Autoimmune gastritis (AIG) in its advanced atrophic stage is characterized by reduced acid secretion, dysbiosis, and gastric cancer (GC) risk. Swallowed oral bacteria surviving in increased intragastric pH may play a carcinogenic role. Oral microbiota was linked to increased GC risk. In AIG, the concomitant assessment of oral and gastric microbiota has not yet been performed. This study aimed to investigate the oral and gastric microbiota in AIG patients to clarify the role of oral bacteria in gastric dysbiosis. A case–control study on n = 20 histologically diagnosed AIG patients and n = 20 controls without AIG is conducted. Saliva samples were obtained from subjects who were fasting and without toothbrushing. Within 1 h, gastroscopy with biopsies (for histopathology and DNA extraction) was performed. Saliva (n = 40) and biopsy (n = 40) samples were frozen at −20 °C. DNA was extracted and prepared; paired-end sequencing was performed (IlluminaMiSeq-sequencer, San Diego, CA, USA). Bacterial abundance in biopsies was higher in AIG than in controls (p = 0.06), but was not different in the saliva (p = 0.54) samples. In biopsies, AIG showed a lower Shannon-Index than controls (p = 0.001). In saliva studies, AIG showed a higher Shannon-Index than controls (p = 0.0). In biopsies, Streptococcus oralis, Fusobacterium pseudoperiodonticum, Veillonella rogosae, and Gemella sanguinis were more frequent in AIG (p < 0.03). The most abundantly shared taxa between saliva and biopsy were S. oralis and Prevotella histicola; Gemella sanguinis, Fusobacterium pseudoperidonticum, and Veillonella rogosae were shared in AIG patients only. This study confirmed gastric dysbiosis in AIG. Oral taxa were more commonly associated with AIG and shared between the mouth and the stomach. In AIG, the oral microbiota is associated with gastric dysbiosis, highlighting the importance of oral eubiosis in patients with impaired gastric acid secretion.

BACKGROUND AND AIMS:Autoimmune gastritis (AIG) is characterized by chronic hypergastrinemia and is associated with an increased risk of gastric neuroendocrine neoplasms (gNENs). Because proton pump inhibitors (PPIs) further increase gastrin secretion, concerns have been raised regarding a potential additive effect on gastric neoplastic risk. This study aimed to evaluate the association between PPI exposure and gNEN occurrence in patients with AIG using a large real-world database. METHODS:We conducted a retrospective propensity score-matched cohort study using the TriNetX Global Collaborative Network. Patients with AIG were identified using diagnostic codes for chronic atrophic gastritis or pernicious anaemia, excluding Helicobacter pylori infection, gastric cancer, multiple endocrine neoplasia or other competing gastric conditions. Two cohorts were defined: patients with AIG receiving PPIs and patients without PPI exposure. The primary outcome was the overall occurrence of gNENs. A prespecified secondary analysis excluded patients with gNENs diagnosed before the index date to evaluate incident tumours. Secondary outcomes included hypergastrinemia, intestinal metaplasia and gastric polyps. RESULTS:A total of 153,687 patients with AIG were identified. After 1:1 propensity score matching, 40,489 patients were included in each cohort. After propensity score matching, gNENs were recorded in 241 patients (0.60%) without PPI exposure and 360 patients (0.89%) receiving PPIs. PPI exposure was associated with a significantly higher occurrence of gNENs (risk ratio [RR] 1.49, 95% CI 1.27-1.76), which was confirmed by time-to-event analysis (hazard ratio [HR] 1.44, 95% CI 1.22-1.70; log-rank p < 0.001). The association persisted after exclusion of patients with pre-existing gNENs (RR 1.61, 95% CI 1.26-2.06; HR 1.52, 95% CI 1.19-1.95). PPI exposure was also associated with higher occurrences of hypergastrinemia (HR 1.17, 95% CI 1.00-1.37), intestinal metaplasia (HR 1.53, 95% CI 1.36-1.71) and gastric polyps (HR 2.48, 95% CI 2.25-2.73). No gastric adenocarcinomas were identified during follow-up. CONCLUSIONS:In this large real-world propensity score-matched study, PPI exposure was associated with a greater occurrence of both overall and incident gNENs in patients with AIG. PPI use was also consistently associated with gastric mucosal alterations, including hypergastrinemia, intestinal metaplasia and gastric polyps. Although the absolute risk of gNENs remained low, these findings support judicious long-term PPI prescribing in patients with AIG and reinforce the importance of appropriate endoscopic surveillance in this high-risk population.

