Malnutrition and sarcopenia are highly prevalent and robustly associated with reduced quality of life, disease progression, and poor outcomes, including complications and mortality, in patients with cirrhosis. Their pathophysiology is multifactorial, involving inadequate dietary intake and malabsorption, impaired liver functional reserves, altered energy, protein, and ammonia metabolism, systemic inflammation, hormonal dysregulation, and lifestyle or environmental influences. Despite extensive research, unresolved issues remain regarding optimal diagnostic criteria, as current approaches vary and lack global standardization. Regarding the diagnostic criteria for malnutrition, the usefulness of the Global Leadership Initiative on Malnutrition criteria has been proposed by international nutrition societies. However, evidence supporting their applicability in hepatology remains insufficient. For sarcopenia, differences in disease concept and diagnostic methods among societies indicate that no unified diagnostic standard exists, and clinicians should approach diagnosis with an understanding of the strengths and limitations of each method. Nutritional strategies emphasize adequate energy and protein intake, late evening snacks, and branched-chain amino acid supplementation, while deficiencies in micronutrients require tailored replacement. Nutritional therapy alone has limited effect on sarcopenia, but when combined with exercise it improves muscle mass, physical performance, and outcomes. Comprehensive approaches integrating optimized nutrition, micronutrient support, and structured exercise are essential to alleviate the burden of malnutrition and sarcopenia and to improve prognosis in patients with cirrhosis. This review addresses malnutrition and sarcopenia in cirrhosis by highlighting their prevalence, pathophysiology, clinical impact, and approaches for screening and diagnosis, and by emphasizing personalized nutritional, pharmacological, and exercise interventions to improve patient outcomes.

Alcohol-associated intestinal dysbiosis and bacterial overgrowth can lead to a dysregulation of tryptophan metabolism and lower production of indoles. Several of these indole derivatives are aryl hydrocarbon receptor ligands that, in turn, are involved in antimicrobial defense via induction of interleukin-22 (IL-22). IL-22 increases the expression of intestinal regenerating islet-derived 3 (Reg3) lectins, which maintain low bacterial colonization of the inner mucus layer and reduce bacterial translocation to the liver. Chronic alcohol consumption is associated with reduced intestinal expression of Reg3β and Reg3γ, increased numbers of mucosa-associated bacteria and bacterial translocation. Translocated microbial products and viable bacteria reach the liver and activate the innate immune system. Release of inflammatory molecules promotes inflammation, contributes to hepatocyte death and results in a fibrotic response. This review summarizes the mechanisms by which chronic alcohol intake changes the gut microbiota and contributes to alcohol-associated liver disease by changing microbial-derived metabolites.

Intestinal bacteria contribute to the pathogenesis of non-alcoholic fatty liver disease(NAFLD).Recently developed microbial profiling techniques are beginning to shed light on the nature of the changes in the gut microbiota that accompany NAFLD and non-alcoholic steatohepatitis(NASH).In this review,we summarize the role of gut microbiota in the development of NAFLD,NASH,and hepatocellular carcinoma(HCC).We highlight the mechanisms by which gut microbiota contribute to NAFLD/NASH,including through alterations in gut epithelial permeability,choline metabolism,endogenous alcohol production,release of inflammatory cytokines,regulation of hepatic Toll-like receptor(TLR),and bile acid meta-bolism.In addition,we analyze possible mechanisms for enhanced hepatic carcinogenesis,including alterations in bile acid metabolism,release of inflammatory cytokines,and expression of TLR-4.Finally,we describe therapeutic approaches for NAFLD/NASH and preventive strategies for HCC involving modulation of the intestinal microbiota or affected host pathways.Although recent studies have pro-vided useful information,large-scale prospective studies are required to better characterize the intestinal microbiota and metabolome,in order to demonstrate a causative role for changes in the gut microbiota in the etiology of NAFLD/NASH,to identify new therapeutic strategies for NAFLD/NASH,and to develop more effective methods of preventing HCC.

No abstract available.
*Hospitalization ; Humans ; *Liver Cirrhosis

Alcoholic liver disease is a leading cause of morbidity and liver-related death worldwide. Intestinal bacterial overgrowth and dysbiosis induced by ethanol ingestion play an important role in the pathogenesis of alcoholic liver disease. After exposure to alcohol in the lumen, enteric bacteria alter their metabolism and thereby disturb intestinal homeostasis. Disruption of the mucosal barrier results in the translocation of microbial products that contribute to liver disease by inducing hepatic inflammation. In this review, we will discuss the effects of alcohol on the intestinal microbiome, and in particular, its effects on bacterial metabolism, bacterial translocation and ecological balance. A better understanding of the interactions among alcohol, the host and the microbiome will reveal new targets for therapy and lead to new treatments.
Bacterial Translocation/physiology ; Central Nervous System Depressants/metabolism ; Ethanol/metabolism ; Humans ; Intestines/*microbiology ; Lipopolysaccharides/physiology ; Liver Diseases, Alcoholic/*microbiology ; Microbiota/*physiology ; Permeability