Reply: Comments by Professor Xiaoran Sun on “Endoscopic Features of Background Gastritis Associated With Remnant Gastric Cancer: A Multicenter Retrospective Study”

To the Editor:

We sincerely thank the authors for their thoughtful and constructive comments regarding our study on the endoscopic findings associated with remnant gastric cancer (RGC) surveillance [1,2].

First, regarding the diagnosis of Helicobacter pylori infection, the retrospective multicenter nature of our study made it difficult to collect standardized objective data, such as histopathological findings or urea breath test results, for all patients. Therefore, we performed endoscopic assessment based on the Kyoto classification, which is widely used in routine clinical practice.

As appropriately pointed out, mucosal findings in the remnant stomach may be modified by bile reflux and postoperative anatomical alterations, and the diagnostic accuracy of the Kyoto classification in this setting may not be equivalent to that in the non-operated stomach. We acknowledge this as an important limitation of our study.

However, the primary objective of our study was not to establish a definitive diagnosis of H. pylori infection, but instead to evaluate the association between background mucosal findings and RGC development in the remnant stomach. Accordingly, we interpreted the Kyoto classification-based findings not as a direct surrogate for infection status but as endoscopic phenotypes reflecting the background mucosal environment.

Future prospective studies incorporating urea breath testing, serological assays, and histopathological evaluation are required to further validate the applicability of the Kyoto classification in the remnant stomach and to clarify the relationship between H. pylori status, eradication history, and endoscopic findings.

We appreciate your valuable comments regarding the reconstruction method. In our cohort, patients who underwent Roux-en-Y reconstruction tended to exhibit fewer endoscopic features, such as anastomotic redness, indicating an association between reduced bile reflux and remnant gastritis.

Simultaneously, the proposed scoring system was designed primarily to exploratorily identify endoscopic features associated with RGC risk. Notably, detailed stratification based on the reconstruction method was beyond the scope of the current analysis. As suggested by the authors, incorporating the reconstruction method as a modifying factor may improve individualized risk stratification, and should be addressed in future studies.

Finally, we agree that the timing of H. pylori eradication may significantly influence the carcinogenic risk, particularly before advanced atrophic changes have been established. Unfortunately, detailed information regarding the eradication timing and treatment success was not available for the present retrospective cohort. Future time-to-event analyses incorporating eradication history, timing of eradication, and eradication success may provide further insights into the relationships among atrophic changes, disappearance of the regular arrangement of collecting venules, and subsequent RGC development.

We sincerely appreciate the authors’ insightful comments and valuable suggestions, which will contribute to the further refinement of clinically applicable risk stratification models for RGC.