duodenitis

The activity of duodenitis was dependent on the neutrophilic infiltration.

Table II describes the patients with active chronic duodenitis.

This, together with its close association with active duodenitis, is in agreement with the findings of two other studies.

His ailment was diagnosed as duodenitis, basically an inflammation of the upper gastrointestinal tract.

In 1979, gastroscopy showed antral gastritis and duodenitis.

Duodenitis is inflammation of the duodenum.

This emphasises the role of H pylori in the pathogenesis of active duodenitis.

Symptoms are often non-specific including, colitis, oedematous duodenitis, and fever with somnolence.

Known causes of duodenitis include:

While hospitalized in February 1990, he had upper gastrointestinal bleeding; endoscopy revealed chronic gastritis and duodenitis.

Chronic duodenitis - in the presence of mucosal mononuclear cell infiltration and epithelial damage.

Chronic active duodenitis was diagnosed when intramucosal neutrophils were seen in patients scoring four or more.

In the nine H pylori negative non-uraemic patients, one had erosive duodenitis and another a deformed duodenum.

The number of ulcers, their site and shape, and any associated duodenitis, erosions, or complicating features such as scarring were noted.

Active chronic duodenitis was also less common in our patients taking NSAIDs.

In 17 patients with an endoscopic picture of diffuse duodenitis the average extent of gastric metaplasia was 15%.

In accordance with Wyatt et al we found a significant association between the extent of gastric metaplasia and microscopic signs of duodenitis.

Duodenitis follows and this inflammation inpairs mucosal defences, ultimately leading to ulceration.

Patients in the NSAID group had fewer cases of active chronic duodenitis.

Some strains of this bacterium are pathogenic to humans as it is strongly associated with peptic ulcers, chronic gastritis, duodenitis, and stomach cancer.

H pylori positive gastritis, and the combination of active duodenitis and gastric metaplasia were independent predictors of duodenal ulceration.

Table IV shows the prevalence of active duodenitis and gastric metaplasia in the presence of absence of the various types of gastritis.

Table V shows the distribution of NSAIDs, with or without second line drugs in patients with active duodenitis and gastric metaplasia.

Thus both H pylori infection and acid induced gastric metaplasia are considered to be prerequisites for the development of duodenitis with polymorphonuclear activity and duodenal ulcer.

Duodenitis was graded according to the degree of neutrophilic and plasma cell infiltration, villus height, Brunner's gland prolapse, and gastric metaplasia.