Background and Objectives: Corpus atrophic gastritis (CAG) is associated with vitamin B12 deficiency due to impaired gastric acid and intrinsic factor secretion. Untreated vitamin B12 deficiency can lead to pernicious anemia, severe neurological consequences, and acute cardiocerebral-vascular events. Timely vitamin B12 supplementation is relevant; however, the dosage of intramuscular (IM) vitamin B12 supplementation has not been standardized to date. The objective was to assess the efficacy of a 1st and 2nd treatment schedule of IM-cyanocobalamin treatment in CAG patients with vitamin B12 deficiency at long-term follow-up and to identify the predictors of increased cyanocobalamin requirement. Methods: This monocentric real-life cohort study included 213 CAG patients with vitamin B12 deficiency. Inclusion criteria were adult age, histological diagnosis of CAG with vitamin B12 deficiency (<220 pg/mL), and follow-up of more than 12 months. The 1st-treatment-schedule (TxA) was 5000 µg IM cyanocobalamin every 5 days for 3 times, followed by 5000 µg IM cyanocobalamin every 3 mos (20,000 µg/yr); the 2nd-treatment-schedule (TxB) was 5000 µg IM cyanocobalamin every 5 days for 3 times, followed by 5000 µg IM cyanocobalamin every 2 mos (30,000 µg/yr). The treatment endpoint was serum vitamin B12 normalization. Clinical-biochemical follow-up was scheduled every 12 ± 6 mos: patients who satisfied the endpoint maintained the TxA, otherwise, TxB was prescribed. Results: Of the 213 CAG patients with vitamin B12 deficiency, 48.3% had anemia, and 26.3% macrocytosis without anemia. TxA efficaciously corrected vitamin B12 deficiency in 146 (68.5%) patients, maintaining efficacy until the longest available follow-up (42.2 ± 2.6 months). The remaining 67 patients (31.5%) were switched to TxB due to persistent vitamin B12 deficiency observed at 12 (6-36) months and were maintained until the longest available follow-up (50.2 ± 4.1 months). At the longest available follow-up, a significant increase in Hb (TxA: 11.9 ± 0.2 to 13.1 ± 0.1 g/dL, p < 0.001; TxB: 12.2 ± 0.3 to 13.6 ± 0.2 g/dL, p = 0.003) and serum vitamin B12 (TxA: 168 ± 7 to 402 ± 19 pg/mL, p < 0.0001; TxB: 157 ± 12 to 340 ± 24 pg/mL, p < 0.0001) was shown in both schedules. A significant decrease in MCV was shown in TxB only (p = 0.0003). In logistic regression, switching to TxB was significantly associated with severe corpus intestinal metaplasia (OR 11.0, 95% CI 2.8-43.7), macrocytosis at CAG diagnosis (OR 2.7, 95% CI 1.2-6.3), and male sex (OR 2.4, 95% CI 1.1-5.2). Conclusions: In this real-world setting, at long-term follow-up, nearly 70% of CAG patients with vitamin B12 deficiency restored their vitamin B12 levels with 20,000 µg/yr of cyanocobalamin, while the remaining 30% required 30,000 µg/yr. Male vitamin B12-deficient CAG patients with advanced gastric damage and severe macrocytosis required higher dosages of cyanocobalamin. They should be carefully monitored to avoid suboptimal supplementation and potentially dangerous consequences of vitamin B12 deficiency.

