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DEN Open· 2026Q2

Reconsidering the Mechanism of Proton Pump Inhibitor‐Associated Fundic Gland Polyps: Absence of Re‐enlargement during Potassium‐Competitive Acid Blocker Therapy

Yoshitsugu Misumi, Tatsuyuki Marumo, Shinichi Ban, Kouichi Nonaka

Short summary

Fundic gland polyps (FGPs) that enlarged on PPIs did not re-enlarge during long-term potassium-competitive acid blocker (PCAB) therapy, even with significantly elevated gastrin levels (up to 753.7 pg/mL).

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Key points

  • FGPs enlarged during 7 years of PPI therapy in a patient with GERD.
  • FGPs markedly regressed within 4 months of switching to PCAB therapy.
  • No re-enlargement of FGPs was observed during continued PCAB therapy.
  • Serum gastrin levels remained elevated (491.9 and 753.7 pg/mL) during PCAB use.

AI-generated from the title and abstract; the full text is not read.

Abstract

ABSTRACT Fundic gland polyps (FGPs) may enlarge during long‐term proton pump inhibitor (PPI) therapy, potentially in association with acid suppression and hypergastrinemia. Potassium‐competitive acid blockers (PCABs) provide potent and sustained acid suppression and may induce comparable or greater elevations in serum gastrin levels than PPIs. We report a case of FGPs in which regression was documented after changes in acid‐suppressive therapy, with no subsequent re‐enlargement during long‐term use of PCABs. A woman in her 60s with gastroesophageal reflux disease developed progressive enlargement of FGPs during 7 years of rabeprazole therapy. Rabeprazole was discontinued because of marked redness of the enlarged FGPs and concern for possible bleeding and was replaced with an H2‐receptor antagonist. After reintroduction of rabeprazole, treatment was switched to a PCAB because of insufficient symptom control. Four months after PCAB initiation, esophagogastroduodenoscopy demonstrated marked regression of the FGPs, with no subsequent re‐enlargement during continued PCAB therapy. Serum gastrin levels were elevated at both measurements during PCAB use (491.9 and 753.7 pg/mL). Histological examination revealed similar fundic gland changes characteristic of FGPs in both a residual polyp and the endoscopically non‐polypoid background mucosa, without dysplasia. Because the exact timing of FGP regression could not be determined, the regression observed 4 months after vonoprazan initiation cannot be solely attributed to vonoprazan therapy and may have occurred, at least in part, during the preceding period of PPI discontinuation. Nevertheless, no subsequent re‐enlargement was observed during long‐term vonoprazan therapy. Clinical Trial Registration: Clinical trial registration was not applicable because this was a single case report.

The authors' abstract, as published at the source. DEN Open, 2026 · DOI ↗

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Field: Gastroenterology

GastroenterologyMedicine