A Case Report of Pancreatic Acinar Metaplasia of the Distal Esophagus Mimicking Barrett’s Esophagus: A Diagnostic Pitfall

Abstract

Background:

Pancreatic acinar metaplasia (PAM) is defined as the presence of islands of exocrine pancreatic glands in areas outside of the pancreas. It is most commonly detected incidentally within the upper gastrointestinal tract. Histologically, PAM typically contains lobular or nested aggregates of epithelial cells with basal nuclei and abundant cytoplasm, which is acidophilic and finely granular in the apical and middle portion and basophilic in the basal compartment, closely resembling pancreatic acinar cells.

Case Presentation:

We report a rare case of PAM located at the gastroesophageal junction (GEJ). Endoscopic examination revealed a lesion mimicking Barrett’s esophagus. Histopathological analysis demonstrated a focus of pancreatic acinar metaplasia comprised of acinar-like cells, located at the squamocolumnar junction of esophagus, consistent with PAM.

Conclusion:

PAM of the esophagus is an exceptionally rare entity that may mimic other esophageal conditions on endoscopic evaluation. Accurate diagnosis relies on histopathological assessment, which is essential for differentiating this uncommon lesion from more prevalent esophageal pathologies.

Learning points

• Pancreatic acinar metaplasia of the gastroesophageal junction is an uncommon histological finding that can endoscopically mimic Barrett’s esophagus.

• Definitive diagnosis of Barrett’s esophagus requires histopathological confirmation of intestinal metaplasia, highlighting the importance of systematic biopsy sampling during endoscopy.

• Recognition of pancreatic acinar metaplasia is important to avoid misdiagnosis and unnecessary long-term surveillance or treatment for Barrett’s esophagus.

Introduction

Pancreatic acinar metaplasia (PAM) refers to the occurrence of clusters of exocrine pancreatic tissue located outside the pancreas. It is most frequently observed in the gastric antrum, though it may develop anywhere along the gastrointestinal tract, including the gastroesophageal junction (GEJ). ¹ When present at the GEJ, it can complicate diagnosis, particularly because it may coexist with Barrett’s esophagus. The endoscopic features of pancreatic metaplasia in the GEJ and distal esophagus remain poorly characterized, and its clinical significance in this region is not fully understood. ²

We herein report a case of PAM at the level of the GEJ disguised as Barrett’s esophagus.

Case Report

A 56-year-old woman with no history of tobacco or alcohol use presented with epigastric pain refractory to proton pump inhibitor (PPI) therapy. She denied the use of nonsteroidal anti-inflammatory drugs (NSAIDs), and her family history was negative for gastric or esophageal malignancy.

Esophagogastroduodenoscopy revealed salmon-colored mucosal changes in the distal esophagus suggestive of Barrett’s esophagus (Figure 1). Targeted biopsies were obtained for histopathological evaluation. Pending histological confirmation, the patient was initiated on a full-dose PPI regimen for 4 weeks along with sodium alginate, with plans to continue therapy on an as-needed basis should Barrett’s esophagus not be confirmed.

Figure 1.

Endoscopic view of the distal esophagus showing salmon-colored mucosa suspicious for Barrett’s esophagus (white arrow).

Histopathological examination of the biopsy specimens demonstrated clusters of pancreatic-type acinar cells within the lamina propria consistent with pancreatic acinar metaplasia. No intestinal metaplasia was identified, excluding a diagnosis of Barrett’s esophagus. Furthermore, there was no evidence of epithelial dysplasia or malignancy.

Pancreatic acinar metaplasia of the distal esophagus is a rare histological finding that may endoscopically mimic Barrett’s esophagus, underscoring the importance of histopathological confirmation before establishing the diagnosis.

Furthermore, gastric biopsies were positive for Helicobater pylori prompting bismuth-containing quadruple therapy for H. pylori eradication for a duration of 10 days. The patient reported complete resolution of her symptoms upon follow up, incriminating H. pylori as the causal agent for her symptoms and the GEJ lesion was an incidental histologic explanation for an endoscopic abnormality (Figure 2).

Figure 2.

HES stain of specimens from the cardia of the esophagus (A), where a gastric-type glandular epithelial lining with a closed mucosal pole (B) is observed alongside a non-keratinizing squamous epithelium (C), in which a tubulo-glandular islet showing pancreatic metaplasia is identified, without associated intestinal metaplasia (no goblet cells). Indeed, this islet (B and D) resembles an exocrine pancreatic acinus, with the presence of ducts lined by simple columnar epithelium associated with glands whose cells have cytoplasm containing red secretory granules at their apical pole and a more basophilic basal appearance. If an immunohistochemical study were conducted (not performed here as it is not essential), these cells would be positive for lipase, trypsinogen, and amylase. (A) (×12), (B and C) (×10), (D) (×40). Histologic findings reveal clusters of pancreatic-type acinar cells within the lamina propria consistent with acinar metaplasia. No intestinal metaplasia was identified, excluding a diagnosis of Barrett’s esophagus. Furthermore, there was no evidence of epithelial dysplasia or malignancy.

