Background: MicroRNA molecules, among them the intensely studied miRNA-155 (miR-155), are regarded as potential biomarkers of chronic gastric inflammation and premalignant lesion progression. However, literature data are scarce in terms of pediatric studies and in the evaluation of the predictive role of miRNA in early gastric inflammation. This study aims to assess the differential expression of miR-155 in relation to pediatric gastritis. Methods: The present research was conducted on 192 patients with chronic dyspeptic symptoms who underwent upper digestive endoscopy. Bioptic samples were harvested for histopathological analysis and tissue miR-155 depiction. MiR-155 expression analysis was carried out through quantitative real-time polymerase chain reaction (qRT-PCR). The study population was divided into two groups: controls (93 patients) and study group (99 patients) with inflammatory modifications. Results: MiR-155 expression was augmented in patients with gastritis but did not differ significantly from controls (p = 0.16). An increase in miR-155 expression was noted in relation to chronic gastritis, H. pylori infection, or increase in gastritis severity, but these variations were not important (p = 0.30, p = 0.44, and p = 0.45, respectively). Conclusions: According to our study, pediatric gastritis increases, but does not greatly influence, miR-155 expression. Dynamic evaluation of miR-155 might enlighten its prognostic role in pediatric gastritis.

Background: Type 2 diabetes mellitus (T2DM) affects up to 10% of adults globally, and its complications can mask the risk of gastrointestinal bleeding or malignancy. Methods: Our study enrolled 633 endoscopic patients stratified according to T2DM presence (4:1 ratio in favor of the control group). Results: T2DM patients referred for endoscopy experienced lower prevalence of epigastric pain and heartburn (OR = 0.637/OR = 0.346, p < 0.05). Often being anemic (OR = 2.23, p < 0.001), they had significantly lower hemoglobin (p = 0.001) and serum iron (p = 0.02), but serum cholesterol was higher in non-diabetics. Ulcers, erosions and mucosal hemorrhages were comparable between groups (p < 0.05), although low-dose aspirin use was more prevalent in diabetics (p = 0.000, OR = 2.34). T2DM was associated with the increased frequency of antro-corporal active gastritis (OR = 1.451/OR 1.501), with smokers presenting a higher frequency of active H. pylori infection (OR = 3.37). T2DM predicted anemia (adjusted OR = 1.70) and the absence of gastroesophageal reflux symptoms (adjusted OR = 0.37), but not active H. pylori gastritis or premalignant lesions. Conclusion: In an endoscopic population, patients with T2DM had lower hemoglobin and serum iron levels. There was an inverse correlation between T2DM and heartburn. H. pylori gastritis and premalignant lesions occurred more frequently in diabetic patients (predominantly pangastritis) before adjusting for age or associated comorbidities, with smoking increasing the risk for active infection.

Background/Objectives: Gastric mucosal lesions represent a significant health burden, with Helicobacter pylori infection being the primary cause of chronic gastritis worldwide. However, the role of modifiable lifestyle factors in modulating the severity of gastric lesions remains incompletely characterized, particularly in Eastern European populations. This study aimed to analyze the relationship between dietary behaviors, smoking, alcohol consumption, and the severity of endoscopic gastric lesions in Romanian patients. Methods: We conducted a cross-sectional study including 361 patients who underwent upper gastrointestinal endoscopy at Târgu Mureș County Clinical Emergency Hospital between 2019 and 2025. Endoscopic lesion severity was classified on an ordinal scale (0 = normal; 1 = edema/erythema; 2 = erosions; 3 = ulcer/bleeding). Dietary intake was assessed using a validated food frequency questionnaire, with foods classified as pro-inflammatory or protective. Ordinal logistic regression models were used to examine associations between lifestyle factors and the severity of gastric lesions, adjusted for age, sex, and H. pylori status. Results: Among participants (median age 65 years, 46.5% male), 45.2% had clinically significant lesions (≥2). H. pylori infection was present in 31.6% of participants. Current smoking (15.2% of participants) showed a trend toward increased severity of gastric lesions (fully adjusted OR 1.59, 95% CI 0.93–2.71, p = 0.092), though not statistically significant. Among current smokers, 52.7% had clinically significant lesions versus 43.8% among non/former smokers. The smoking–alcohol interaction was not statistically significant (interaction OR = 1.19, 95% CI: 0.34–4.17, p = 0.780). Dietary balance score showed no association with the severity of gastric lesions (OR = 1.061 per 10-unit increase, p = 0.355). NSAID use emerged as the strongest predictor (OR = 1.68, 95% CI 1.01–2.78, p = 0.044). The number of cumulative risk factors correlated significantly with clinically significant lesions (Spearman r = 0.107, p = 0.042), with prevalence increasing from 34.5% in patients with 0–1 factors to 83.3% with 6+ factors. Conclusions: Current smoking showed a trend toward increased severity of gastric lesions in this Romanian cohort, though not reaching statistical significance. NSAID use was the only significant independent predictor. The dose–response relationship between cumulative risk factors and the severity of lesions emphasizes the importance of comprehensive risk assessment and multi-factorial interventions in gastric disease prevention. However, as a cross-sectional study, these associations cannot establish causality and should be confirmed in prospective cohorts.

