Mucosal changes in gastric ulceration and their response to carbenoxolone sodium.

Abstract

SUMMARY The epithelial differences between the normal stomach (six subjects) and 47 patients with gastric ulcers were compared. The concentrations of intraepithelial lymphocytes and polymorphonuclear leucocytes in lesser curve and prepyloric gastric ulcers were compared, and the effect of treatment with carbenoxolone sodium was studied. There is a statistically significant reduction in the total number of intraepithelial polymorphonuclear leucocytes before and after successful treatment with carbenoxolone sodium. There is also a statistically significant decrease in the quantity of intraepithelial lymphocytes in those patients with lesser curve gastric ulcers successfully treated with carbenoxolone sodium, whereas there is a significant increase in those patients with prepyloric gastric ulcers successfully treated and those patients in whom treatment failed. The value of counts of migrating white blood cells as a method of objectively assessing the effect of healing drugs upon the gastric mucosa is discussed.Pseudomonas aeruginosa was found in many specimens obtained, and evidence is presented that this was not a contaminant. Carbenoxolone appeared to increase the amount of mucus but had little effect upon the number of bacteria found. The possible contribution of Pseudomonas aeruginosa to gastric ulceration is discussed.

Pathogenesis and therapy of gastric and duodenal ulcer disease

“…In the early 1980s, Marshall and Warren [7] first cultured the bacterium associated with gastritis and introduced investigators to the potential role of bacterial infection in the pathogenesis of gastritis, peptic ulcer, and gastric cancer [8]. Investigators rapidly met the challenge.…”

Helicobacter pylori: 20 years on

“…It was thought that all these facts were unrelated, and that gastric urease was actually secreted by the gastric epithelial cells, until Charles Lieber showed that it could be suppressed with tetracycline 5 , and Delluva showed that germ-free animals did not develop gastric urease 6 . The presence of spiral bacteria in the human stomach was reported several times, most notably by Freedberg in 1940 7 and Steer and Colin-Jones in 1975 8 , well before the bacteria were found to cause peptic ulcer and gastric cancer 1,9 . The history of H. pylori is the subject of a recent book, Helicobacter pioneers: firsthand accounts from the scientists who discovered helicobacters, 1892-1982 10 .…”

Species differentiation and identification in the genus ofHelicobacter

“…Interest in the role of gastric bacteria in the pathogenesis of peptic ulcer disease was rekindled when Steer and Colin Jones [6] reported the presence of bacteria deep in the mucus layer of gastric mucosa in patients with gastric ulceration. It was suggested that the bacteria might cause a reduction in gastric mucosal resistance via predisposal to ulceration.…”

“…Attempts to culture this bact erium yielded growth of Pseudomonas aeruginosa. Retrospectively, careful examination of the figures in this publication [6] suggests that the organism seen on the mucosa is a spiral bacterium, a morphological form not associated with P. aeruginosa. It is now assumed that the culture of P. aeruginosa by these authors represents a contaminant cultured from the endoscope.…”