D Popiolek1, E Kahn, J Markowitz, F Daum. 1. Department of Laboratories, North Shore University Hospital, New York University School of Medicine, Manhasset 11030, USA.
Abstract
BACKGROUND: 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. OBJECTIVE: To clarify the origin of PAT at the GEJ. METHODS: 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. RESULTS: 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. CONCLUSIONS: Our data suggest that PAT at the GEJ develops independently of inflammation and is, therefore, likely to be congenital.
BACKGROUND: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. OBJECTIVE: To clarify the origin of PAT at the GEJ. METHODS: 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. RESULTS: 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. CONCLUSIONS: Our data suggest that PAT at the GEJ develops independently of inflammation and is, therefore, likely to be congenital.