Aluated by the 51Cr-ethylenediaminetetraacetic acid (51Cr-EDTA) permeability test in 52 LC patients and in 48 sex- and age-matched controls. The presence of 51Cr-EDTA was also evaluated in ascitic fluid after therapeutic paracentesis in all LC patients with ascites. RESULTS: An altered IP was found in 45% of LC patients compared with 4% of controls (P<0.00001). IP impairment was significantly associated with Child–Pugh status (75% of Child C patients vs. 39% of Child B and 22% of Child A patients), with the presence of ascites (60% in ascitic patients vs. 31% in nonascitic patients), and with a history of SBP (100% of patients with SBP vs. 50% of those without SBP). 51Cr-EDTA was present in all ascitic samples obtained from patients with SBP compared with 22% of patients without SBP. CONCLUSIONS: IP derangement was a common finding in LC, especially in patients with more advanced disease (presence of ascites and history of SBP). The presence of 51Cr-EDTA in ascites in patients with SBP suggests an altered permeability of splancnic vessels and/or peritoneal membranes. Further studies are required to assess 51Cr-EDTA urine and ascite cutoffs to set up SBP preventive strategies....

Fusobacterium nucleatum, a gram-negative anaerobic bacterium, has emerged as a significant player in colorectal cancer (CRC) pathogenesis. The bacterium causes a persistent inflammatory reaction in the colorectal mucosa by stimulating the release of pro-inflammatory cytokines like IL-1β, IL-6, and TNF-α, creating an environment conducive to cancer progression. F. nucleatum binds to and penetrates epithelial cells through adhesins such as FadA, impairing cell junctions and encouraging epithelial-to-mesenchymal transition (EMT), which is associated with cancer advancement. Additionally, the bacterium modulates the host immune system, suppressing immune cell activity and creating conditions favorable for tumor growth. Its interactions with the gut microbiome contribute to dysbiosis, further influencing carcinogenic pathways. Evidence indicates that F. nucleatum can inflict DNA damage either directly via reactive oxygen species or indirectly by creating a pro-inflammatory environment. Additionally, it triggers oncogenic pathways, especially the Wnt/β-catenin signaling pathway, which promotes tumor cell growth and longevity. Moreover, F. nucleatum alters the tumor microenvironment, impacting cancer cell behavior, metastasis, and therapeutic responses. The purpose of this review is to elucidate the molecular mechanisms by which F. nucleatum contributes to CRC. Understanding these mechanisms is crucial for the development of targeted therapies and diagnostic strategies for CRC associated with F. nucleatum.

Introduction.Helicobacter pylorieradication therapy has the potential burden of antibiotic-associated gastrointestinal (GI) side effects. The occurrence of side effects is among the major drawbacks of such regimens. GI manifestations may be related to alterations in the intestinal microflora. Probiotics can prevent or reduce antibiotic-associated side effects and have an inhibitory effect onH. pylori.Methods. To define the efficacy ofLactobacillus reuterisupplementation inH. pylorieradication and in preventing GI-associated side effects during a second-line levofloxacin triple therapy. 90H. pylori-positive patients receive for 7 days a second-line triple therapy with esomeprazole, levofloxacin, and amoxicillin withL. reuterifor 14 days (group 1) and without probiotic supplementation (group 2). Each subject received a validated questionnaire to record symptoms everyday for 4 weeks from the start of therapy.H. pyloristatus and side effects were assessed 6 weeks after treatment.Results. The eradication rate was significantly influenced by probiotic supplementation withL. reuteri(group 1: 36/45, 80%; group 2: 28/45 62%;P<0.05). The incidence of nausea and diarrhoea in group 1 was significantly lower than that in group 2.Conclusion. InH. pylori-positive subjectsL. reuterisupplementation increases the eradication rate while reducing the incidence of the most common side effects associated with antibiotic therapy in second-line treatment.