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

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.