Background/Objectives: Autoimmune gastritis (AIG), celiac disease (CD), and gastric surgery (GS) often cause iron deficiency anemia (IDA) due to iron malabsorption. In this clinical context, IDA treatment is often challenging. The first-line IDA treatment is oral iron supplementation followed by intravenous (IV) iron administration when ineffective or not tolerated. Ferric carboxymaltose (FCM) showed efficacy in various clinical settings. Prospective data evaluating the efficacy of IV FCM in IDA patients secondary to iron malabsorption are scant. The aim of the current study was to assess the tolerability, efficacy, and QoL impact of IV FCM for the treatment of IDA patients with iron malabsorption. Methods: Study design: single-center, prospective observational study: n = 37 adults with AIG, CD, or GS with IDA receiving IV FCM were consecutively included. Endpoints were (i) safety tolerability, (ii) efficacy on IDA recovery (Hb normalization), and (iii) QoL impact. At baseline (T0) and 12 weeks after treatment (T12), a QoL-SF12 questionnaire was assessed. Complete blood count (CBC) and iron status (ferritin, iron, transferrin, transferrin saturation (TS)) were assessed at T0, 4 weeks (T4), and T12 after treatment. Results: Of the 37 IDA patients, 19 (51.4%) had AIG, 9 (24.3%) CD, and 9 (24.3%) GS; Based on Ganzoni’s formula, 24 (64.9%) patients received a single IV FCM infusion (mean ± SEM dosage of 975 ± 12 mg); 13 (35.1%) required two IV infusion sessions with a mean ± SEM cumulative dose of 1400 ± 77 mg. One patient (2.7%) experienced mild adverse events without need for treatment interruption or hospitalization. At T0, anemia was moderate in 7 (18.9%) patients and severe in 1 (2.7%). IDA recovery was achieved in 26 (70.3%) patients at T4 and in 29 (78.4%) at T12. At T4, mean ± SEM Hb increased from 10.8 ± 0.2 g/dL to 12.7 ± 0.1 g/dL, ferritin from 28.5 ± 11.2 ng/mL to 188.2 ± 25.7 ng/mL, and TS from 6.7 ± 0.5% to 23.7 ± 1.9% (p < 0.0001). At T12, mean ± SEM Hb further increased to 13.1 ± 0.2 g/dL (p < 0.05 vs. T4), ferritin slightly decreased to 125 ± 26.7 ng/mL, and TS to 22.7 ± 2.8%. At T12, nonsignificant increases in QoL scores relative to baseline were observed. Conclusions: IV FCM is a safe and effective treatment leading to IDA recovery in nearly 80% of patients at T12. Thus, when oral iron treatment is not feasible or has failed, IV FCM treatment might be considered a first-line therapeutic option for IDA consequent to iron malabsorption.

BACKGROUND:Autoimmune atrophic gastritis (AAG) is an immune-mediated disorder affecting the gastric oxyntic mucosa. Two pathogenetic models are proposed: a pure autoimmune disorder or gastric autoimmunity triggered by Helicobacter pylori (Hp)-infection. In AAG, histological diagnosis of Hp may be challenging and serology can help assess exposure to Hp-infection. This study aimed to determine seroreactivity to Hp-antigens in AAG patients by using Hp-multiplex serology assay. METHODS:A single-centre case-control study on 178 adults: 75 patients with serological and histological AAG diagnosis, 25 controls with histologically Hp-positive-non-atrophic gastritis (Ctr-NAG-Hp+) and 78 subjects with a healthy stomach (Ctr-HS). Sera were analysed using Hp-multiplex serology assay allowing simultaneous detection of antibodies to 13 Hp-proteins. Overall positivity cutoff: seroreactivity to more than 3 Hp-antigens. RESULTS:The number of seroreactive Hp-antigens was higher in AAG than in Ctr-HS(mean±SEM 2.2±0.3 vs 1.4±0.22,p=0.02) and lower than in Ctr-NAG-Hp+ patients (mean±SEM 5.4±0.5,p<0.001).Overall Hp-seropositivity in AAG was two-fold higher than in Ctr-HS but not statistically significant (21.1% vs 10.3%,p=0.06) and lower than in Ctr-NAG-Hp+(80%,p<0.0001). Complete absence of seroreactivity was similar in AAG and Ctr-HS (29.3% vs 38.5%, p=0.23) and significantly higher than in Ctr-NAG-Hp+ (4%, p=0.009). Main immunogenic Hp-proteins were HP0010(GroEL),HP1098(HcpC),HP0695(HyuA),HP0875(Catalase),HP1564,HP0547(CagA) and HP0243(NapA) with seroreactivity in >50% of AAG patients. CONCLUSIONS:By Hp-multiplex serology, 30% of histologically Hp-negative AAG pts had no seroreactivity, likely belonging to the pure AAG type. Conversely, 20% of AAG pts showed Hp exposure, indicating that infection might have triggered gastric autoimmunity. The remaining AAG patients showed seroreactivity below cut-off for seropositivity and thus not definitively categorisable by this approach.

