Atrophic gastritis is an autoimmune gastritis that is characterised by the production of antibodies to parietal cells and intrinsic factor of the stomach. It is uncommon in paediatrics, as a result, is not usually in the differential diagnosis. A boy in middle childhood presented with a history of auditory hallucinations and fatigue, his workup only showed iron deficiency anaemia which responded to oral iron replacement but rebounded off therapy. There was no underlying cause found until years later, when he presented with Raynaud's phenomenon leading to an autoimmune workup being done which showed him being weakly antinuclear antibody (ANA) positive and strongly positive for antiparietal cell antibody. This led to the patient undergoing endoscopy where the histopathology findings revealed antral-like gastric mucosa with mild mixed chronic inflammation. There was a decrease in parietal cell numbers and t focal evidence of intestinal metaplasia, but no evidence of dysplasia or malignancy. This confirmed the diagnosis of atrophic gastritis which is extremely rare in the paediatric population.

Celiac disease (CD) is a chronic immune-mediated enteropathy characterized by gluten-induced small intestinal mucosal injury and a broad spectrum of clinical manifestations. Emerging evidence suggests that CD may also be associated with gastric mucosal abnormalities, including Helicobacter pylori-negative chronic gastritis (HPNCG). This study aimed to investigate the clinical, laboratory, and histopathological features of patients with CD complicated by HPNCG and to identify factors associated with this condition. A total of 60 patients with CD were retrospectively enrolled and divided into 2 groups: CD alone (n = 26) and CD with HPNCG (n = 34). Demographic characteristics, gastrointestinal symptoms, comorbidities, laboratory parameters, and histopathological findings were compared between groups. Univariate and multivariate logistic regression analyses were performed to identify factors independently associated with CD complicated by HPNCG. Receiver operating characteristic curve analysis was used to evaluate discriminatory performance. Among the 60 patients, 45.0% were male and 55.0% were female, with a mean age of 41.8 ± 15.2 years. Compared with the CD-alone group, patients with CD and HPNCG had significantly higher prevalence of abdominal bloating (61.8% vs 30.8%, P = .018), anemia (58.8% vs 26.9%, P = .013), osteopenia/osteoporosis (38.2% vs 15.4%, P = .048), and liver function abnormalities (23.5% vs 3.8%, P = .036). Histopathologically, Marsh grade IIIb-IIIc (88.2% vs 61.5%, P = .019) and moderate-to-severe chronic gastric inflammatory infiltration (64.7% vs 34.6%, P = .022) were more frequent in the CD with HPNCG group. Multivariate logistic regression identified Marsh grade IIIb-IIIc as the only factor independently associated with CD complicated by HPNCG (odds ratio = 3.96, 95% confidence interval: 1.05-14.91, P = .042). Receiver operating characteristic analysis showed that Marsh grade IIIb-IIIc alone yielded an area under the curve of 0.73, while the combined model achieved an area under the curve of 0.81. Patients with CD complicated by HPNCG present with a heavier burden of gastrointestinal symptoms, nutritional impairments, and mucosal injury compared to those with CD alone. Severe duodenal villous atrophy, reflected by Marsh grade IIIb-IIIc, is independently associated with HPNCG in CD and may serve as a clinically useful indicator for identifying this high-risk subgroup.

The contact-induced epithelium gene A (iceA), with allelic variants iceA1 and iceA2, remains a controversial virulence factor in Helicobacter pylori due to inconsistent clinical outcomes. In this study, we analyzed 1,427 H. pylori genomes from the NCBI database and 200 clinical isolates from Shenzhen, China, to elucidate the global distribution of iceA genotypes and their associations with other virulence factors, bacterial gene expression, and the relationship with gastric diseases. We found that iceA genotypes varied significantly across regions, with iceA1 predominating in Asia and Europe, and iceA2 being more prevalent in North America. This suggests adaptive evolution to regional host environments. The association between iceA genotypes and cagA status also exhibited regional patterns. Additionally, iceA1 was linked to higher ureA expression, potentially enhancing acid resistance and colonization potential (P < 0.05). Importantly, patients infected with iceA1 genotype strains were more likely to present with gastric erosion (P < 0.05); however, they showed no association with peptic ulcer disease in any region. These findings highlight the geographical heterogeneity of iceA1 genotypes and their potential role in H. pylori-related gastric diseases.

