Endoscopic Features of Early Autoimmune Gastritis: Insights From a Case Study in a Young Male Patient

Figure 1. Endoscopic findings of early autoimmune gastritis. Early Endoscopic Findings of Autoimmune Gastritis. Autoimmune gastritis, historically termed type A gastritis by Strickland and Mackey [1], is an autoimmune disorder targeting the parietal cells of the fundic glands, resulting in inflammation and atrophy predominantly in the corpus and fundus. Traditionally, patients with autoimmune gastritis present with neurological symptoms secondary to vitamin B12 or iron deficiency, often leading to diagnoses such as pernicious anemia or iron deficiency anemia in advanced stages [2]. However, the majority of cases are asymptomatic and frequently discovered incidentally. Diagnosis relies on a combination of clinical, endoscopic, histological, and serological findings, though standardized diagnostic criteria for autoimmune gastritis have yet to be universally established. In 2023, the “Study Group on Establishment of Diagnostic Criteria for Type A Gastritis,” an adjunctive group of the Japanese Society of Gastrointestinal Endoscopy (JSGE), proposed new diagnostic criteria [3]. According to these criteria, autoimmune gastritis is definitively diagnosed when characteristic endoscopic or histological findings are accompanied by positive gastric autoantibodies (anti-parietal cell or anti-intrinsic factor antibodies). Despite increasing global interest in the early-stage endoscopic features of autoimmune gastritis, reports in young adults remain scarce [3,4,5,6]. A 22-year-old male presented with complaints of epigastric pain and lower back pain. He had received two COVID-19 vaccinations and had undergone Helicobacter pylori eradication therapy at another hospital three months prior to his visit. Laboratory investigations revealed no evidence of anemia (red blood cell count: 5.20 × 10⁶/μL; hemoglobin: 17.4 g/dL; hematocrit: 49.8%; mean corpuscular volume: 95.9 fL), normal iron metabolism (serum iron: 161 μg/dL [40-188]; total iron-binding capacity: 336 μg/dL [253–366]; ferritin: 58.2 ng/mL [31-325]), and normal serum levels of gastrin (170 pg/mL [0-200]) and vitamin B12 (497 pg/mL [180-914]). Anti-parietal cell antibody levels were slightly elevated (10-fold; reference range: 0–9). An upper gastrointestinal endoscopy was performed using the Olympus GIF-290 endoscope. An upward view of the lesser curvature of the gastric body revealed a regular arrangement of collecting venules (RAC) [7], a hallmark endoscopic feature indicative of H. pylori-negative status, in the lower body. A sharply demarcated atrophic border was observed between the lower and middle corpus. A downward view of the greater curvature of the body revealed no atrophic changes in the lower segment but extensive atrophy in the middle and upper segments. Scattered diffuse redness and atrophy were visible in the upper body and fundus. The antral mucosa showed transvascular findings without severe atrophy or intestinal metaplasia. The natural history of autoimmune gastritis is thought to progress through four stages. In the first stage, serum anti-parietal cell and anti-intrinsic factor antibodies become positive, representing a condition referred to as potential autoimmune gastritis, which lacks histological evidence of corpus-predominant atrophic gastritis [8]. In the second stage, histological abnormalities develop in the corpus mucosa, but no endoscopic atrophic changes are observed. The third stage is characterized by evident corpus atrophy on endoscopy, while most patients remain asymptomatic. In the final stage, clinical manifestations such as vitamin B12 deficiency and anemia emerge. Notably, childhood autoimmune gastritis may present with symptoms and histological or serological abnormalities despite the absence of endoscopic atrophic changes [9]. Reports on the early-stage endoscopic findings of autoimmune gastritis are limited. Childhood cases are often discovered incidentally due to anemia or comorbidities such as chronic thyroiditis or type 1 diabetes mellitus [9,10]. The low prevalence and asymptomatic nature of most cases have limited the routine use of endoscopy for diagnosis. In Japan, where gastric cancer screening is prevalent, most cases of atrophic gastritis are attributed to H. pylori infection, often associated with pangastritis caused by the cytotoxin-associated gene A (CagA) virulence factor [11,12,13]. Eradication therapy for H. pylori has uncovered cases of atrophic gastritis unrelated to infection, with corpus-predominant atrophy increasingly recognized as autoimmune gastritis [14,15]. Studies have reported that autoimmune gastritis is more frequently observed in patients with multiple failed H. pylori eradication attempts, potentially due to achlorhydria allowing the survival of urease-positive bacteria other than H. pylori [14,15,16,17,18]. This phenomenon may lead to false-positive urea breath test results [16]. As interest in autoimmune gastritis grows, the adjunctive study group of the JSGE has proposed diagnostic criteria that incorporate endoscopic findings [3]. However, early-stage endoscopic features remain poorly defined due to limited case accumulation. Kotera et al. recently described characteristic endoscopic findings, including longitudinal pseudo-polyps and erythematous swelling, in 12 patients with early-stage autoimmune gastritis (mean age: 56.2 years; range: 41–71 years) [6]. Notably, these findings have not been reported in younger patients. In this case, we report the endoscopic findings of ear-ly-stage autoimmune gastritis in a 22-year-old male. Although the endoscopic appearance did not exhibit bamboo-like or salmon-like patterns described by Kotera et al., a distinct atrophic border demarcating the pyloric and fundic glands was observed. Despite the absence of histological examination and only a slightly elevated anti-parietal cell antibody titer, this case highlights unique endoscopic features of early-stage autoimmune gastritis in a young adult.