BACKGROUND:International comparative data on autoimmune gastritis (AIG) remain limited. OBJECTIVE:We aimed to describe AIG features and quantify the risk of gastric adenocarcinoma and type 1 gastric neuroendocrine tumours (NETs). DESIGN:Retrospective study across eight tertiary centres in Europe, Türkiye, Latin America, the USA and Japan. Adults with histologically confirmed AIG were included. Clinical and follow-up data were collected to estimate adenocarcinoma and NET incidence and associated factors. RESULTS:1240 patients were included (female:male 2:1; median age 59, IQR 48-67; median follow-up 68 months, IQR 36-108). Macrocytic anaemia predominated in Europe (45.6%), microcytic anaemia in Türkiye (56.1%) and Latin America (64.7%). Autoimmune comorbidities were most frequent in Latin America (67.7%). 36 (2.9%) gastric adenocarcinomas and 132 (10.6%) NETs occurred. No incident adenocarcinomas were reported in Latin America or Japan cohorts. Crude incidence rates ranged from 1.15 to 1.47 for adenocarcinoma and 0.70 to 1.62/100 person-years for NETs. Factors associated with adenocarcinoma included age >65 years (OR 4.50, 95% CI 2.18 to 9.27), intestinal metaplasia (OR 1.51, 95% CI 1.16 to 1.97), gastrin-17 >1316 pg/mL (OR 15.52, 95% CI 3.61 to 66.71) and prior proton pump inhibitor (PPI) (OR 5.74, 95% CI 2.13 to 15.47). For NETs, prior PPI (OR 2.69, 95% CI 1.12 to 6.46), smoking (OR 2.45, 95% CI 1.75 to 3.42), intestinal metaplasia (OR 2.88, 95% CI 1.38 to 6.01) and gastrin-17 >1316 pg/mL (OR 3.25, 95% CI 1.42 to 7.45), were associated with higher odds, while Helicobacter pylori eradication was associated with lower odds of NETs (OR 0.25, 95% CI 0.07 to 0.88). CONCLUSION:AIG presentation and neoplastic risks differ by region, warranting further research and potentially region-specific follow-up strategies.

OBJECTIVES:Autoimmune gastritis (AIG) has been poorly described in childhood. We sought to identify the patterns of manifestations of pediatric AIG at onset and to describe its laboratory, clinical, and histopathological features. METHODS:This was a retrospective, longitudinal, multicenter, cohort study enrolling histologically proven AIG patients with an onset in the pediatric age (<18 years old). We retrieved laboratory and clinical data at the time of onset and at last follow-up when available. Differences between Helicobacter pylori-exposed versus H. pylori-naïve, and anti-parietal cell antibody (PCA)-positive versus PCA-negative patients were investigated. RESULTS:Overall, 51 pediatric AIG patients (median age: 13 years, interquartile range: 11-16; F:M ratio 1.7:1) were included. Most patients were diagnosed with the overt type of AIG (47; 92.1%), while four (7.8%) were still in the potential phase. Atopic dermatitis (9.8%), rhinitis (7.8%), and asthma (5.9%) were common comorbidities, suggesting a link with T helper 2 (Th2) disorders. Two patients (3.9%) were found to have had previous or concurrent eosinophilic esophagitis, and five (9.8%) had eosinophilic gastritis. Notably, four patients (7.8%) presented with collagenous gastritis. On histological examination, the majority of patients were negative for H. pylori infection, except for 1 case out of 51 (2.0%) who had an active infection. CONCLUSIONS:AIG may affect pediatric patients and lead to complications in this population. At presentation, the disease may exhibit histologic patterns attributed to collagenous and/or eosinophilic gastritis. Moreover, a possible association between AIG and Th2 disorders has been observed, warranting further research.

