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<p>The relationship between autoimmune gastritis (AIG) and <i>Helicobacter pylori</i> (<i>H. pylori</i>) gastritis remains unclear, particularly whether there is any interaction. Herein, we report a case of early-stage AIG diagnosed in an elderly patient with highly active <i>H. pylori</i> gastritis, who subsequently underwent eradication therapy. We were able to follow the changes in these two types of gastritis immediately before and after eradication therapy, through observation over a period of 5&#xa0;years and 5&#xa0;months. Despite the previous state of predominant <i>H. pylori</i> gastritis, eradication therapy led to rapid exacerbation of atrophic changes, which was especially evident in endoscopic findings. In addition, the anti-parietal cell antibody titer increased constantly from 1:320 to 1:1280. We concluded that AIG activity was enhanced compared to that before eradication therapy. This course suggests the following two possibilities: early-stage AIG may have progressed steadily regardless of <i>H. pylori</i> gastritis status, or its activity may have been suppressed until the time of eradication therapy.</p>

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Enhanced activity of autoimmune gastritis following Helicobacter pylori eradication therapy

  • 期刊论文

  • 发表日期：

    2025年1月13日

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  • Takashi Ihara,
  • Ryoji Kushima,
  • Ken Haruma

摘要

The relationship between autoimmune gastritis (AIG) and Helicobacter pylori (H. pylori) gastritis remains unclear, particularly whether there is any interaction. Herein, we report a case of early-stage AIG diagnosed in an elderly patient with highly active H. pylori gastritis, who subsequently underwent eradication therapy. We were able to follow the changes in these two types of gastritis immediately before and after eradication therapy, through observation over a period of 5 years and 5 months. Despite the previous state of predominant H. pylori gastritis, eradication therapy led to rapid exacerbation of atrophic changes, which was especially evident in endoscopic findings. In addition, the anti-parietal cell antibody titer increased constantly from 1:320 to 1:1280. We concluded that AIG activity was enhanced compared to that before eradication therapy. This course suggests the following two possibilities: early-stage AIG may have progressed steadily regardless of H. pylori gastritis status, or its activity may have been suppressed until the time of eradication therapy.