Pancreatic acinar tissue (PAT) at the gastroesophageal junction (GEJ) has been reported in 3% of adults with Barrett esophagus (BE) and in 24% of healthy subjects. The pathogenesis of this ectopic tissue is controversial. Both an acquired metaplastic process in the setting of BE and a congenital abnormality have been suggested in adults.
To clarify the origin of PAT at the GEJ.
We reviewed material obtained from the GEJ in 69 children and young adults. Each specimen was evaluated by 3 levels stained with hematoxylin-eosin for the presence of PAT, BE, esophagitis, and gastritis. Selected cases were also examined with immunohistochemical stains for lipase, trypsin, and amylase.
In 16% of the study population, PAT was present at the GEJ and was not associated with BE. The prevalence of esophagitis and/or gastritis did not vary significantly between patients with and without PAT.
Our data suggest that PAT at the GEJ develops independently of inflammation and is, therefore, likely to be congenital.