INTRODUCTION:Helicobacter pylori (Hp)-related atrophic gastritis (AG) affects corpus and antral mucosa, resulting in multifocal AG (MF-AG); autoimmunity-driven AG is corpus-restricted (CR-AG). AG carries increased gastric dysplasia (GD) and gastric cancer (GC) risk, well established in MF-AG, but debated in CR-AG. This study aimed to assess clinical, endoscopic-histological characteristics of GD-GC in patients with MF-AG and CR-AG. METHODS:This was the multicenter cross-sectional study across 11 Italian gastroenterology centers on data of non-cardia GD-GC in adult patients with MF-AG or CR-AG based on clinical, endoscopic, and histological charts. RESULTS:Eighty-four patients were included with MF-AG and CR-AG in 45 (53.6%) and 39 (46.4%), respectively. Low-grade GD, high-grade GD, and GC were diagnosed in 31 (36.9%), 6 (7.1%), and 47 (56.0%), respectively. GD-GC similarly occurred in patients with MF-AG and CR-AG: high-grade GD in 4 (8.9%) vs 2 (5.1%), low-grade GD in 17 (37.8%) vs 14 (35.9%), and GC in 24 (53.5%) vs 23 (59.0%) ( P > 0.05). Compared with MF-AG, in patients with CR-AG, GD-GC were more commonly polypoid (51.6% vs 27.3%, P = 0.048) and more frequent in the corpus (55.3% vs 28.6%, P = 0.02), but occurred also in the antrum (34.2%) and incisura (10.5%). Surgery was more frequent in CR-AG than in MF-AG (48.6% vs 23.1%, P = 0.02). Corpus atrophy severity and intestinal metaplasia were not different ( P > 0.05), histological Hp positivity was low in both (2.3% vs 2.9%, P = 0.87), but in Hp negatives, active inflammation was present in the antrum in 26.7% and 7.7% ( P = 0.02), and in the corpus in 31.1% and 21.5% ( P = 0.27). DISCUSSION:Non-cardia GC and GD may occur in both MF-AG and CR-AG, displaying differences in topography and endoscopic presentation but similarities in nonlesional mucosa, differentiation, and staging. Surveillance should be considered in corpus AG, regardless of extension and supposed etiology. BACKGROUND:La gastrite atrofica (AG) Helicobacter pylori (Hp)-relata interessa la mucosa dell'antro e del corpo-fondo dando luogo alla gastrite atrofica multifocale (MF-AG); la gastrite atrofica autoimmune invece è limitata al corpo-fondo risparmiando l'antro (CR-AG). L'AG è ad aumentato rischio per displasia (GD) e cancro gastrico (GC). Questo rischio è ben stabilito nella MF-AG, ma ancor adibattuto nella CR-AG. Questo studio ha come scopo di valutare le caratteristiche cliniche e endoscopico-istologiche di pazienti affetti da GD o GC in MF-AG e CR-AG. METODI:E' stato condotto uno studio trasversale multicentrico in 11 centri gastroenterologici italiani su dati di pazienti adulti con GD o GC non cardiali in MF-AG o CR-AG basati su schede cliniche e referti endoscopici e istologici. RISULTATI:Sono stati inclusi 84 pazienti, di cui 45 (53.6%) con MF-AG e 39 (46.4%) con CR-AG. GD di basso (LG-GD) e di alto grado (HG-GD) e GC sono stati diagnosticati in 31 (36.9%), 6 (7.1%), and 47 (56.0%) pazienti, rispettivamente. GD e GC sono stati riscontrati con frequenza simile in pazienti con MF-AG e CR-AG: HG-GD in 4 (8.9%) vs 2 (5.1%), LG-GD in 17 (37.8%) vs 14 (35.9%), e GC in 24 (53.5%) vs 23 (59.0%) (p>0.05). Rispetto ai pazienti con MF-AG, nei pazienti con CR-AG GD e GC erano più frequentemente di aspetto polipoide (51.6% vs 27.3%, p=0.048) e più frequentemente localizzati nel corpo-fondo (55.3% vs 28.6%, p=0.02), ma venivano riscontrati anche nell'antro (34.2%) e a livello dell'incisura (10.5%). Il trattamento chirurgico era più frequente nei pazienti con CR-AG rispetto a coloro con MF-AG (48.6% vs 23.1%, p=0.02). La severità dell'atrofia del corpo-fondo e la presenza di