Escherichia/Shigella, SCFAs, and Metabolic Pathways—The Triad That Orchestrates Intestinal Dysbiosis in Patients with Decompensated Alcoholic Cirrhosis from Western Mexico

Gut microbiota undergoes profound alterations in alcohol cirrhosis. Microbiota-derived products, e.g., short chain fatty acids (SCFA), regulate the homeostasis of the gut-liver axis. The objective was to evaluate the composition and functions of the intestinal microbiota in patients with alcohol-decompensated cirrhosis. Fecal samples of 18 patients and 18 healthy controls (HC) were obtained. Microbial composition was characterized by 16S rRNA amplicon sequencing, SCFA quantification was performed by gas chromatography (GC), and metagenomic predictive profiles were analyzed by PICRUSt2. Gut microbiota in the cirrhosis group revealed a significant increase in the pathogenic/pathobionts genera Escherichia/Shigella and Prevotella, a decrease in beneficial bacteria, such as Blautia, Faecalibacterium, and a decreased α-diversity (p < 0.001) compared to HC. Fecal SCFA concentrations were significantly reduced in the cirrhosis group (p < 0.001). PICRUSt2 analysis indicated a decrease in acetyl-CoA fermentation to butyrate, as well as an increase in pathways related to antibiotics resistance, and aromatic amino acid biosynthesis. These metabolic pathways have been poorly described in the progression of alcohol-related decompensated cirrhosis. The gut microbiota of these patients possesses a pathogenic/inflammatory environment; therefore, future strategies to balance intestinal dysbiosis should be implemented. These findings are described for the first time in the population of western Mexico

Position statement on the use of albumin in liver cirrhosis

Cirrhosis is characterized by a prolonged asymptomatic period in which the inflammation persists, increasing as the disease progresses. Proinflammatory cytokines and pro-oxidant molecules are key in the development of organ dysfunction. Cirrhosis progression and worsening of portal hypertension bring about bacterial translocation and systemic dissemination via portal circulation of bacterial products, and molecular patterns associated with damage, which exacerbate the systemic Inflammation. Albumin is a molecule that undergoes structural and functional changes as liver damage progresses, affecting its antioxidant, immunomodulatory, oncotic, and endothelial stabilizing properties. Our knowledge of the properties of albumin reveals a molecule with multiple treatment options, capable of targeting several physiopathological aspects of cirrhosis. For the elaboration of the present manuscript on the uses of albumin in liver cirrhosis, several experts in the field of hepatology in Mexico were divided into 5 working groups to summarise and formulate, when appropriate, position statements: 1)pathophysiology of cirrhosis and properties of albumin; 2)proven uses of albumin [large-volume paracentesis, spontaneous bacterial peritonitis (SBP), hepatorenal syndrome (HRS)]; 3)controversial/emerging uses of albumin (long-term use, acute decompensation, liver transplant, non-HRS kidney injury, muscle cramps, non-SBP infections, hyponatremia, encephalopathy); 4)use of albumin in acute-on-chronic liver failure, immunomodulation, and systemic Inflammation; 5)pharmacoeconomics