Rising antimicrobial resistance has reduced the effectiveness of empirical eradication regimens for Helicobacter pylori (H. pylori) infection, particularly those containing clarithromycin. Local resistance surveillance and identification of clinical predictors of resistance are essential to guide treatment strategies. This study evaluated antimicrobial resistance patterns and clinical determinants of resistance in a real-world tertiary-care cohort. A retrospective observational study was performed, which included 352 adult patients with confirmed H. pylori infection managed between November 2022 and November 2025. Of these, 168 patients underwent culture and antibiotic susceptibility testing, while 184 received empirical therapy. Resistance rates were calculated according to the number of isolates tested for each antimicrobial agent (available-case analysis). Multivariable logistic regression analysis was used to identify independent predictors of resistance. Among susceptibility-tested patients, resistance to at least one antimicrobial agent was detected in 44.6%. Clarithromycin resistance was most frequent (42.5%), followed by metronidazole (36.4%) and levofloxacin (14.0%), whereas amoxicillin resistance remained low (2.4%). Multidrug resistance (MDR) based on available susceptibility data was observed in 12.5% of cases, most commonly involving dual clarithromycin–metronidazole resistance. Prior eradication therapy was independently associated with resistance (adjusted Odds Ratio aOR 2.41; 95% Confidence Interval CI 1.29–4.51; p = 0.006), while demographic factors were not. Clarithromycin resistance substantially exceeds recommended thresholds for empirical triple therapy in this setting. Prior eradication therapy is the principal predictor of resistance, supporting resistance-informed and stewardship-oriented management strategies.

Background and Objectives: Superior mesenteric artery syndrome (SMAS) is an uncommon cause of proximal duodenal obstruction that requires clinicoradiological correlation. Materials and Methods: We retrospectively reviewed 13 patients with SMAS identified at the Clinical County Emergency Hospital Bihor, Romania, during 2019–2024. Clinical records and contrast-enhanced computer tomography (CT) examinations were reviewed descriptively. Results: The cohort included 13 adults aged 19–85 years (mean 45.5 ± 17.8; median 43 years). Abdominal pain was reported in 12/13 patients (92.3%), vomiting or emetic symptoms in 6/13 (46.2%), feeding difficulty or appetite disturbance in 5/13 (38.5%), and documented weight loss in 3/13 (23.1%). CT measurements were available for the aortomesenteric angle in 7/13 patients (range, 10–25°) and for the aortomesenteric distance in 8/13 (range, 3–8 mm); direct third-part duodenal compression and proximal dilatation were interpreted together with compatible symptoms. Imaging showed Nutcracker-type left renal vein compression in 3/13 patients (23.1%) and possible May–Thurner anatomy in 1/13 (7.7%); these findings were not adjudicated as clinical syndromes without corresponding manifestations. Based on the management labels, 9/13 patients (69.2%) underwent surgery at some point and 4/13 (30.8%) received medical therapy only. Standardized follow-up and procedure-level outcome data were not available for all patients. Conclusions: This small, retrospective series is descriptive and cannot estimate prevalence, diagnostic delay, or comparative treatment effectiveness. It illustrates heterogeneous adult presentations and supports interpreting aortomesenteric measurements together with compatible symptoms and evidence of duodenal obstruction.

Background/Objectives: The increasing prevalence of antimicrobial resistance has become a major challenge in the management of Helicobacter pylori infection and is a leading cause of eradication failure. Resistance to clarithromycin and fluoroquinolones is primarily mediated by mutations in the 23S rRNA and gyrA genes, respectively. This study aimed to evaluate the prevalence of resistance-associated mutations in the 23S rRNA and gyrA genes, investigate their relationship with phenotypic antimicrobial resistance, assess their impact on eradication outcomes, and develop a prediction model for treatment failure. Methods: This retrospective real-world cohort study included 294 adult patients with confirmed H. pylori infection evaluated at the Oradea County Emergency Clinical Hospital, Romania, between November 2022 and November 2025. Clinical, endoscopic, histopathological, microbiological, molecular, and treatment outcome data were collected from medical records. Resistance-associated mutations in the 23S rRNA (A2143G, A2142G, and A2142C) and gyrA (N87K, D91G, and D91N) genes were analyzed and correlated with phenotypic antimicrobial resistance and eradication outcomes. Independent predictors of eradication failure were identified using multivariable logistic regression, and a prediction model was subsequently developed. Results: Overall, 101 patients (34.4%) harbored 23S rRNA mutations and 64 (21.8%) carried gyrA mutations, while 27 patients (9.2%) exhibited mutations in both genes. A2143G was the most frequent mutation (25.2%). Resistance-associated mutations showed strong concordance with phenotypic antimicrobial resistance. Patients with wild-type strains achieved eradication rates exceeding 90%, whereas significantly lower success rates were observed among patients carrying A2143G, A2142G, or gyrA mutations. Multivariable analysis identified previous eradication attempts (aOR 3.12, 95% CI 1.71–5.68), A2143G mutation (aOR 4.86, 95% CI 2.43–9.72), gyrA mutation (aOR 2.91, 95% CI 1.45–5.84), increasing age (aOR 1.03, 95% CI 1.01–1.05), and treatment with clarithromycin-based triple therapy (aOR 2.18, 95% CI 1.02–4.63) as independent predictors of eradication failure. The prediction model demonstrated excellent discriminatory performance (AUC 0.88, 95% CI 0.84–0.92), with a sensitivity of 82.5%, specificity of 80.1%, and satisfactory calibration (Hosmer–Lemeshow p = 0.68). Conclusions: Resistance-associated mutations in the 23S rRNA and gyrA genes are strongly associated with phenotypic antimicrobial resistance and reduced H. pylori eradication success. Molecular resistance testing may facilitate individualized treatment selection and improve clinical outcomes. The proposed prediction model, integrating clinical characteristics, treatment regimen, and molecular resistance markers, demonstrated excellent performance and may represent a useful tool for identifying patients at increased risk of eradication failure.

Food allergy is increasingly recognized across geographic regions and age groups, although temporal trends are difficult to separate from differences in diagnostic criteria and surveillance. This narrative review examines how diet and nutrition interact with the wider exposome to influence food allergy risk, oral tolerance, and clinical phenotypes across the lifespan. We critically synthesize evidence on early-life allergen introduction, dietary diversity, fiber and microbial metabolites, Westernized and ultra-processed dietary patterns, epithelial barrier dysfunction, medication exposures, pollution, and changing food systems. Randomized trials support early peanut introduction and, with greater heterogeneity, early egg introduction as preventive approaches; by contrast, causal evidence linking most other nutritional and environmental exposures to clinically confirmed food allergy remains limited. The diet–microbiome–immune axis offers plausible pathways connecting dietary substrates and microbial metabolites to epithelial integrity and immune regulation, but human mechanistic and longitudinal evidence remains incomplete. Globalization, migration, alternative protein sources, and climate-related exposures may reshape allergen encounters. Adult-onset food allergy, pollen–food allergy syndrome, alpha-gal syndrome, and cofactor-dependent reactions further illustrate how environmental influences may alter clinical expression beyond infancy. We propose an integrated life-course framework linking nutritional and non-nutritional exposures, underlying biological pathways, and emerging allergic phenotypes, while explicitly distinguishing intervention-supported findings from observational associations and mechanistic hypotheses. Future studies should combine standardized clinical outcomes with dietary assessment, environmental exposure measurements, functional microbiome profiling, metabolomics, and immune phenotyping to identify modifiable pathways relevant to food allergy prevention.