PubMed · 8371820
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H J Jebbink, A J Smout, L M Akkermans, G P van Berge Henegouwen. 1993-08-28. [Functional dyspepsia].. https://pubmed.ncbi.nlm.nih.gov/8371820/
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There is good evidence to suggest that gastric metaplasia in the proximal duodenum and Helicobacter pylori gastritis are essential requirements for the development of duodenal ulceration in most cases. Gastric metaplasia is most likely to be a defence response or adaptation to excess acid reaching the duodenum. The appearance of gastric-type epithelium over the duodenal villi probably results from substitution by cells migrating from Brunner's gland ducts. These metaplastic foci provide sites for colonization by H. pylori passing through the duodenum; the organisms do not attach to native duodenal epithelial cells. Having colonized the metaplastic areas, H. pylori provokes an active chronic inflammatory response akin to that seen in the gastric mucosa. Active chronic duodenitis leads to a weakening of mucosal defence against acid-peptic attack, and erosion and ulceration may ensue. Healing of ulcers by conventional acid-reducing treatments does not influence the extent of gastric metaplasia, (although there may be some reduction with long-term proton pump inhibitors); nor do such regimens affect the background duodenitis. Only with eradication of H. pylori is there resolution of inflammation, but studies to date indicate that eradication alone has no substantial effect on the prevalence or extent of gastric metaplasia. Nevertheless the elimination of H. pylori appears to remove one of the essential co-factors for duodenal ulceration and the patient can be considered cured, despite the persistence of gastric metaplasia.
In this article the histological features of acute and chronic gastritis are reviewed. The histopathological gastric biopsy report can now encompass an aetiological, topographical (when antrum and corpus are sampled) and morphological comment on the gastric mucosa. The degree of detail included in the report (e.g. grading of the severity of inflammation, atrophy, density of Helicobacter pylori) will vary according to local requirement. However, the distinct recognisable patterns of inflammation categorised in the Sydney system provide a common terminology for a succinct diagnosis. The overall condition of the patient's gastric mucosa assigns him/her to one of the H. pylori-positive or negative categories of chronic gastritis. This may not only have relevance to current clinical management, but may be a valuable record if the patient returns with dyspeptic symptoms in the future. For example, duodenal ulcers are unlikely to develop except in patients with antrum predominant H. pylori-associated gastritis. Knowledge of the natural history of different types of gastritis is rapidly evolving, and the biopsy provides a permanent 'snapshot' of the state of the gastric mucosa at the time of the endoscopy.
The prevalence of peptic ulcer in cirrhotic patients is similar to that reported for the general population. Although gastric acid outputs ar normal or lower in cirrhotic subjects compared with non-cirrhotics, the frequency of non-response to histamine H2-receptor antagonists is higher. Peptic ulcer disease in the cirrhotic seems to pursue a more virulent course compared with that in the non-cirrhotic subject. Peptic ulcer prevalences in patients dying of uraemia or in uraemic patients on maintenance dialysis treatment are comparable with those in the general population. However, the frequency of peptic ulcer, especially complicated ulcer, is increased following renal transplantation. Ulcer complications in this context are associated with a high mortality rate. Pre-transplant risk factors for subsequent development of peptic ulcer remain to be identified and the value of histamine H2-receptor antagonists in prophylaxis is as yet unproven.