Gastroduodenal inflammation in patients with nonulcer dyspepsia

Abstract

Proper control and quantitation are important in the accurate evaluation of gastroduodenal inflammation in dyspeptic patients without ulcers or erosions as proved by endoscopy. The endoscopic findings and the gastroduodenal mucosal inflammatory cell count in 31 patients with non-ulcer dyspepsia were compared with an age-matched group of 32 healthy controls. Endoscopy revealed similar mucosal changes and in similar frequency in both groups. Differential mucosal inflammatory cell count showed a statistically significant (P less than 0.001) increase in the neutrophil count in the gastric body, antrum, and duodenal cap of the dyspeptic group, as well as a slight but significant (P less than 0.05) increase in the round cell and eosinophil count of the duodenal mucosa alone. No correlation was found between the endoscopic changes and an increase in neutrophil count above a normal level determined by the healthy controls. However, an endoscopically normal mucosa was more likely to be associated with a normal neutrophil count. Active inflammation of the gastroduodenal mucosa likely accounts for the symptoms in patients with non-ulcer dyspepsia.

The Correlation of Endoscopic and Histological Diagnosis of Gastric Atrophy

“…Furthermore, when the histological atrophic grade was compared between the group with atrophy absent by endoscopy and the group with atrophy present the histological atrophic grade was significantly higher in the group with atrophy present by endoscopy than in the group with atrophy absent. These results are consistent with the findings that the concordance was good in the severe forms of gastritis [11][12][13][14][15][16][17].…”

“…Research regarding the concordance between the findings of endoscopy and histology in cases with gastritis has been made, but the outcomes showed a kind of disappointing correlation [11][12][13][14][15]. However, in general, the concordance was good in the severe forms of gastritis and normal endoscopy has excluded active gastritis [11][12][13][14][15][16][17].…”

Campylobacter pylori and gastroduodenal disease

“…The prevalence of C. pylori in patients with NUD is 45 to 70% and the prevalence of gastritis is similar (68,77,109,110,126,127), suggesting possible involvement of the organism in the disease. One of the problems with assessing these data is that there is an age-related increase in the prevalence of the organism (43,50,92), and, thus, C. pylori is found in about 50% of asymptomatic individuals 50 to 60 years old.…”

Studies of Luminal and Mucosal pH in Reflux Esophagitis and Antral Gastritis

“…Though this variety of gastritis has been well defined morphologically [42], both its pathophysiology and relationship to clinical symptoms remain uncertain [13. [43][44][45][46][47], Thus, some consider that the primary problem in antral gastritis is abnormal duodenogastric bile reflux, consequent on abnor malities of gastropyloroduodenal coordina tion [10,48], Support for this concept of bilerelated gastritis comes from in vitro studies which have clearly demonstrated the ability of bile both to disrupt the mucus layer [49] and to inhibit gastric bicarbonate secretion [50], thus allowing easy access for damaging hydrogen ions to the sensitive mucosa. Our observations suggest furthermore that the at tack-defense equilibrium in the antrum may already be set on a knife edge, the additional presence of bile in certain pathological condi tions tilting the balance and resulting in mu cosal damage.…”