S3707 Pancreatic Acinar Metaplasia at the Gastroesophageal Junction in a Patient With Chronic Reflux

Abstract

Introduction: Pancreatic acinar metaplasia (PAM) is defined as pancreatic glandular tissue forming acini outside of the pancreas. Recent studies have shown a possible association between chronic use of proton pump inhibitors (PPIs) and nonsteroidal anti-inflammatory drugs (NSAIDs). Here, we present a case of PAM in a patient with chronic reflux on PPIs without a history of NSAID use. Case Description/Methods: A 41-year-old female with a longstanding history of gastroesophageal reflux disease (GERD) presented to clinic for evaluation of chronic reflux. The patient reported having symptoms of reflux for over 20 years. Over this time, she trialed multiple medications such as PPIs and antacids, but denied the use of NSAIDs. She also underwent multiple esophagogastroduodenoscopies (EGDs) for evaluation of her reflux, the last being 5 years ago, which showed mild gastric erythema but was otherwise unremarkable. Due to persistent symptoms despite medical management, she was scheduled for repeat EGD. EGD showed salmon-colored mucosa and gastric erythema. Pathology from esophagus biopsies revealed junctional mucosa with focal pancreatic acinar metaplasia (PAM). The patient was transitioned to Dexlansoprazole for symptomatic management and was scheduled for repeat EGD in 1 year for surveillance of PAM. Discussion: Pancreatic acinar metaplasia (PAM) is a term used to describe pancreatic glandular tissue organized in nests found outside of the pancreas. It is most commonly found in the gastric antrum, but can be found elsewhere in the gastrointestinal tract such as at the gastroesophageal junction (GEJ). While endoscopic findings of PAM differ, one study showed that the most commonly found appearance is salmon-colored mucosa. PAM is diagnosed histologically by pancreatic acinar-like cells that have a prominent cytoplasm with eosinophilic apical areas and basophilic basal areas. The exact pathogenesis of PAM is unknown; studies have shown that PAM may be associated with chronic NSAID or PPI use. While our patient used PPIs for years, she denies a history of NSAID usage. Another study by Schneider et al. showed that there was no association between PAM and reflux or gastritis, suggesting that PAM be have a congenital component. Further research is needed to determine the etiology of PAM. It can be found in patients with Barrett’s esophagus and may be associated with Helicobacter pylori. Therefore, it is important that these patients undergo routine surveillance.