Sepsis-associated liver injury: Mechanisms and potential therapeutic targets
- PMID: 39563749
- PMCID: PMC11572628
- DOI: 10.3748/wjg.v30.i42.4518
Sepsis-associated liver injury: Mechanisms and potential therapeutic targets
Abstract
In this editorial, we examined a recent article in the World Journal of Gastroenterology that focused on sepsis-associated liver injury (SLI) and its treatment. SLI is a serious complication of sepsis, primarily caused by microcirculatory disturbances, the gut-liver axis, and inflammatory responses. Specific treatment recommendations for SLI are lacking. The gut-liver axis represents a potential therapeutic target, with metformin showing promise in modulating the gut microbiome and enhancing intestinal barrier function. Although immunomodulatory therapies are being explored, anti-tumor necrosis factor agents and interleukin-1 receptor antagonists have not demonstrated significant clinical benefits. Statins may reduce liver inflammation and prevent injury in sepsis, but their clinical application is limited. Reduced D-related human leucocyte antigen expression on monocytes and lymphocytes suggests immune suppression in patients, indicating that corticosteroids could reverse clinical deterioration in severe infections and address adrenal cortical insufficiency. Current large-scale studies on glucocorticoid therapy for sepsis have yielded mixed results, likely due to inadequate assessment of the immune status of the host. Future research should prioritize the development of personalized immunotherapy tailored to patients' immune profiles, focusing on identifying novel indicators of immune status and advancing immunomodulatory targets and therapeutics for septic patients.
Keywords: Adrenal cortical insufficiency; Glucocorticoid; Gut-liver axis; Immune dysregulation; Immunosuppression; Inflammation; Sepsis; Sepsis-associated liver injury.
©The Author(s) 2024. Published by Baishideng Publishing Group Inc. All rights reserved.
Conflict of interest statement
Conflict-of-interest statement: The authors declare that there are no financial or other conflicts of interest that could influence the content or conclusions of this manuscript.
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