metaplasia intestinale non erano differenti (p>0.05), mentre la positività istologica per l'Hp era bassa in ambedue i gruppi ((2.3% vs 2.9%, p=0.87), ma nei Hp negativi l'attività infiammatoria era presente nell'antro nel 26.7% e 7.7% (p=0.02), e nel corpo-fondo nel 31.1% e 21.5% (p=0.027). CONCLUSIONI:GD e i GC non cardiali possono sviluppare sia in pazienti con MF-AG che con CR-AG, con differenze nella topografia e nella presentazione endoscopica ma con similitudini nella mucosa non lesionale circostante, nella differenziazione e nella stadiazione. Pertanto, la sorveglianza dovrebbe essere considerata in tutti i pazienti con AG del corpo, a prescindere dall'estensione e dalla presunta eziologia.

BACKGROUND:Type 1 gastric neuroendocrine tumors (T1-gNETs) are typically indolent. Current guidelines suggest endoscopic surveillance for lesions ≤10 mm, mainly based on expert consensus. AIM:To evaluate outcomes in patients with T1-gNETs ≤10 mm managed by endoscopic surveillance. METHODS:This dual-center retrospective study (2000-2023) included patients from two Western ENETS Centers of Excellence with T1-gNETs ≤10 mm under surveillance. Primary endpoints were disease progression rate and progression-free survival (PFS); p < 0.05 was considered significant. RESULTS:A total of 125 patients (66.4 % female; median age 59.5 years) with a median tumor size of 3 mm were analyzed. Most tumors were G1 (92.8 %), and 75.2 % had ≤5 lesions. Over a median follow-up of 72 months, progression occurred in 5 patients (4 %), with no metastases. Low-grade dysplasia was found in 2.4 % and early gastric cancer in 1.6 %. Eleven patients (8.8 %) died, none from tumor-related causes. Restricted mean survival time was 266.5 months. The 5-year PFS rate was 97.8 %. Having ≤5 lesions was significantly associated with lower progression risk (HR = 0.14, 95 % CI: 0.014-0.76, p = 0.022). CONCLUSIONS:T1-gNETs ≤10 mm show low progression risk and can be safely managed with lifelong surveillance. In patients with solitary or few lesions, extended intervals may be appropriate.

Autoimmune atrophic gastritis (AAG) is a non-self-limiting immune-mediated disorder exerting growing interest. The main autoantigen, the beta subunit of the proton pump (H+, K+-ATPase), is localised on the oxyntic mucosa parietal cells, limiting the autoimmune inflammatory damage to this stomach compartment. Clinical manifestations of AAG may occur late, once corpus-fundus atrophy occurs, and are characterised by loss of gastric acidity, impaired iron and/or cobalamin malabsorption, and increased risk of gastric type 1 neuroendocrine neoplasms and possibly gastric adenocarcinoma. Many topics regarding epidemiology, clinical features, pathogenesis, diagnosis, and management remain to be clarified. AAG patients are frequently misdiagnosed or diagnosed with delay. AAG still represents a clinical challenge and a great opportunity for advancing our knowledge on gastrointestinal autoimmune diseases and gastric precancerous conditions. The timely and correct diagnosis of AAG patients is clinically relevant to avoid potentially harmful consequences due to micronutrient deficiencies and related anaemia and neoplastic complications. The current position paper addresses AAG in adults and reflects the views of the Autoimmune gastRitis Italian netwOrk Study grOup (ARIOSO) on its epidemiology, clinical features, pathogenesis, diagnosis, and management. Improving the understanding of AAG would facilitate timely and accurate diagnosis, enhance clinical management and patients' quality of life, and reduce the economic and social burden of this underrecognized condition.

