The clinical data of 4 pediatric patients with collagenous gastritis (CG) diagnosed at the Department of Pediatrics of Peking University Third Hospital between January 2021 and October 2025 were retrospectively analyzed. The median age at onset was 10.8 years. All patients presented with iron-deficiency anemia, and two also experienced abdominal pain. Gastroscopy in all cases revealed a nodular gastric mucosal appearance. Histopathological examination confirmed subepithelial collagen band thickness greater than 10 μm in all patients, with varied patterns of inflammatory infiltrate, including two cases with eosinophil-predominant inflammation and one with lymphocytic gastritis. Two patients were found to have collagenous duodenitis, while none showed collagenous colitis. Serological testing identified one patient with low-titer positive antinuclear antibodies and another with elevated gastrin-17 levels. Treatment consisted of iron supplementation in all cases, combined with gastric mucosal protectants in three patients and glucocorticoid therapy in one patient. Follow-up of three patients showed clinical improvement with resolution of anemia, and two also demonstrated histological improvement with reduced gastric inflammation and collagen deposition. Pediatric CG is characterized primarily by iron-deficiency anemia and nodular gastric mucosal changes, accompanied by duodenal involvement in some patients. These findings underline the importance of a comprehensive evaluation of the entire gastrointestinal tract. Diagnosis relies on distinct endoscopic and pathological features, while attention should also be paid to potential biomarkers. A combined treatment approach, including iron supplementation, mucosal protection, and glucocorticoids when necessary, may lead to clinical and histological remission.

Immune checkpoint inhibitors (ICIs) have transformed the treatment landscape across multiple malignancies. However, their expanding use has been accompanied by an increasing spectrum of immune-related adverse events (irAEs), particularly those affecting the gastrointestinal (GI) tract. GI toxicities may involve both the upper and lower GI tract and range from mild, nonspecific symptoms to severe inflammatory complications requiring treatment interruption, hospitalization, or selective immunosuppressive therapy. This review summarizes the current evidence regarding the pathogenesis, clinical presentation, endoscopic and histopathologic findings, and management of GI irAEs associated with ICIs. Upper GI involvement, including esophagitis, gastritis, and duodenitis, is relatively uncommon and typically presents with nonspecific symptoms and heterogeneous endoscopic findings, which may occur despite a macroscopically normal-appearing mucosa. Lower GI toxicity, particularly diarrhea and colitis, is more common and clinically significant, especially in patients receiving anti-CTLA-4-based and combination regimens. Endoscopic evaluation with mucosal biopsy remains central to diagnosis because clinical severity does not always correlate with endoscopic or histopathologic activity. Histopathologic patterns are heterogeneous and may overlap with those of other inflammatory or infectious GI disorders, making clinicopathologic correlation essential. Current management is largely guided by expert consensus and includes supportive care, corticosteroids, and biologic rescue therapy with agents such as infliximab or vedolizumab for steroid-refractory disease. Early recognition, appropriate grading, exclusion of alternative etiologies, and multidisciplinary collaboration among oncologists and gastroenterologists are critical to optimize outcomes while preserving the benefits of cancer immunotherapy.

Pernicious anemia (PA) is an autoimmune cause of vitamin B12 deficiency, often secondary to chronic atrophic gastritis, which increases the risk of gastric malignancies. Early signs, like mild macrocytosis, are frequently overlooked, especially in patients with other risk factors such as long-term metformin use. We present a case illustrating the full clinical trajectory from long-standing, unexplored macrocytosis to severe anemia, ultimately leading to the diagnosis of PA and detection of early-stage gastric adenocarcinoma on surveillance esophagogastroduodenoscopy (EGD). Informed consent was obtained from the patient to publish the case. The patient was a 59-year-old man with type 2 diabetes, treated with metformin 2 g daily for over four years, who presented with severe symptomatic macrocytic anemia after approximately one year of unexplored macrocytosis on routine laboratory testing. Evaluation revealed profound vitamin B12 deficiency with evidence of hemolysis, and serologic testing confirmed PA. Surveillance EGD identified a gastric polyp, which was resected for histopathologic evaluation. Examination of the lesion revealed a moderately differentiated adenocarcinoma with associated high-grade dysplasia and submucosal invasion. Random gastric biopsies demonstrated chronic inflammation with focal atypia and were negative for Helicobacter pylori. Subsequent staging investigations confirmed stage I disease (cT1b, cN0, and cM0). The patient underwent partial gastrectomy and continued intramuscular vitamin B12 therapy, with excellent clinical recovery and no evidence of recurrent disease on follow-up. Our case highlights that persistent macrocytosis should not be overlooked, particularly in patients with risk factors for vitamin B12 deficiency such as long-term metformin use. Early evaluation may uncover important underlying diagnoses such as PA, prevent severe hematologic complications, and facilitate detection of associated gastric malignancies at a potentially curable stage.

Gastric ectopic pancreas is an uncommon congenital anomaly that is usually asymptomatic but can mimic gastric malignancy when inflamed. We report the case of a 33-year-old previously healthy woman who presented with acute severe epigastric pain and inability to tolerate oral intake. Endoscopy demonstrated annular thickening of the gastric antrum, congested and friable mucosa, and poor gastric distensibility. Contrast-enhanced computed tomography demonstrated irregular circumferential antral wall thickening with an enhancing endoluminal mass, perigastric lymphadenopathy, and minimal free intraperitoneal fluid, raising a strong suspicion for gastric malignancy. Fibroblast activation protein inhibitor positron emission tomography demonstrated a tracer-avid gastric antral lesion. Endoscopic ultrasound showed a large hypoechoic mural lesion with loss of normal wall-layer architecture and perigastric lymph nodes. Conventional biopsy showed Helicobacter pylori-associated chronic gastritis without malignancy, while endoscopic ultrasound-guided sampling revealed spindle cells with eosinophilic inflammatory infiltrate and only mild cytological atypia. Immunohistochemistry helped exclude gastrointestinal stromal tumour, schwannoma, carcinoma, and inflammatory myofibroblastic tumour. Following H. pylori eradication therapy and conservative management, symptoms resolved completely. Repeat endoscopy at three months demonstrated resolution of antral thickening and a residual centrally umbilicated subepithelial lesion, supporting the presumed inflamed gastric ectopic pancreas. This case highlights that fibroblast activation protein inhibitor avidity should be interpreted as a marker of fibroblast activation rather than proof of malignancy and that interval reassessment can prevent unnecessary radical surgery in clinically stable patients with discordant imaging and histology.