(1) Background: The aim was to evaluate the effectiveness of the probiotic containing Saccharomyces boulardii in the treatment of small intestinal bacterial overgrowth (SIBO) in patients with decompensated cirrhosis. (2) Methods: This was a blinded, randomized, placebo-controlled study. (3) Results: After 3 months of treatment, SIBO was absent in 80.0% of patients in the probiotic group and in 23.1% of patients in the placebo group (p = 0.002). The patients with eliminated SIBO had decreased frequency of ascites and hepatic encephalopathy, the increased platelets and albumin levels, the decreased blood levels of total bilirubin, biomarkers of bacterial translocation (lipopolysaccharide [LPS]) and systemic inflammation (C-reactive protein), and positive changes in markers of hyperdynamic circulation compared with the state at inclusion. There were no significant changes in the claudin 3 level (the intestinal barrier biomarker) in these patients. No significant changes were observed in the group of patients with persistent SIBO. The serum level of nitrate (endothelial dysfunction biomarker) was lower in patients with eradicated SIBO than in patients with persistent SIBO. One (5.3%) patient with eradicated SIBO and six (42.9%) patients with persistent SIBO died within the first year of follow-up (p = 0.007). (4) Conclusions: SIBO eradication was an independent predictor of a favorable prognosis during the first year of follow-up.

We aimed to systematize the results of published studies on the use of Saccharomyces boulardii (SB) for the treatment of various liver disorders (CRD42022378050). Searches were conducted using PubMed and Scopus on 1 August 2022. The PubMed search was updated on 15 June 2024. The review included sixteen studies: ten experimental animal studies (EASs) and six randomized controlled trials (RCTs). The CNCM I-745 strain was used in 68.8% of the included studies. SB reduced the severity of many manifestations of cirrhosis, and lowered the Child–Pugh scores in RCT. SB reduced the serum concentrations of TNF-α, IL-1β, IL-6, and IL-4 in animals with metabolic dysfunction-associated steatotic liver disease (MASLD); lowered the serum TNF-α and IL-6 levels in experimental cirrhosis in rats; and reduced the CRP levels in decompensated cirrhosis. The EAS of MASLD revealed that SB reduced liver steatosis and inflammation and lowered the liver expression of genes of TNF-α, IL-1β, interferon-γ, and IL-10. In studies on experimental cirrhosis and MASLD, SB reduced the liver expression of genes of TGF-β, α-SMA, and collagen as well as liver fibrosis. SB reduced the abundance of Escherichia (Proteobacteria), increased the abundance of Bacteroidetes in the gut microbiota, prevented an increase in intestinal barrier permeability, and reduced bacterial translocation and endotoxemia.

Aim: to review the current literature on the potential link between Helicobacter pylori ( H. pylori ) infection and iron deficiency and vitamin B ₁₂ deficiency anemia. Key points. Published studies have shown that iron deficiency anemia of unknown cause may be due to H. pylori infection, especially in pediatric practice. This infection can lead to impaired iron absorption through various mechanisms. Eradicating H. pylori infection can contribute to restoring normal red blood cell parameters. Additionally, patients infected with H. pylori have lower blood levels of vitamin B ₁₂ compared to uninfected individuals. The mechanisms contributing to impaired vitamin B ₁₂ absorption in patients with H. pylori infection may be associated with the progression of multifocal atrophic gastritis, as well as the production of antibodies against parietal cells and intrinsic factor. Many national gastroenterology societies and consensus meetings recommend testing for H. pylori infection patients with iron deficiency anemia or B ₁₂ deficiency anemia of unknown origin and, if positive, eradicating it. Conclusion. There is a positive association between H. pylori infection and the development of unexplained iron deficiency anemia. The relationship between H. pylori infection and vitamin B ₁₂ deficiency anemia has not been sufficiently studied and requires further research.