Original Article Antralization of the Gastric Mucosa of the Incisura Angularis and its Gastrin Expression
Carlos A. Rubio, Edgar Jaramillo, Gaku Suzuki, Pernilla Lagergren and Gabriella Nesi
Departments of 1Pathology and Endoscopy, Karolinska University Hospital, Unit of Esophageal and Gastric Research (ESOGAR); Department of Molecular Medicine and Surgery, Karolinska Institute, Stockholm, Sweden and Department of Human Pathology and Oncology, University of Florence, Florence, Italy
Received 18 April 2008; Accepted in revision 7 May 2008; Available online 20 May 2008
Abstract: The frequency of antrum-type mucosa and gastrin expression in gastric biopsies from the incisura angularis was assessed in 60 consecutive patients having gastrointestinal symptoms. Following the recommendations from the updated Sydney System for the classification and grading of gastritis, two biopsies were taken from the antrum, one from the incisura and two from the corpus. Sections were stained with H&E, Giemsa and for gastrin. Gastrin-positive cells were semi-quantified as: 0 (none), ≤ 9, 10- 49 cells and ≥50 gastrin-labelled cells/40x field. Antrum-type mucosa at the incisura (called antralization) occurred in 30% of the biopsies without inflammation, but in 69% of those with H. pylori-induced gastritis, and in 64% of those with autoimmune gastritis. At the incisura, gastrin-labelled cells (≥10) were found in 62% (18/29) of biopsies showing antralization, but in only 20% (3/15) of those having transitional-type mucosa (p<0.05) and in none of the 16 biopsies having fundic-type mucosa. The similarity in gastrin expression between the mucosa of the gastric antrum and the antral-type mucosa at the incisura substantiates the notion that antralization is a metaplastic transformation. The significantly higher frequency of antral-type mucosa at the incisura in patients with gastritis than in those without gastritis strongly suggests that chronic inflammation per se triggers antralization of the incisura, irrespective of the presence or absence of H. pylori infection. (IJCEP804002).
Address all correspondence to: Carlos A Rubio, MD, PhD, Gastrointestinal and Liver Pathology Research Laboratory, Department of Pathology, Bldg P1/R8:02, Karolinska Institute and University Hospital, 17176, Stockholm, Sweden. Fax: 46 8 51774524; Email: Carlos. Rubio@ki.se