S6284 Gastric Mucosal Hyperplasia in the Setting of Long-Term Proton Pump Inhibitor Use Mimicking Submucosal Tumor

Introduction: Long-term proton pump inhibitor (PPI) use has been known to cause various changes in the gastric mucosa, including hypertrophy. The mechanism of these changes is not fully understood; however, they are mostly considered benign. Here we present a case in which a patient with long-term PPI use was found to have thickened gastric mucosa resembling a submucosal tumor. Case Description/Methods: A 72-year-old man with history of long segment non-dysplastic Barrett’s esophagus (BE) and long-term PPI use (>15 years) presented with a 2-week history of nausea, vomiting, abdominal pain, and diarrhea. He had surveillance esophagogastroduodenoscopy (EGD) 4 years ago which showed BE without dysplasia. Computed tomography (CT) showed mass-like thickening of the fundus of the stomach with a hypertrophied blood vessel. EGD revealed C2M4 non-dysplastic BE, a 3 cm hiatal hernia, and a submucosal mass in the fundus. Follow up endoscopic ultrasound (EUS) showed a dilated mucosa up to 20 mm, but no vascular abnormality and no submucosal or muscularis propria abnormality. Biopsy revealed benign gastric tissue with negative immunohistochemical stain for Helicobacter pylori. A diagnosis of Menetrier’s disease was considered. Therefore, a repeat EGD was performed and 2 large pieces of the lesion were removed via endoscopic mucosal resection. Pathology revealed benign oxyntic gastric mucosa with gland hyperplasia, which seems to suggest long-term PPI use as the cause. The patient finally underwent positron emission tomography-CT (PET-CT) 1 month later which revealed no worrisome hypermetabolic activity within the thickened folds at the gastric fundus or in the rest of the stomach. No hypermetabolic foci concerning for malignancy were found throughout the remainder of the body either. His symptoms eventually subsided. Discussion: The patient’s chief complaint along with the CT findings lead to multiple EGD and EUS evaluations of the ultimately benign gastric mucosal hypertrophy, followed by a normal PET-CT. It was this unique combination of factors that resulted in such a thorough workup, and it underscores the latent effects of PPIs, a class of medications that are so commonly used.

Publication Details

Journal
The American Journal of Gastroenterology
Published
2025-10-01
DOI
https://doi.org/10.14309/01.ajg.0001153596.85760.d9
Primary Topic
Esophageal Cancer Research and Treatment
Type
article
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article

S6284 Gastric Mucosal Hyperplasia in the Setting of Long-Term Proton Pump Inhibitor Use Mimicking Submucosal Tumor

The American Journal of Gastroenterology
Esophageal Cancer Research and Treatment
article

S6284 Gastric Mucosal Hyperplasia in the Setting of Long-Term Proton Pump Inhibitor Use Mimicking Submucosal Tumor

article en

Abstract

Introduction: Long-term proton pump inhibitor (PPI) use has been known to cause various changes in the gastric mucosa, including hypertrophy. The mechanism of these changes is not fully understood; however, they are mostly considered benign. Here we present a case in which a patient with long-term PPI use was found to have thickened gastric mucosa resembling a submucosal tumor. Case Description/Methods: A 72-year-old man with history of long segment non-dysplastic Barrett’s esophagus (BE) and long-term PPI use (>15 years) presented with a 2-week history of nausea, vomiting, abdominal pain, and diarrhea. He had surveillance esophagogastroduodenoscopy (EGD) 4 years ago which showed BE without dysplasia. Computed tomography (CT) showed mass-like thickening of the fundus of the stomach with a hypertrophied blood vessel. EGD revealed C2M4 non-dysplastic BE, a 3 cm hiatal hernia, and a submucosal mass in the fundus. Follow up endoscopic ultrasound (EUS) showed a dilated mucosa up to 20 mm, but no vascular abnormality and no submucosal or muscularis propria abnormality. Biopsy revealed benign gastric tissue with negative immunohistochemical stain for Helicobacter pylori. A diagnosis of Menetrier’s disease was considered. Therefore, a repeat EGD was performed and 2 large pieces of the lesion were removed via endoscopic mucosal resection. Pathology revealed benign oxyntic gastric mucosa with gland hyperplasia, which seems to suggest long-term PPI use as the cause. The patient finally underwent positron emission tomography-CT (PET-CT) 1 month later which revealed no worrisome hypermetabolic activity within the thickened folds at the gastric fundus or in the rest of the stomach. No hypermetabolic foci concerning for malignancy were found throughout the remainder of the body either. His symptoms eventually subsided. Discussion: The patient’s chief complaint along with the CT findings lead to multiple EGD and EUS evaluations of the ultimately benign gastric mucosal hypertrophy, followed by a normal PET-CT. It was this unique combination of factors that resulted in such a thorough workup, and it underscores the latent effects of PPIs, a class of medications that are so commonly used.

The American Journal of GastroenterologyVol. 120(10S2)
Good health and well-being
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Esophageal Cancer Research and Treatment
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S6284 Gastric Mucosal Hyperplasia in the Setting of Long-Term Proton Pump Inhibitor Use Mimicking Submucosal Tumor · The American Journal of Gastroenterology (2025) | TGRS Research Map | TGRS