Nicole Vienneau

Thank you for your thoughtful and insightful commentary on our manuscript regarding autoimmune metaplastic atrophic gastritis (AMAG)

Balamuthia mandrillaris is a rare cause of cutaneous amebiasis that can progress to central nervous system infection, almost always resulting in death. It is a free‐living, opportunistic ameba found globally in dust, soil, and freshwater that can infect people of all ages regardless of the status of the host immune system. Herein, we report a case of B. mandrillaris infection in Canada in an 83‐year‐old man presenting to the hospital with altered mental status and a chronic wound of 4‐year duration. A skin biopsy of the chronic wound revealed extensive dermal granulomatous and mixed inflammatory infiltrate with abundant multinucleated giant cells. Inspection of multiple level sections revealed structures concerning for amebic trophozoites. After the patient's death, lesional tissue from the skin and brain was sent to the Centers for Disease Control (CDC) for further subtyping, which confirmed B. mandrillaris as the causative organism. This case raises awareness for this organism as a possible cause of cutaneous infections and highlights the necessity for dermatopathologists and pathologists alike to have a heightened suspicion for amebic infections when non‐specific granulomatous inflammation is identified in the skin.

Background/Objectives : Autoimmune metaplastic atrophic gastritis (AMAG) is a chronic, autoimmune-mediated condition associated with increased risk of malignancy and nutritional deficiencies, yet diagnostic and follow-up processes remain inconsistent and unclear. This study investigates follow-up testing performance in patients with AMAG and neuroendocrine tumors (NET), as well as the correlation between endoscopic impressions and histologic findings. Methods: We retrospectively analyzed 65 gastric biopsies with final diagnoses or comments mentioning the possibility of AMAG, 12 of which included well-differentiated WHO grade 1 NET arising in AMAG. H&E slides were reviewed to assess atrophy severity, the presence or absence of enterochromaffin-like (ECL) cell hyperplasia, and Helicobacter organisms. The final diagnostic line or comments made were scored from 1 to 5, based on the strength of the language used to alert the treating clinician to the likelihood of AMAG. Corresponding endoscopy reports were scored from 1 to 5 based on the likelihood of the reports documenting AMAG features. Data regarding follow-up laboratory testing relevant to AMAG and biopsy performance were collected from the electronic medical records. Results: Endoscopy scores showed no significant associations with the histology comment score or atrophy grade. The histology comment score was positively associated with performing at least a total of three laboratory tests (p = 0.03). No association was found between the presence or absence of follow-up biopsy and histology comment score (p = 0.60). Follow-up biopsy was more common in patients with NET than those with AMAG without NET (p < 0.001). Conclusions: Poor endoscopic–histologic correlation with variable follow-up practices highlights the need for standardized protocols in AMAG management. Enhanced adherence to biopsy guidelines, standardized pathology reporting, and consistent surveillance, particularly for patients with AMAG without NET, are imperative to improve diagnosis and outcomes. Future research should focus on optimizing endoscopic techniques, standardizing serological tests, and establishing evidence-based surveillance protocols for AMAG patients.