Background: Efficacy of eradication regimens in Helicobacter pylori (Hp) infection is commonly reported with proton pump inhibitors (PPIs). In patients with corpus atrophic gastritis, characterized by impaired acid secretion, PPI treatment is questionable. Objectives: The current study aimed to assess in clinical practice the tolerability and eradication rate of modified eradication regimens without PPI as first-line treatment in patients with histologically Hp-positive corpus atrophic gastritis. Design: Real-life longitudinal observational study. Methods: Overall, 76 patients (77.6% females, age 58.5 (26–88) years) with histologically Hp-positive corpus atrophic gastritis were consecutively diagnosed (2001–2022). First-line eradication treatment was prescribed without PPIs: concomitant or sequential amoxicillin-based therapy (ABT) until 2016 ( n = 30), then single-pill bismuth treatment (SPBT; n = 46). Treatment adherence and adverse events were clinically evaluated and treatment efficacy was assessed by histopathology (updated Sydney system) at 6 ± 3 months after treatment. Results: Only mild adverse events not requiring medical treatment were observed in four patients treated with SPBT without PPIs (vomiting, self-limiting diarrhoea, nausea, abdominal discomfort) and in two treated with ABT without PPIs (vomiting and abdominal discomfort). Overall, 71/76 (93.4%) corpus atrophic gastritis patients completed the treatment: 43/46 (93.5%) SPBT without PPIs and 28/30 (93.3%) ABT without PPIs. Successful cure of Hp was observed in 64/71 patients: overall eradication rate 90.1%, 95%CI 69.4%–115.1%. 42/43 corpus atrophic gastritis patients treated with SPBT without PPIs were successfully cured against 22/28 of those treated with ABT without PPIs. The eradication rate was higher for SPBT than ABT: 97.7%, 95%CI 70.4%–132.0% vs 78.6%, 95%CI 49.2%–118.9%, p = 0.013. Conclusion: In clinical practice, Hp cure can be achieved without PPIs as first-line treatment in about 90% of patients with corpus atrophic gastritis.

Background First-degree relatives of gastric cancer (GC) patients are known to have an increased risk of developing GC. However, guidelines in low-intermediate incidence regions often lack specific recommendations for managing both asymptomatic and symptomatic relatives at risk. Aim This study aimed to evaluate the differences in relevant histological findings (e.g. Helicobacter pylori infection, gastric precancerous and neoplastic conditions) between asymptomatic patients undergoing esophagogastroduodenoscopy due to first-degree relatives with GC and patients with symptoms or other clinical indications and presence of first-degree relatives with GC. The secondary aim was to identify the patient’s risk factors of relevant histological findings. Methods This single-center retrospective study included patients undergoing esophagogastroduodenoscopy with biopsies with the indication for first-degree relatives with GC from January 2008 to September 2022. They were analyzed in two groups based on whether they had additional symptoms or clinical indications for esophagogastroduodenoscopy. Results Overall, 283 patients were included (54.5% asymptomatic vs. 45.5% symptomatic). Histological findings that led to changes in patient management were identified in 32% of cases. No significant differences in histological findings between the two groups were observed ( P = 0.077). A subanalysis revealed that patients with male relatives affected by GC had a higher incidence of relevant histological findings than those with female family members with GC ( P = 0.013) with an odds ratio of 3.10. Conclusion First-degree relatives of GC patients may be at risk for H. pylori infection and gastric precancerous conditions regardless of symptoms or other indications, and a proactive endoscopic screening could be considered even in countries with low GC incidence.