S2948 Long-Term Proton Pump Inhibitor-Induced Gastric Microcystic Glandular Changes Leading to Gastric Wall Thickening

Abstract

INTRODUCTION: Long term (LT) proton pump inhibitor (PPI) induced gastric microcystic glandular mucosal changes could lead to significant gastric wall thickening which must be further evaluated to exclude underlying neoplastic process. CASE DESCRIPTION/METHODS: An 81-year-old male with GERD and Barrett’s esophagus (BE) on chronic omeprazole 40mg BID was evaluated by endoscopic ultrasound (EUS) for 1cm gastroesophageal junction (GEJ) sub epithelial lesion (SEL) seen on EGD and thickened gastric mucosa (2.6 cm) normalizing just proximal to GEJ identified on an otherwise negative CT abdomen done to evaluate for epigastric pain. EGD showed irregular carpet-like thickened gastric folds with cobble stoning sparing the gastric antrum. EUS showed a small cystic SEL at GEJ and marked diffuse thickening of gastric body mucosa (16 mm) with intact muscularis propria and absence of regional lymphadenopathy. Endoscopic biopsies revealed no H. pylori but gastric mucosa with microcystic glandular changes consistent with gastric mucosal trophic changes secondary to chronic PPI use. Due to BE however, patient was continued on PPI. DISCUSSION: PPIs remain the cornerstone for GERD treatment. Adverse effects from inappropriate PPI use are more clinically manifested in the elderly population. These include drug-drug interactions and increased risk of LT PPI adverse effects on digestive and extra-digestive organs (such as dementia, decreased bone density, and community acquired pneumonia). LT PPI use can lead to fundic gland polyp formation, small intestinal bacterial overgrowth, and collagenous colitis. Gastric trophic changes were found to occur secondary to LT PPI use in the form of parietal cell protrusion into the gastric lumen and fundic gland polyp formation resulting from increased serum gastrin level. Hypertrophic changes due to LT PPI induce gastric mucosal changes that can be appreciated endoscopically as gastric cobblestone-like lesions (GCLL). Sparing of the antrum in our patient of such changes can be explained by parietal cells being anatomically present in gastric fundic glands located primarily in the gastric fundus and body. Histopathology of gastric biopsies in these cases show fundic microcystic glandular change, parietal cell hyperplasia, and cytoplasmic vacuolation. A gastroenterologist should be familiar with such changes due to LT PPI use and, yet, must biopsy the gastric mucosa to exclude any underlying gastric infiltrative and neoplastic process.Figure 1.: Endoscopic view of gastric corpus showing thickened folds, carpet like polypoid lesions.Figure 2.: Radial EUS showing markedly thickened gastric mucosa and intact muscularis propria.Figure 3.: Histopathology of gastric corpus biopsies showing microcystic glandular conformation.