Campylobacter pylori, duodenal ulcer, and gastric metaplasia: possible role of functional heterotopic tissue in ulcerogenesis
Autor: | M Ralston, Hazell Sl, Adrian Lee, J Carrick, G Daskalopoulos |
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Jazyk: | angličtina |
Rok vydání: | 1989 |
Předmět: |
Adult
Male medicine.medical_specialty Choristoma/*complications Gastritis/etiology/pathology Duodenum Choristoma Gastroenterology Duodenal Ulcer/*etiology Duodenal Neoplasms Risk Factors Metaplasia Internal medicine Duodenal bulb Campylobacter Infections medicine Gastric mucosa Pyloric Antrum Humans Duodenal Infection Antrum Duodenal Neoplasms/*complications Duodenal Neoplasm Gastric Mucosa Aged business.industry Pyloric Antrum/pathology Duodenum/pathology Middle Aged digestive system diseases medicine.anatomical_structure Campylobacter Infections/*complications Duodenal Ulcer Gastritis Female medicine.symptom business Research Article |
Popis: | Multiple pinch biopsies were taken from the duodenum and antrum of 137 subjects (46 active duodenal ulceration; 44 healed ulcers; 47 'normal'), and examined for the presence and grade of gastritis, gastric metaplasia, and Campylobacter pylori. These factors, as well as age, sex, cigarette, and anti-inflammatory agent intake were evaluated as possible risk factors for duodenal ulceration. Pentagastrin induced Congo Red staining of the duodenal bulb was performed in an additional 43 cases, to determine the presence of functioning parietal cells in the duodenum. Ninety eight per cent of patients with duodenal infection with C pylori had active or healed duodenal ulcers. Bacteria were confined to areas of gastric metaplasia which was always infiltrated with inflammatory cells. The metaplastic tissue was usually superficial in type, although patients had C pylori associated with heterotopic tissue: this has not been previously described. Congo Red staining of the duodenal bulb showed that functioning endogenous acid producing tissue could be found most often at the edges of duodenal ulcers, but also in non-ulcer subjects. Cigarette smoking, age, sex, and ingestion of non-steroidal anti-inflammatory agents were not to be found to be significant risk factors for duodenal ulceration. In contrast, the presence of duodenal infection with C pylori proved to be a strong risk factor for duodenal ulceration (RR = 51), together with gastric metaplasia (RR = 6.2), and antral C pylori infection (RR = 7.6). These data identify duodenal infection with C pylori as the strongest risk factor for development of duodenal ulceration. Our finding of endogenous acid production around the edges of duodenal ulcers suggests an active role for parietal cells in the duodenum. We postulate a synergistic role for duodenal C pylori and endogenous acid production in the development of duodenal ulceration. Gut |
Databáze: | OpenAIRE |
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