Background and Aims: The importance of sessile serrated lesions (SSLs) in the pathogenesis of colorectal carcinoma has been recently established. These are supposed to cause the so-called “interval cancer”, having a rapidly progressive growth and being difficult to detect and to obtain an endoscopic complete resection. We aimed to establish the most important metabolic risk factors for sessile serrated lesions. Methods: We performed a retrospective case-control study, on a series of 2918 consecutive patients who underwent colonoscopy in Gastroenterology and Endoscopy Unit, County Clinical Emergency Hospital, Târgu-Mureș, Romania between 1 st of January 2015-31 th of December 2017. In order to evaluate the metabolic risk factors for polyps’ development, enrolled participants were stratified in two groups, a study group, 33 patients with SSLs lesions, and a control group, 138 patients with adenomatous polyps, selected by systematic sampling for age and anatomical site. Independent variables investigated were: gender, smoking, alcohol consumption, obesity, arterial hypertension, diabetes, hypercholesterolemia, hypertriglyceridemia, hyperuricemia, nonalcoholic liver disease. Results: For SSLs the most common encountered localization was the right colon in 30.55% of cases. By comparative bivariate analysis between SSLs group and control group, it was observed that hypertension (p=0.03, OR 2.33, 95 %CI 1.03-5.24), obesity (p=0.03, OR 2.61, 95 %CI 1.08-6.30), hyperuricemia (p=0.04, OR 2.72, 95 %CI 1.28-7.55), high cholesterol (p=0.002, OR 3.42; 95 %CI 1.48-7.87), and high triglycerides level (p=0.0006, OR 5.75; 95 %CI 1.92-17.2) were statistically associated with SSLs development. By multivariate analysis hypertension and hypertriglyceridemia retained statistical significance. Conclusions: Our study showed that the highest prevalence of SSLs was in the right colon and hypertension and increased triglycerides levels were associated with the risk of SSLs development. These risk factors are easy to detect in clinical practice and may help identifying groups with high risk for colorectal cancer, where screening is recommended.

Background and Objectives: Metabolic dysfunction-associated steatotic liver disease (MASLD) is now widely acknowledged as belonging to the broader category of metabolic disorders, being closely associated with obesity, insulin resistance, and chronic systemic inflammation. Recent evidence indicates that in MASLD, alterations in the gut–liver axis—particularly increased intestinal permeability may serve as a crucial mechanistic link between metabolic dysfunction and hepatic steatosis. Zonulin, a physiological modulator of intestinal tight junctions, has been suggested as an indicator of compromised barrier integrity; however, its specific role in MASLD remains to be fully elucidated. Materials and Methods: We conducted a prospective observational study including 52 adult patients diagnosed with MASLD. Hepatic steatosis was evaluated using the SteatoTest (FibroMax panel), while fecal zonulin levels were measured by ELISA at baseline. Clinical, anthropometric, and metabolic parameters were assessed. We used ROC curve analysis to explore zonulin’s predictive value for moderate-to-severe steatosis (≥S2). Results: Elevated fecal zonulin (>107 ng/mL) occurred in 26.9% of participants. In a binary logistic model with SteatoTest ≥ S2 as outcome, zonulin was independently associated with clinically significant steatosis (OR per 1 ng/mL = 1.017; 95% CI 1.002–1.032; p = 0.029). Discrimination for ≥S2 was AUC = 0.680 (95% CI 0.535–0.825; p = 0.015). The Youden-optimal cut-off was 57.0 ng/mL (sensitivity 68.2%, specificity 63.3%) versus 40.9%/83.3% at the manufacturer’s 107 ng/mL threshold. Conclusions: Fecal zonulin shows modest discriminatory ability for steatosis and is best used as an adjunct to non-invasive assessment; cohort-specific calibration (57.0 ng/mL) outperformed the generic 107 ng/mL threshold.

Gastric cancer (GC) is the fifth most common malignancy worldwide, with 968,784 new cases reported in 2022. Since 1975, when stomach cancer was the most common cancer, its incidence has declined in many regions. This decline can be attributed to improved food preservation and recognition of Helicobacter pylori (H. pylori) as a group 1 carcinogen in intestinal-type GC. The aim of this review was to summarize current strategies for primary and secondary prevention of GC, with an emphasis on H. pylori management, dietary factors, novel biomarkers, and screening approaches relevant in Europe. Papers from large databases, namely Web of Science, Scopus, and PubMed/MEDLINE, were selected (reviews, guidelines, and peer-reviewed studies) from about the last 1–5 years. The research was conducted using the keywords gastric cancer, prevention, primary prevention, secondary prevention, and endoscopy guidelines on prevention of gastric cancer. Primary prevention of GC is directed at screening for H. pylori and dietary changes. Secondary prevention is supported by traditional tumor markers, pepsinogen-based serological biopsy, newer blood-based markers, and major technological progress in endoscopy. High-definition endoscopy, magnification, virtual chromoendoscopy, and artificial intelligence have improved the detection of preneoplastic lesions and early cancer, while advanced therapeutic techniques such as endoscopic mucosal resection and endoscopic submucosal dissection permit organ-sparing treatment. Large projects, including GISTAR, EUROHELICAN, TOGAS, and EUCanScreen, are expected to clarify optimal screening strategies. Although GC incidence has declined, it remains a common and significant malignancy. Understanding the facets of primary and secondary prevention of GC will lead to a reduction in the burden of this disease.

