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Background: Patients with decompensated cirrhosis face poor prognosis and increased mortality risk. Rifaximin, a non‐absorbable antibiotic, has been shown to have beneficial effects in preventing complications and improving survival in these patients. However, the underlying mechanisms of rifaximin's effects remain unclear. Methods: We obtained fecal samples from decompensated cirrhotic patients undergoing rifaximin treatment and controls, both at baseline and after 6 months of treatment. Shotgun metagenome sequencing profiled the gut microbiome, and untargeted metabolomics analyzed fecal metabolites. Linear discriminant and partial least squares discrimination analyses were used to identify differing species and metabolites between rifaximin‐treated patients and controls. Results: Forty‐two patients were enrolled and divided into two groups (26 patients in the rifaximin group and 16 patients in the control group). The gut microbiome's beta diversity changed in the rifaximin group but remained unaffected in the control group. We observed 44 species with reduced abundance in the rifaximin group, including Streptococcus_salivarius, Streptococcus_vestibularis, Haemophilus_parainfluenzae, etc. compared to only four in the control group. Additionally, six species were enriched in the rifaximin group, including Eubacterium_sp._CAG:248, Prevotella_sp._CAG:604, etc., and 14 in the control group. Furthermore, rifaximin modulated different microbial functions compared to the control. Seventeen microbiome‐related metabolites were altered due to rifaximin, while six were altered in the control group. Conclusion: Our study revealed distinct microbiome‐metabolite networks regulated by rifaximin intervention in patients with decompensated cirrhosis. These findings suggest that targeting these specific metabolites or related bacteria might be a potential therapeutic strategy for decompensated cirrhosis. [ABSTRACT FROM AUTHOR]

Objectives: Covert hepatic encephalopathy (CHE) negatively affects the health‐related quality of life and increases the risk of overt HE (OHE) in patients with liver cirrhosis. However, the impact of CHE on long‐term patient outcomes remains controversial. This study aimed to explore the association between CHE and disease progression and survival among cirrhotic patients. Methods: This was a single‐center prospective study that enrolled 132 hospitalized patients with cirrhosis, with an average follow‐up period of 45.02 ± 23.06 months. CHE was diagnosed using the validated Chinese standardized psychometric hepatic encephalopathy score. Results: CHE was detected in 35.61% cirrhotic patients. During the follow‐up, patients with CHE had a higher risk of developing OHE (log‐rank 5.840, P = 0.016), exacerbation of ascites (log‐rank 4.789, P = 0.029), and portal vein thrombosis (PVT) (log‐rank 8.738, P = 0.003). Cox multivariate regression analyses revealed that CHE was independently associated with the occurrence of OHE, exacerbation of ascites, and PVT. Furthermore, patients with progression of cirrhosis were more likely to be diagnosed as CHE (log‐rank 4.462, P = 0.035). At the end of the follow‐up, patients with CHE had a lower survival rate compared to those without CHE (log‐rank 8.151, P = 0.004). CHE diagnosis (hazard ratio 2.530, P = 0.008), together with elder age and higher Child–Pugh score, were risk factors for impaired survival in cirrhotic patients. Conclusion: CHE is associated with disease progression and poor survival in patients with cirrhosis, indicating that CHE may serve as an independent predictor of poor prognosis among these patients. [ABSTRACT FROM AUTHOR]