Helicobacter pylori
Article Abstract:
Infection of the stomach mucosal tissue by the bacterium Helicobacter pylori is associated with the development of gastritis, the inflammation of the stomach, and duodenal ulcers, lesions in a portion of the small intestine. A review is presented of the physical and biochemical features, optimal laboratory growth conditions, antibiotics to which the bacteria is sensitive or resistant, and methods for identifying different strains. The strongest evidence for a role of H. pylori in the development of gastritis was provided by treatment studies, which showed that the elimination of H. pylori from the stomach is associated with resolution of gastritis. Duodenal ulcer disease is associated with gastritis, but is not directly caused by H. pylori, which is present in the gastric mucosa of 80 percent of adults with duodenal ulcers. Elimination of H. pylori is associated with a reduction in the rate of recurrence of duodenal ulcers. H. pylori is found in 60 percent of patients with gastric ulcers. An association between H. pylori infection of the gastric mucosa, gastritis, and duodenal ulcer disease has also been shown in children. The colonization of H. pylori in the gastric mucosa occurs less often in children than adults, and almost never occurs in children younger than eight years of age. The symptoms of H. pylori infection in children are most often stomach pain and vomiting, and are more evident in duodenal ulcer disease than in gastritis. Elimination of the bacteria with antibiotics improves symptoms, particularly in duodenal ulcer disease. The various methods of diagnosing H. pylori infection are discussed. The incidence of H. pylori infection increases with age and the bacteria are most likely transmitted person to person. Bismuth salts and antibiotics are effective in eliminating the bacteria from the stomach, and reduce the recurrence of infection. The symptoms of duodenal ulcer disease can be treated by drug therapy with histamine-2 antagonists and bismuth salts. Treatment is not necessary for patients with H. pylori-induced gastritis without duodenal ulcer disease. The disease processes relating H. pylori infection, gastritis, and duodenal ulcer disease require further study. (Consumer Summary produced by Reliance Medical Information, Inc.)
Publication Name: Archives of Disease in Childhood
Subject: Health
ISSN: 0003-9888
Year: 1990
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Histamine concentration of gastric mucosa in Helicobacter pylori positive and negative children
Article Abstract:
Duodenal ulcer is a condition in which there is an imbalance between the protective properties of the gastrointestinal mucosa and the destructive properties of gastric acid. The microorganism Helicobacter pylori is now recognized to play a pivotal, perhaps causal role in the development of duodenal ulcer; studies have reported that as high as 100 percent of duodenal ulcer patients test positive for H. pylori. Eradication of H. pylori infection with antibacterial drugs often leads to complete healing of the ulcer. However, the mechanism by which H. pylori leads to the formation of duodenal ulcers remains unknown. If the microorganism causes changes in the rate of gastric acid secretion, this might be reflected in the levels of gastric histamine, a substance formed within the stomach that is thought to be involved in all forms of gastric acid secretion. To evaluate this possibility, a study was carried out with 37 children between the ages of 1 and 16 years; 19 of the subjects tested positive for H. pylori (nine of these patients had an active duodenal ulcer). Biopsy specimens were taken from the children's stomachs and analyzed for histamine content. The concentration of histamine in the stomachs of H. pylori-positive children was approximately half of that found in the stomachs of children who were H. pylori negative. Among children who were H. pylori positive, those with active ulcers had much lower levels of histamine than those without ulcers. These results suggest that H. pylori causes a release of histamine from gastric cells (resulting in a lower level within the cell), thus increasing the levels of gastric acid secretion. (Consumer Summary produced by Reliance Medical Information, Inc.)
Publication Name: Gut
Subject: Health
ISSN: 0017-5749
Year: 1991
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