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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. Plain language summary: Treatment against Helicobacter pylori infection without using acid-blockers (proton pump inhibitors) in patients with corpus atrophic gastritis The common treatment against Helicobacter pylori (Hp) infection, the bug causing gastritis, peptic ulcer, and gastric cancer, is a combination of antibiotics and drugs blocking gastric acid secretion, called proton pump inhibitors (PPIs). Corpus atrophic gastritis, is a particular type of gastritis at increased risk for gastric cancer, in which the gland producing gastric acid are damaged and therefore the use of PPIs does not make sense. It is unknown, whether treatment against Hp using only antibiotics without PPIs works in the same manner. The current research aimed to understand in clinical practice whether in patients with corpus atrophic gastritis and Hp infection, never treated before, the treatment against Hp with antibiotics but without using PPIs, is well tolerated and successful to eradicate the bacterium. This study involved 76 patients with histological Hp infection and corpus atrophic gastritis (ascertained by gastroscopy and biopsies): 30 patients were treated with amoxillin together with another antibiotic, and 46 patients with a single-pill bismuth treatment (SPBT) available since 2016. All treatments were prescribed without using PPIs. At 6 ± 3 months after treatment, adverse events and treatment efficacy, i.e. whether Hp disappeared on gastric biopsies taken during gastroscopy, was checked. What this study found was that adverse events occurred in only 6 patients, all mild and not requiring treatment. Of the 76 patients, 71 completed the treatment. The eradication of the bacterium was yielded in 64 (90.1%) patients. The SPBT worked better compared to the amoxicillin treatment as more patients in the first were successfully cured from the infection: 97.7% against 78.6%. This research shows that in clinical practice in patients with corpus atrophic gastritis, the cure of Hp infection can be achieved without. [ABSTRACT FROM AUTHOR]

INTRODUCTION: Corpus-restricted atrophic gastritis is a chronic inflammatory disorder leading to possible development of type 1 neuroendocrine tumors (T1gNET), intraepithelial neoplasia (IEN), and gastric cancer (GC). We aimed to assess occurrence and predictors of gastric neoplastic lesions in patients with corpus-restricted atrophic gastritis at long-term follow-up. METHODS: A prospective single-center cohort of patients with corpus-restricted atrophic gastritis adhering to endoscopic-histological surveillance was considered. Follow-up gastroscopies were scheduled according to the management of epithelial precancerous conditions and lesions of the stomach guidelines. In case of new/worsening of known symptoms, gastroscopy was anticipated. Cox regression analyses and Kaplan-Meier survival curves were obtained. RESULTS: Two hundred seventy-five patients with corpus-restricted atrophic gastritis (72.0% female, median age 61 [23-84] years) were included. At a median follow-up of 5 (1-17) years, the annual incidence rate person-year was 0.5%, 0.6%, 2.8%, and 3.9% for GC/high-grade IEN, low-grade IEN, T1gNET, and all gastric neoplastic lesions, respectively. All patients showed at baseline operative link for gastritis assessment (OLGA)-2, except 2 low-grade (LG) IEN patients and 1 T1gNET patient with OLGA-1. Age older than 60 years (hazard ratio [HR] 4.7), intestinal metaplasia without pseudopyloric metaplasia (HR 4.3), and pernicious anemia (HR 4.3) were associated with higher risk for GC/HG-IEN or LG-IEN development and shorter mean survival time for progression (13.4, 13.2, and 11.1, respectively, vs 14.7 years, P 5 0.01). Pernicious anemia was an independent risk factor for T1gNET (HR 2.2) and associated with a shorter mean survival time for progression (11.7 vs 13.6 years, P 5 0.04) as well as severe corpus atrophy (12.8 vs 13.6 years, P 5 0.03). DISCUSSION: Patients with corpus-restricted atrophic gastritis are at increased risk for GC and T1gNET despite low-risk OLGA scores, and those aged older than 60 years with corpus intestinal metaplasia or pernicious anemia seem to display a high-risk scenario. [ABSTRACT FROM AUTHOR]

Autoimmune atrophic gastritis is an immune-mediated disease resulting in autoimmune destruction of the specialized acid-producing gastric parietal cells. As a consequence, in autoimmune atrophic gastritis, gastric acid secretion is irreversibly impaired, and the resulting hypochlorhydria leads to the main clinical manifestations and is linked, directly or indirectly, to the long-term neoplastic complications of this disease. In the last few years, autoimmune atrophic gastritis has gained growing interest leading to the acquisition of new knowledge on different aspects of this disorder. Although reliable serological biomarkers are available and gastrointestinal endoscopy techniques have substantially evolved, the diagnosis of autoimmune atrophic gastritis is still affected by a considerable delay and relies on histopathological assessment of gastric biopsies. One of the reasons for the diagnostic delay is that the clinical presentations of autoimmune atrophic gastritis giving rise to clinical suspicion are very different, ranging from hematological to neurological-psychiatric up to gastrointestinal and less commonly to gynecological-obstetric symptoms or signs. Therefore, patients with autoimmune atrophic gastritis often seek advice from physicians of other medical specialties than gastroenterologists, thus underlining the need for increased awareness of this disease in a broad medical and scientific community.