Helicobacter pylori (H. pylori) infection remains highly prevalent worldwide and is strongly associated with chronic gastritis, peptic ulcer disease, and an elevated risk of gastric cancer. In pediatric clinical practice, eradication therapy is challenged by rising antibiotic resistance, inadequate acid suppression, and poor adherence to complex multidrug regimens. Potassium-competitive acid blockers (P-CABs) represent a newer class of antisecretory agents that competitively and reversibly inhibit gastric H+/K+-ATPase, resulting in a more rapid onset and more sustained control of intragastric pH compared with conventional proton pump inhibitors (PPIs). P-CABs offer greater flexibility in dosing timing relative to meals in children, with substantial potential to simplify treatment regimens and improve H. pylori eradication rates in the pediatric population. This narrative review summarizes the pharmacologic rationale for using P-CABs in pediatric H. pylori eradication, synthesizes current clinical evidence-derived mainly from Japanese observational studies of vonoprazan (VPZ)-and discusses key issues regarding resistance, tolerability, and practical clinical application. Published pediatric studies, predominantly involving adolescents and older pediatric cohorts, suggest that VPZ-based regimens may achieve favorable eradication rates, while short-term tolerability appears broadly similar to that of PPI-based therapies in the available comparative data. However, the existing evidence is limited by small sample sizes, narrow geographic scope, and marked heterogeneity in study design, antibiotic backbones, and resistance patterns, which preclude direct cross-study comparisons. Data supporting other P-CABs in pediatric populations remain very scarce. Future research should prioritize pediatric pharmacokinetic/pharmacodynamic studies to optimize weight- and age-based dosing, conduct resistance-stratified comparative trials, and perform cost-effectiveness analyses. Until more robust pediatric evidence becomes available, P-CAB-based regimens may be considered a viable option in selected clinical scenarios, while clinicians should exercise caution when extrapolating adult data and remain vigilant toward local antibiotic resistance epidemiology.

Autoimmune gastritis (AIG) has been traditionally recognised as a precursor to type I gastric neuroendocrine tumours and non-cardia gastric adenocarcinoma. However, emerging but scattered evidence suggests that its oncogenic footprint may extend beyond the gastric body to the cardia, gastro-oesophageal junction (GOJ) and oesophagus. In this review, we synthesise the available epidemiological and clinical studies linking AIG and its late manifestation, pernicious anaemia, to cardia/GOJ adenocarcinoma and oesophageal cancers. We discuss putative histopathological, immunological and other mechanisms, including corpus-predominant atrophy, intestinal metaplasia and vitamin B12 deficiency that may create a carcinogenic microenvironment not only in the distal stomach but also at the GOJ and beyond. We highlight diagnostic and epidemiologic challenges that have obscured these associations, including the difficulties in defining the gastric cardia, disentangling autoimmune versus other potential pathways and the under-recognition of AIG in routine practice. Finally, we outline a research agenda aimed at clarifying the malignancy risk across the stomach-cardia-oesophagus continuum, emphasising the need for well-phenotyped cohorts, biomarker-driven risk stratification and refined surveillance strategies. By reframing AIG as a potential hidden gateway to junctional and oesophageal malignancies, we argue that its true oncological significance may be broader than previously appreciated.

Neonatal vitamin B12 (B12) deficiency can cause neurodevelopmental harm, and newborn screening (NBS) may enable early detection and treatment. We conducted a multicenter pilot project in four Prague university hospitals between 1 June 2022 and 30 June 2025. Algorithms included the determination of propionylcarnitine-derived primary markers using flow-injection tandem mass spectrometry and second-tier methylmalonic acid (MMA), with total homocysteine measured only when MMA was increased. Of 34,302 screened newborns with consent, 1365 (3.98%) triggered second-tier testing; 9 had MMA > 2.5 µmol/L, of which 8 met the case definition after confirmatory testing, giving a birth frequency of 1:4228 (95% CI 1:2176-1:9931). Positive predictive value was 0.59% (95% CI 0.25-1.15%) and 88.89% (95% CI 51.75-99.72%) for the primary test and second-tier MMA, respectively, with a false positive rate of 0.00292% (95% CI 0.000074-0.01625%). All affected infants were treated orally with cyanocobalamin. Maternal work-up identified confirmed B12 deficiency in four of eight mothers and premalignant gastric changes in two of four positive women. These data support the feasibility, low cost, and clinical utility of incorporating B12 deficiency into Czech NBS, with benefits extending beyond newborn health.

Helicobacter pylori infection is a major etiological factor in chronic gastritis, peptic ulcer disease, and gastric cancer, highlighting the demand for sensitive, non-invasive, and operationally simple diagnostic strategies. Herein, we report a pathogen-activated, enzyme-free biosensing platform that directly couples target recognition with signal amplification through a single DNAzyme-hybridization chain reaction (HCR) cascade. Distinct from conventional multicomponent amplification systems, the designed DNAzyme simultaneously functions as both the recognition element and the HCR initiator, enabling a true one-step assay without auxiliary enzymes or intermediate probes. Upon specific activation by H. pylori, the DNAzyme releases an initiator strand that triggers downstream HCR amplification, generating a fluorescence signal-off response under mild isothermal conditions (37 °C). The assay exhibits a linear response over a concentration range of 102-104 CFU mL-1 with a detection limit of 0.11 CFU mL-1 and enables direct analysis of saliva supernatants without complex pretreatment. Recovery studies in artificially contaminated saliva samples show satisfactory accuracy (98.4-104.9%) and reproducibility (RSD < 5%). Owing to its simplified workflow, minimal equipment requirement, and modular design, this strategy provides a generalizable sensing framework for non-invasive pathogen detection.