Background: Metabolic dysfunction-associated steatotic liver disease (MASLD) is increasingly recognized as part of the broader spectrum of metabolic disorders, with links to obesity, insulin resistance, and systemic inflammation. Emerging evidence points to a role of the gut–liver axis, particularly intestinal permeability, in its pathogenesis. Zonulin—a regulator of tight junctions—has been proposed as a marker of impaired barrier function, but its relevance in MASLD remains unclear. Methods: We conducted a prospective observational study including 52 adult patients diagnosed with MASLD. Hepatic steatosis was evaluated using the SteatoTest (FibroMax panel), while fecal zonulin levels were measured by ELISA at baseline. Clinical, anthropometric, and metabolic parameters were assessed. We used ROC curve analysis to explore zonulin’s predictive value for moderate-to-severe steatosis (≥S2). Results: Fecal zonulin levels above 107 ng/mL were found in 26.9% of participants. This group showed a higher frequency of moderate-to-severe steatosis (78.6%) compared to those with lower zonulin levels (55.3%), although the correlation with SteatoTest was weak (r = 0.19, p > 0.05). No significant associations were found between zonulin and liver fibrosis, insulin resistance (HOMA-IR), or the BARD score. The AUC for detecting steatosis ≥ S2 was 0.68. Conclusions: Although limited as a standalone diagnostic tool, fecal zonulin may reflect underlying gut barrier dysfunction in MASLD and show moderate association with hepatic steatosis. Its role as a complementary biomarker in non-invasive stratification frameworks warrants further study, especially in larger cohorts with control groups.

Background/Objectives: Metabolic dysfunction–associated steatotic liver disease (MASLD) is closely linked to atherosclerotic cardiovascular disease (ASCVD), but the prognostic value of liver fibrosis and gut–liver axis alterations remains uncertain. Methods: We conducted a prospective, observational study in two tertiary centers (in Romania and Italy) and compared the outcomes with different tests available for fibrosis (FibroTest in Romania or acoustic radiation force impulse (ARFI) elastography in Italy) and intestinal permeability (IP) (by fecal zonulin in Romania or lactulose/mannitol ratio in Italy). Liver steatosis was confirmed at ultrasonography. Analyses followed a within-cohort strategy. Ten-year ASCVD categories were summarized separately per cohort, and within-cohort associations with elevated ASCVD risk (≥7.5%) were explored using univariate logistic regression with age-adjusted two-parameter checks. A pooled robustness analysis (n = 132) was then performed using multivariable logistic regression models for intermediate–high ASCVD risk (≥7.5%), adjusted for age (per 5 years), waist circumference (per 5 cm), total cholesterol (per 10 mg/dL), diabetes, and hypertension. A higher threshold (≥20%) yielded the same qualitative interpretation. Results: ASCVD was computable for 52 Romanian (low 78.8%, borderline 5.8%, intermediate 7.7%, high 7.7%) and 80 Italian participants (low 80.0%, borderline 6.2%, intermediate 12.5%, high 1.2%). In both cohorts, age was associated with higher ASCVD. Fibrosis severity (FibroTest or ARFI) and IP (zonulin or LA/MA) showed no associations with ASCVD. In pooled adjusted models, neither significant fibrosis nor high intestinal permeability was independently associated with ASCVD, whereas age and cardiometabolic comorbidities remained the dominant correlates. Conclusions: Across both cohorts, 10-year ASCVD risk was mainly determined by age and major cardiometabolic comorbidities. Neither liver fibrosis nor intestinal permeability contributed additional prognostic value in this setting, regardless of the assessment method. These data support prioritizing aggressive metabolic risk management and call for harmonized, longitudinal studies to clarify gut–liver contributions to cardiovascular outcomes.

Helicobacter pylori infection represents a well-established risk factor for the development of gastric carcinogenesis, yet reliable clinical or endoscopic predictors of infection remain poorly defined. Identifying non-invasive or endoscopic markers of this infection could improve early detection, which is crucial for effective prevention and clinical management. This single-center study included 737 patients who underwent upper gastrointestinal endoscopy. We compared clinical, laboratory, and endoscopic features between H. pylori-positive and H. pylori-negative individuals. A total of 263 with H. pylori-positive gastric biopsies and 474 with H. pylori-negative biopsies were enrolled in our study. Cerebrovascular disease (9.51% vs. 5.51%, p = 0.04, OR = 1.80), type 2 diabetes mellitus (T2DM—22.05% vs. 15.86%, p = 0.04, OR 1.5), and alcohol consumption (18.96% vs. 9.3%, p = 0.00, OR = 2.28) were significantly more prevalent among H. pylori-positive patients. Heartburn was more commonly reported in H. pylori-negative individuals (23.77% vs. 15.38%, p = 0.01, OR = 0.58). Laboratory parameters showed no significant differences between groups. Regarding endoscopic findings, corporal erythema (26.92% vs. 16.17%, p = 0.00, OR = 1.91), corporal erosions (11.54% vs. 5.32%, p = 0.00, OR = 2.32), and submucosal hemorrhages (20.91% vs. 11.6%, p = 0.00, OR = 2.01) were associated with H. pylori infection. In the multivariate logistic regression models, alcohol consumption and corporal lesions remained independent predictors of H. pylori-associated gastritis, even after adjusting for age, sex, and PPI use. This study identifies alcohol consumption and specific corporal mucosal changes as novel, independent predictors of H. pylori infection. Heartburn was negatively associated with active H. pylori infection, while the rest of the symptoms did not predict infection or mucosal lesions. The laboratory parameters did not differ significantly between groups. These findings underscore the potential of targeted endoscopic evaluation and risk-based screening (particularly among T2DM and alcohol-consuming populations) to enhance early detection and management of H. pylori-associated disease.