The role of cytomegalovirus (CMV) in the flare-up of ulcerative colitis (UC) is not clearly understood. CMV can cause similar symptoms in different clinical contexts, which may be attributed to the natural evolution of the viral infection, the patient’s immune status, or its association with inflammatory bowel disease (IBD). This study aims to delineate the diverse manifestations of CMV-related lesions from clinical, endoscopic, and histopathological perspectives, alongside a brief narrative review of the literature. In managing IBD patients, it is crucial to be vigilant for signs of CMV reactivation, especially before the initiation of more intensive therapies.

Background: Autoimmune gastritis (AIG) and Helicobacter pylori gastritis are distinct etiologies of chronic gastritis, yet comparative data on their long-term progression remain limited. Objectives: We compared the evolution of precancerous gastric lesions in patients with AIG and H. pylori-associated gastritis. Methods: This retrospective single-center cohort included 116 patients (52 histologically defined AIG, 64 H. pylori-associated gastritis) who underwent two upper endoscopies with Sydney-protocol biopsies at least 12 months apart between 2013 and 2024 (median follow-up 60 and 49 months). The primary outcome was the development of glandular atrophy or intestinal metaplasia (IM) not present at baseline. Results: New atrophy or IM developed in 61.5% (32/52) of AIG and 34.4% (22/64) of H. pylori patients (adjusted odds ratio [OR] 3.81, 95% confidence interval [CI] 1.53–9.49). Incident atrophy was more frequent in AIG (65.1% vs. 31.5%), including in comparison with baseline H. pylori-positive patients only (adjusted OR 3.02, 95% CI 1.08–8.46), whereas differences in IM were less consistent. Progression occurred in 42.9% of patients who were H. pylori-negative after treatment and 55.6% of persistently infected patients (p = 0.70). Proton pump inhibitor (PPI) use, an exploratory clinical risk score, and symptom changes were not associated with progression. Conclusions: In this selected cohort with repeat endoscopy, histologically defined AIG was associated with more frequent histological progression, particularly glandular atrophy, than H. pylori-associated gastritis. Prospective studies with serologically confirmed AIG and neoplastic endpoints are needed to inform risk stratification.

Background: Liver cirrhosis is associated with portal hypertension and its gastrointestinal complications, but non-variceal gastroduodenal mucosal injury and its relationship to Helicobacter pylori (H. pylori) infection and hepatic disease severity remain incompletely characterized. Methods: This retrospective, cross-sectional study included 162 patients undergoing first upper gastrointestinal endoscopy (61 with cirrhosis, 101 controls), assessed using a composite gastroduodenal mucosal injury score (range 0–16) across the antrum, gastric corpus, duodenal bulb, and second duodenal portion. Results: Cirrhosis was independently associated with a higher injury burden after adjusting for H. pylori status, nonsteroidal anti-inflammatory drug (NSAID), antiplatelet, anticoagulant, and proton pump inhibitor (PPI) use (adjusted count ratio [aCR] = 1.33, 95% CI: 1.09–1.63, p = 0.006); and H. pylori infection was independently and separately associated with higher injury burden (aCR = 1.25, 95% CI: 1.01–1.54, p = 0.037), while none of the four medication classes showed an independent association. This excess injury was concentrated almost exclusively in the gastric corpus (adjusted aCR = 3.04, p < 0.0001), with no significant differences at other sites. Injury severity did not correlate with Child–Pugh class or tests of the liver’s biosynthetic capacity (all p > 0.05). Only patients with concurrent cirrhosis and H. pylori infection showed significantly elevated injury relative to unexposed controls (adjusted aCR = 1.87, 95% CI: 1.38–2.53, p < 0.0001), with a significant, exploratory cirrhosis × H. pylori interaction (aCR = 1.56, p = 0.037). Conclusions: Cirrhosis is therefore associated with a corpus-predominant pattern of gastroduodenal injury, compatible with, though not proof of, a portal hypertension-related mechanism, and shows a significant positive multiplicative interaction with concurrent H. pylori infection; given the exploratory nature of this analysis, these findings are hypothesis-generating and warrant prospective confirmation before informing endoscopic screening or infection-screening practice.