C A Rubio1. 1. Gastrointestinal and Liver Pathology Research Laboratory, Karolinska Institute and Hospital, 171 76 Stockholm, Sweden. Carlos.Rubio@onkpat.ki.se
Abstract
AIMS: The diagnosis of duodenal gastric metaplasia (DGM) is based on the demonstration of periodic acid Schiff (PAS) positive mucin in duodenal columnar cells. Recently, groups of duodenal columnar cells were seen to be autofluorescent in haematoxylin and eosin (H&E) stained sections from a patient with DGM. MATERIALS AND METHODS: Consecutive archival gastric and duodenal H&E sections from 30 patients with chronic gastritis and DGM (CG+DGM), from 30 with chronic gastritis without DGM (control group I), from 30 with normal gastric and duodenal mucosa (control group II), and from five patients with coeliac disease (control group III) were reviewed on a fluorescent microscope. RESULTS: The surface epithelium of the gastric mucosa in all 95 cases had autofluorescent material. In 31 cases with DGM (including one unreported case in control group I), groups of columnar duodenal cells also had autofluorescent material. In the remaining 64 cases, duodenal columnar cells were not autofluorescent. Results were confirmed with the PAS stain. CONCLUSIONS: The method described detected apical mucin secretion in columnar cells, both in the stomach and in the duodenum from patients with DGM. The autofluorescence was induced by eosin (which binds to neutral mucin). Observing H&E stained duodenal biopsies under a fluorescence microscope may be sufficient to confirm DGM or to detect incipient DGM. Despite long observation periods and a long exposure time while photographing, the autofluorescence did not fade away. Because re-cuttings for special staining (PAS) are no longer required when this method is used, both final diagnosing time and laboratory costs can be reduced.
AIMS: The diagnosis of duodenal gastric metaplasia (DGM) is based on the demonstration of periodic acid Schiff (PAS) positive mucin in duodenal columnar cells. Recently, groups of duodenal columnar cells were seen to be autofluorescent in haematoxylin and eosin (H&E) stained sections from a patient with DGM. MATERIALS AND METHODS: Consecutive archival gastric and duodenal H&E sections from 30 patients with chronic gastritis and DGM (CG+DGM), from 30 with chronic gastritis without DGM (control group I), from 30 with normal gastric and duodenal mucosa (control group II), and from five patients with coeliac disease (control group III) were reviewed on a fluorescent microscope. RESULTS: The surface epithelium of the gastric mucosa in all 95 cases had autofluorescent material. In 31 cases with DGM (including one unreported case in control group I), groups of columnar duodenal cells also had autofluorescent material. In the remaining 64 cases, duodenal columnar cells were not autofluorescent. Results were confirmed with the PAS stain. CONCLUSIONS: The method described detected apical mucin secretion in columnar cells, both in the stomach and in the duodenum from patients with DGM. The autofluorescence was induced by eosin (which binds to neutral mucin). Observing H&E stained duodenal biopsies under a fluorescence microscope may be sufficient to confirm DGM or to detect incipient DGM. Despite long observation periods and a long exposure time while photographing, the autofluorescence did not fade away. Because re-cuttings for special staining (PAS) are no longer required when this method is used, both final diagnosing time and laboratory costs can be reduced.