World journal of gastrointestinal endoscopy · 2025
Gyrus-like endoscopic changes in autoimmune gastritis with past Helicobacter pylori infection: Two case reports and review of literature.
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Tan Chuan-Chuan, Shangguan Xue-Li, Lei Xiao-Ming, Deng Fang-Fang, Wu Yang-Peng, Zhang Guo-Min
Аннотация
BACKGROUND: Autoimmune gastritis (AIG) is recognized endoscopically by the presence of antrum-sparing corpus-dominant atrophy, known as reverse atrophy. However, a past Helicobacter pylori (H. pylori) infection can obscure this classic pattern. We present two cases of AIG with past H. pylori infection and highlight a novel endoscopic sign that may aid AIG recognition when typical features are absent.
CASE SUMMARY: One patient reported postprandial fullness, while the other was asymptomatic. Neither had a history of H. pylori eradication therapy. Both tested negative on a urea breath test and positive for anti-parietal cell antibodies. In both patients, endoscopy revealed mucosal atrophy involving both the corpus and antrum, which was counter to the characteristic reverse atrophy pattern typically seen in AIG. Beyond the atrophic border, we observed a distinct pattern of gyrus-like changes, manifesting as elevated mucosa between deep fissures. Histologically, targeted biopsies from these gyrus-like areas revealed parietal cell degeneration, lymphocytic infiltration, and hyperplasia of enterochromaffin-like cells, consistent with early histopathologic changes seen in AIG. These results supported diagnoses of AIG with past H. pylori infection.
CONCLUSION: Gyrus-like changes may serve as a novel endoscopic clue of AIG with past H. pylori infection.
CASE SUMMARY: One patient reported postprandial fullness, while the other was asymptomatic. Neither had a history of H. pylori eradication therapy. Both tested negative on a urea breath test and positive for anti-parietal cell antibodies. In both patients, endoscopy revealed mucosal atrophy involving both the corpus and antrum, which was counter to the characteristic reverse atrophy pattern typically seen in AIG. Beyond the atrophic border, we observed a distinct pattern of gyrus-like changes, manifesting as elevated mucosa between deep fissures. Histologically, targeted biopsies from these gyrus-like areas revealed parietal cell degeneration, lymphocytic infiltration, and hyperplasia of enterochromaffin-like cells, consistent with early histopathologic changes seen in AIG. These results supported diagnoses of AIG with past H. pylori infection.
CONCLUSION: Gyrus-like changes may serve as a novel endoscopic clue of AIG with past H. pylori infection.