Reconsidering the Mechanism of Proton Pump Inhibitor-Associated Fundic Gland Polyps: Absence of Re-enlargement during Potassium-Competitive Acid Blocker Therapy.
- 1Department of Digestive Endoscopy Tokyo Women's Medical University Hospital Tokyo Japan.
- 2Department of Gastroenterology Ina Hospital Saitama Japan.
- 3Department of Pathology Dokkyo Medical University Saitama Medical Center Saitama Japan.
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.
Related
- Acute Enlargement of a Frontal Calvarial Lesion in Polyostotic Fibrous Dysplasia Associated with McCune–Albright Syndrome: A Case Report
- Lipoprotein(a) Is Associated with Coronary Plaque Vulnerability and Compensatory Vascular Enlargement: An Intravascular Ultrasound Study
- Preoperative lymph-node enlargement is associated with favorable survival for patients with pathological stage II colorectal cancer
- Corticosteroid-refractory checkpoint inhibitor pneumonitis in lung cancer: biological heterogeneity and mechanism-informed management
- Role and mechanism of ribosomal protein S3 in tyrosine kinase inhibitor resistance in chronic myeloid leukemia
BibTeX
@article{misumi2026reconsidering,
title = {{Reconsidering the Mechanism of Proton Pump Inhibitor-Associated Fundic Gland Polyps: Absence of Re-enlargement during Potassium-Competitive Acid Blocker Therapy.}},
author = {Yoshitsugu Misumi and Tatsuyuki Marumo and Shinichi Ban and Kouichi Nonaka},
journal = {DEN open},
year = {2026},
month = nov,
doi = {10.1002/deo2.70463},
url = {https://europepmc.org/article/MED/42968916},
note = {CC BY},
}
RIS
TY - JOUR
TI - Reconsidering the Mechanism of Proton Pump Inhibitor-Associated Fundic Gland Polyps: Absence of Re-enlargement during Potassium-Competitive Acid Blocker Therapy.
AU - Yoshitsugu Misumi
AU - Tatsuyuki Marumo
AU - Shinichi Ban
AU - Kouichi Nonaka
PY - 2026
DA - 2026/11/01
JO - DEN open
DO - 10.1002/deo2.70463
UR - https://europepmc.org/article/MED/42968916
AB - 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.
SN - 2692-4609
ER -