A 93-year-old male presented with unspecific abdominal discomfort. Upon upper endoscopy, the cardiac mucosa appeared polypoid and irregular. Multiple biopsies were taken.
Histologically, the background mucosa revealed a chronic-atrophic gastritis with intestinal metaplasia (Panel A). The surface epithelium demonstrated a gastric foveolar phenotype with pale eosinophilic cytoplasm. The nuclei were oval, enlarged, but only slightly irregular. The chromatin content was increased and nuclear polarisation retained, respectively. Mitoses were inconspicuous (Panels A-D).
Immunohistochemistry confirmed the gastric foveolar phenotype, with positivity for MUC5AC (Panel E), MUC6 (Panel F) and negativity for MUC2 (Panel G). The Ki67 labelling index was 35% (Panel H).
The “intestinal” type of gastric carcinomas usually develops via an atrophy-metaplasia-dysplasia-carcinoma sequence. Traditionally, the gastric dysplasia occurring against a background of intestinal metaplasia shows an intestinal phenotype that recapitulates the morphology of colonic adenomas (MUC2 positive, MUC5AC and MUC6 negative). The same phenotype dominates the picture in Barrett’s dysplasia.
In recent years, several types of non-intestinal, that is, non-adenomatous dysplasia have been recognized. Of these, gastric foveolar dysplasia, as illustrated in our case, is the most frequent. It may be encountered within the stomach and at the gastro-esophageal junction, that is, in Barrett’s oesophagus. Gastric foveolar dysplasia is characterized by low columnar cells with clear / light eosinophilic cytoplasm (due to apical neutral mucin) and oval to round, often only slightly irregular nuclei.
It is of note that gastric foveolar dysplasia, even when appearing low grade, may give rise to very well differentiated adenocarcinomas. Therefore, the biopsy material needs to be examined thoroughly, e.g., by cutting multiple levels, not to overlook invasion. The inter-observer agreement in separating low-grade foveolar dysplasia from reactive gastric mucosa and low-grade adenomatous dysplasia appears to be poor. Greater awareness and agreed criteria are needed to prevent misdiagnosis of low-grade foveolar dysplasia as reactive, and vice versa.
Endoscopic removal of the dysplastic lesion by endoscopic mucosal resection (EMR) or endoscopic submucosal dissections (ESD) is the treatment of choice.
