[Gastroduodenal ulcer disease: update on pathogenesis].
Gastroduodenal ulcer disease comprises a heterogeneous group of different diseases resulting uniformly in a mucosal defect reaching beyond the muscularis mucosae. Consequently, a single unifying pathogenesis of ulcer disease does not exist but only a rather general concept that ulcers develop when mucosa-injuring factors outweigh the mucosa-protecting factors. According to this concept, ulcers develop within a broad range of different possibilities in the relation of mucosa-injuring factors to impaired mucosal protection. The main histological and physiological elements for the understanding of peptic ulcer disease are briefly summarized, followed by a short survey of the important known 'traditional' abnormalities of possible pathogenetic importance in duodenal and gastric ulcer patients. Gastroduodenal ulcer disease represents a typical example of a multifactorial disease, where different combinations of both hereditary and environmental factors produce the same morphological lesion. By far the most exciting data of the last ten years originate from the still increasing understanding of the role of Helicobacter pylori in gastroduodenal ulcer disease. The most important evidence and hypotheses are presented of how and where Helicobacter pylori is or could be involved in the complicated pathogenetic network of ulcer disease. The infection of gastric epithelium by Helicobacter pylori has become the second main factor besides acid/pepsin in the pathogenesis of ulcer disease. Beside the improved insights in ulcer pathogenesis, the translation of the new data into clinical medicine has led and will lead to remarkable progress. Most important: a causal therapy of ulcer disease has become available in contrast to the so far practiced sole symptomatic treatment of single ulcer episodes. What has treatment of single ulcer episodes. What has been a domain of ulcer surgery has come into reach of drug therapy.
Wirth
H P
HP
Department für Innere Medizin, Universitätsspital Zürich.
D000900:Anti-Bacterial Agents / Q000627:therapeutic use; D005744:Gastric Acid / Q000378:metabolism; D005746:Gastric Emptying; D005753:Gastric Mucosa / Q000503:physiopathology; D020022:Genetic Predisposition to Disease; D016481:Helicobacter Infections / Q000188:drug therapy; D006801:Humans; D010437:Peptic Ulcer / Q000209:etiology / Q000503:physiopathology* / Q000628:therapy; D013312:Stress, Physiological / Q000503:physiopathology
D000900:Anti-Bacterial Agents
Gastroduodenale Ulkuskrankheit: Neues zur Pathogenese.