Discussion

Pancreatic acinar metaplasia (PAM) refers to the presence of pancreatic-type glandular tissue arranged in small clusters or nests located outside the pancreas. This entity is most frequently identified in the gastric antrum, although it has also been observed in other regions of the gastrointestinal tract, including the gastroesophageal junction (GEJ). ¹ The endoscopic appearance of PAM can vary considerably; however, some studies have reported that it most commonly presents as areas of salmon-colored mucosa, which may resemble Barrett’s esophagus and thus require careful evaluation. ²

Definitive diagnosis of PAM relies on histological examination. Microscopically, the lesion is characterized by cells that resemble pancreatic acinar cells, displaying abundant cytoplasm with distinct staining patterns—specifically, eosinophilic (pink-staining) apical regions and basophilic (blue-staining) basal portions. These features help distinguish PAM from other types of metaplastic or neoplastic changes within the gastrointestinal mucosa. ³

The underlying pathogenesis of PAM remains unclear. Some studies have suggested a potential association with chronic use of medications such as nonsteroidal anti-inflammatory drugs (NSAIDs) raising the possibility that long-term mucosal irritation or chemical exposure may contribute to its formation.^4,5

Recent literature has provided additional insight into the clinical significance of PAM, particularly at the gastroesophageal junction. A study by Andersen et al examined PAM in the context of gastroesophageal reflux disease and its relationship to intestinal metaplasia. The authors found that PAM and intestinal metaplasia rarely coexist and that patients with PAM were significantly less likely to demonstrate intestinal metaplasia on biopsy. ⁶ This aligns with our case report findings whereby histologic results revealed pancreatic acinar metaplasia without intestinal metaplasia, excluding a diagnosis of Barrett’s esophagus.

Similarly, case reports described by Varda et al have documented PAM identified incidentally during endoscopic evaluation in a female patient being investigated for reflux symptoms. This report consistently describes benign histologic features without evidence of dysplasia or malignant transformation, reinforcing the notion that PAM is typically a non-neoplastic entity. Varda and colleagues also emphasized the importance of clinical correlation and appropriate surveillance strategies. ⁷

PAM has also been identified in patients with Barrett’s esophagus and may show an association with Helicobacter pylori infection, suggesting that it could coexist with or arise in the context of other gastrointestinal pathologies as was exemplified in our case report.

Given these potential associations, it is important for patients diagnosed with PAM to undergo regular clinical and endoscopic surveillance. Continued research is essential to better understand the etiology, clinical significance, and long-term implications of this condition, as well as to clarify whether it represents a benign incidental finding or a marker of underlying gastrointestinal disease.

The histological examination in our case has found clusters of pancreatic-type acinar cells within the lamina propria consistent with PAM. No intestinal metaplasia was identified, excluding the diagnosis of Barrett’s esophagus. Furthermore, there was no evidence of epithelial dysplasia or malignancy.

This case report explicitly highlights that Barrett’s is an endoscopic-histologic diagnosis, that salmon-colored mucosa alone is insufficient, and that systematic biopsies prevented an incorrect surveillance label in our case report.

In summary, PAM is an uncommon finding that can occur at various sites throughout the gastrointestinal tract. PAM of the distal esophagus is a rare histological finding that may endoscopically mimic Barrett’s esophagus, underscoring the importance of histopathological confirmation before establishing the diagnosis.

This case report presents several limitations that warrant consideration. Foremost, as an observation derived from a single patient, its findings are inherently limited in scope and lack external validity, precluding any generalization to wider populations or inference of causality. Moreover, the absence of longitudinal follow-up restricts the ability to assess the natural history, clinical evolution, and potential long-term implications of pancreatic acinar metaplasia at the gastroesophageal junction. Although the histopathological evaluation was sufficient to establish the diagnosis, the lack of adjunctive immunohistochemical analysis may be viewed as a limitation, as such techniques could have provided additional confirmatory and phenotypic detail. The concomitant presence of Helicobacter pylori infection further introduces a potential confounding factor, rendering any putative association with pancreatic acinar metaplasia speculative. Finally, in light of the rarity of this entity and the paucity of data in the existing literature, definitive conclusions regarding its clinical significance, pathogenesis, and optimal management strategies remain to be established.