Taha A S, Huxham I M, Motley P, Morton R, Beattie A D
The Gastrointestinal Centre, Southern General Hospital, Scotland, UK.
Eur J Gastroenterol Hepatol. 1998 Dec;10(12):1001-5. doi: 10.1097/00042737-199812000-00004.
OBJECTIVES/DESIGN: Chronic inflammation is increasingly being linked to ischaemia, but the mechanism is poorly understood, and little is known about its effect on local gastric endothelial microvessels. We aimed at studying the number and surface area of gastric mucosal endothelial microstructures in the presence or absence of chronic gastritis.
Immunohistochemical assessments were carried out on gastric antral and body biopsies taken from patients with chronic gastritis and others with normal histology. The primary antibody (QB-END/10) was raised against CD34 antigen within the endothelial cell membranes. A computer attached to a microscope was used to count the number and measure the surface area of mucosal endothelial entities.
In patients with Helicobacter pylori gastritis (n = 19), the median number of endothelial microstructures per section was 43 in the antrum and 86 in the gastric body, compared with 205 (P = 0.00004) and 165 (P = 0.002), respectively, in subjects with normal gastric histology (n = 11). The median surface area of the endothelial microstructures was also reduced in patients with gastritis. The normal gastric antrum had more endothelial entities than the normal body (median of 205 vs 165; P = 0.007).
Within the normal stomach, the antrum is more richly vascularized than the gastric body. However, active chronic gastritis is associated with reduction in both the number and surface area of mucosal endothelial microstructures, with the reduction being more marked in the antrum. This is different from acute inflammation, and is relevant to our understanding of the natural history of mucosal defence, particularly the greater susceptibility of the gastric antrum to ulceration, compared with the gastric body.
