Abstract
Advanced chronic liver disease is characterized by metabolic-associated liver disease,
metabolic-associated steatohepatitis, and cirrhosis. This clinical setting is associated
with platelet activation, which has been suggested to play a role in the progression
of liver disease; thus, platelet activation has been detected in portal circulation
as well within liver sinusoids. Experimental studies with antiplatelet drugs and observational
studies in human suggested a role for platelet activation in the mechanism of the
disease. Furthermore, advanced chronic liver disease may be complicated by atherosclerotic
complications, where the role of platelet activation is well consolidated. Platelet
activation may represent a unique mechanism leading to liver disease on one hand and
to atherosclerotic complications on the other hand. Several studies pointed to the
role of gut dysbiosis as key step for eliciting platelet activation via the production
of pro-aggregating metabolites such as trimethylamine N-oxide or translocation of
bacterial products such as lipopolysaccharide into the systemic circulation. The aims
of this narrative review are to show the experimental and clinical evidence relating
platelets with advanced chronic liver disease, to explore the role of gut microbiota
as mechanism for platelet activation, and to suggest novel therapeutic strategies
to inhibit gut microbiota–platelet axis.
Keywords
blood platelets - dysbiosis - lipopolysaccharide - liver cirrhosis - liver diseases
