Investigating the link between alcohol use disorder and the severity of acute respiratory distress syndrome

Abstract

Background. Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) are acute respiratory failure syndromes with a high mortality rate. Byproducts of alcohol metabolism like acetaldehyde and reactive oxygen species lead to oxidative stress and inflammation which could worsen recovery outcomes, due to increased risks for conditions like systemic inflammation, sepsis and immune dysfunction. Objective of study. Investigate the mechanisms by which alcohol use helps the development of ALI and ARDS. Explore Wnt/β-catenin pathway as a therapeutic target to counteract these effects. Material and methods. This article is based on information gathered from publications and literature published on PubMed, Google Scholar and NCBI. Results. Patients with alcohol use disorder (AUD) have a 2-4 times higher risk of developing ARDS. People with a history of alcohol abuse have twice the risk of developing sepsis and patients with sepsis are twice as likely to develop ARDS. Alcohol is a major risk factor for the development of ALI/ARD as it increases the risk of aspiration and pulmonary infection and disrupts the immune system and nonimmunologic host defense mechanisms leading to immune dysregulation of alveolar macrophages and dysfunction of the alveolar epithelial barrier. Alcohol Use Disorder (AUD) heightens ALI/ARDS risk by decreasing immune defenses and lung barrier functions via affecting membrane permeability, glutathione depletion and impairment of macrophage function. Wnt/β-catenin pathway offers therapeutic potential by suppressing epithelial mesenchymal transition for reducing lung injury. Conclusion. Alcohol consumption greatly increases the risk of ALI and ARDS by disrupting immune defenses and weakening lung barriers, causing enhanced inflammation and oxidative stress. Targeting mechanisms like the Wnt/β-catenin pathway may offer therapeutic benefits to counteract these effects.