnosis of subjacent liver disease in otherwise healthy patients with AUD is intriguing [4] and there is an interest in obtaining markers to better stratify the risk of progressive liver injury among patients with unhealthy alcohol use [5]. All of the aforementioned pathological features (intestinal permeability, microbial translocation, systemic inflammation, and monocyte activation) have been thoroughly studied in patients with overt end-stage liver disease or severe alcoholic hepatitis [6,7,8,9], but they have been far less frequently assessed in patients with AUD without end-stage liver disease admitted for hospital treatment of the disorder [10,11]. SCD14 and sCD163 are markers of monocyte activation [2], with sCD14 levels representing monocyte activation dependent on lipopolysaccharide (LPS)
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