title: Helicobacter pylori and its involvement in gastritis and peptic ulcer formation.
abstract: Modern gastroenterology started in early 19(th) century with the identification by W. Prout of the inorganic (hydrochloric) acid in the stomach and continued through 20(th) century with the discoveries by I.P. Pavlov of neuro-reflex stimulation of gastric secretion for which he was awarded first Nobel Prize in 1904. When concept of nervism or complete neural control of all digestive functions reached apogeum in Eastern Europe, on the other side of Europe (in United Kingdom), E. Edkins discovered in 1906 that a hormone, gastrin, may serve as chemical messenger in stimulation of gastric acid secretion, while L. Popielski revealed in 1916 that histamine is the most potent gastric secretagogue. K. Schwartz, without considering neural or hormonal nature of gastric secretory stimulation, enunciated in 1910 famous dictum; "no acid no ulcer"; and suggested gastrectomy as the best medication for excessive gastric acid secretion and peptic ulcer. In early 70s, J.W. Black, basing on earlier L. Popielski's histamine concept, identified histamine-H(2) receptors (H(2)-R) and obtained their antagonists, which were found very useful in the control of gastric acid secretion and ulcer therapy for which he was awarded in 1972 second Nobel Prize in gastrology. With discovery by G. Sachs in 1973 of proton pumps and their inhibitors (PPI), even more effective in gastric acid inhibition and ulcer therapy than H(2)-R antagonists, gastric surgery, namely gastrectomy, practiced since first gastric resection in 1881 by L. Rydygier, has been considered obsolete for ulcer treatment. Despite of the progress in gastric pharmacology, the ulcer disease remained essentially "undefeated" and showed periodic exacerbation and relapses. The discovery of spiral bacteria in the stomach in 1983 by B.J. Marshall and R.J. Warren, Australian, clinical researches, awarded in 2005 the Nobel Prize for the third time in gastrology, has been widely considered as a major breakthrough in pathophysiology of gastritis and peptic ulcer, which for the first time can be definitively cured by merely eradication of germ infecting stomach. This overview presents the mechanism of induction of gastritis and peptic ulcer by the H. pylori infection and describes accompanying changes in gastric acid and endocrine secretion as well as the effects of germ eradication on gastric secretory functions and gastroduodenal mucosal integrity.
authors.affiliation: Department of Clinical Physiology, Jagiellonian University Medical College, Cracow, Poland. mpkontur@cyf-kr.edu.pl
authors.forename: S J
authors.initials: SJ
authors.lastname: Konturek
authors.forename: P C
authors.initials: PC
authors.lastname: Konturek
authors.forename: J W
authors.initials: JW
authors.lastname: Konturek
authors.forename: M
authors.initials: M
authors.lastname: Plonka
authors.forename: M
authors.initials: M
authors.lastname: Czesnikiewicz-Guzik
authors.forename: T
authors.initials: T
authors.lastname: Brzozowski
authors.forename: W
authors.initials: W
authors.lastname: Bielanski
mesh_terms: D000818:Animals; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000009:adverse effects; D000897:Anti-Ulcer Agents / Q000627:therapeutic use; D005744:Gastric Acid / Q000378:metabolism; D005756:Gastritis / Q000453:epidemiology / Q000209:etiology* / Q000378:metabolism; D016481:Helicobacter Infections / Q000150:complications* / Q000378:metabolism; D016480:Helicobacter pylori; D006801:Humans; D010437:Peptic Ulcer / Q000188:drug therapy / Q000453:epidemiology / Q000209:etiology* / Q000378:metabolism
chemical_list: D000894:Anti-Inflammatory Agents, Non-Steroidal; D000897:Anti-Ulcer Agents