Aim: To establish whether the addition of probiotics to a globally accepted Helicobacter pylori (H. pylori)-eradication scheme may reduce the rates of side effects and increase the eradication rates. Methods. Prospective, randomized, placebo-controlled trial of patients receiving eradication therapy for H. pylori in the eight participating centers. All patients received a 10-day proton pump inhibitor containing non-bismuth quadruple therapeutic regimen for H. pylori eradication (omeprazole 20 mg, amoxycillin 1 g, clarithromycin 500 mg, and metronidazole 500 mg all twice daily orally) and were randomized to receive either probiotics (group A) or placebo (group B). The probiotic used combined four probiotic strains, i.e., Lactobacillus Acidophilus, Lactiplantibacillus plantarum, Bifidobacterium lactis, and Saccharomyces boulardii. Results. Data were analyzed for 329 patients in group A and 335 patients in group B. Fifty six (17.0%) patients in group A and 170 (50.7%) patients in group B reported the occurrence of an H. pylori treatment-associated new symptom or the aggravation of a pre-existing symptom of any severity (p < 0.00001). H. pylori was successfully eradicated in 303 patients in group A (92.0%) and 291 patients in group B (86.8%), (p = 0.028). Conclusion: Adding probiotics to the 10-day concomitant non-bismuth quadruple H. pylori eradication regimen increases the eradication rate and decreases side effects.

Background/Objectives: The role of intestinal dysbiosis as an important driver of inflammation in metabolic disorders is becoming increasingly evident. Beta-defensin 2 is an antimicrobial peptide that contributes to innate immunity, while recently it has been suggested as a novel biomarker of gut dysbiosis. However, its role in obesity remains unexplored. This study aimed to compare circulating beta-defensin 2 levels between individuals with overweight and obesity and lean controls. An additional objective was to explore potential correlations between beta-defensin 2 and other inflammatory markers in this population. Methods: The study population consisted of 81 participants (61.7% females) divided into obesity (n = 27), overweight (n = 34), and normal body mass index (n = 20) groups. All participants were free of infection and diabetes mellitus. Beta-defensin 2, interleukin-6, presepsin, high-sensitivity C-reactive protein (hs-CRP), and ferritin were evaluated in the study groups. Results: We did not find significant differences in beta-defensin 2 levels between the groups (p = 0.936). In contrast, hs-CRP levels were higher in people with obesity compared to the sum of participants in the overweight and control groups (p = 0.044), after adjusting for the effects of age, sex, smoking, and vitamin D status. Furthermore, a positive correlation was established between beta-defensin 2 and presepsin values (p = 0.012). Conclusions: The results of the present study demonstrate that obesity is characterized by an aggravation of inflammation, as expressed by elevated hs-CRP levels. Although the study design cannot prove causal relationships, our findings also suggest that beta-defensin 2 levels correlate with the magnitude of systemic inflammation in infection-free individuals living with obesity. The value of the combined evaluation of different biomarkers in obesity-related outcomes warrants further investigation by larger studies.

Background/Objectives: Ustekinumab has been approved for the treatment of moderate to severe ulcerative colitis. Real-world data regarding its efficacy and the discovery of predictive factors of response need to be studied further. We aimed to evaluate the efficacy and identify predictors of response to induction treatment with ustekinumab in patients with ulcerative colitis. Methods: This is a multicenter, prospective cohort study. Clinical response (CR) at week 16 was the primary endpoint, and steroid-free clinical remission (SFCRem) and endoscopic response were the secondary endpoints. Baseline histology, mucosal gene expression, and pharmacokinetics were studied for their effect on response to treatment. Results: We included 123 patients (mean age = 50.3 years). CR was recorded in 70.8% (75/106), SFCRem in 48% (59/123), endoscopic improvement in 71.4% (40/56), and mucosal healing in 28.6% (16/56). Higher PRO-stool frequency (OR = 0.49, p = 0.027), concomitant use of 5-ASA (OR = 3.69, p = 0.021), platelet number of ≥284 × 10⁹/L (OR = 6.52, p = 0.001) at baseline, and a drop in the total count of platelets by 10⁸/L (OR = 1.23, p = 0.022) at week 8 were independently associated with CR. Elevated trough levels of ustekinumab at week 16 were associated with a higher probability of endoscopic improvement (median difference = 3784 ng/mL, p = 0.013), with an optimal cut-off value of 3500 ng/mL (AUC = 0.82, 95% CI: 0.66–0.96). Increased mucosal mRNA expression for IL-23 (p = 0.007) and IL-23R (p = 0.031) at baseline was associated with increased probability of CR. Higher continuous Geboes scores at baseline were associated with a lower probability of CR (OR = 0.80, p = 0.045), with an optimal cut-off value of 14 (AUC = 0.75, 95% CI: 0.57–0.93). Conclusions: Clinical, laboratory, and molecular markers may identify patients with ulcerative colitis who are more likely to respond to ustekinumab.