Helicobacter pylori and acid secretion: where are we now?
It is now widely recognized that H. pylori gastritis can produce marked alterations in gastric acid secretion. In subjects with an antral predominant gastritis there is increased release of gastrin and consequently increased acid secretion. Such subjects are at risk of developing duodenal ulcers. In other subjects the infection produces a marked body gastritis and this is associated with marked hyposecretion of acid or complete achlorhydria. These subjects have an increased risk of developing gastric cancer. Between these two ends of the disease spectrum lie the majority of H. pylori-infected subjects who have gastritis of both the antrum and body and no overall change in acid secretion. The reason why the infection exerts these divergent effects on gastric morphology and function remains unclear and is a challenge for ongoing research.
McColl
K E
KE
Department of Medicine and Therapeutics, Western Infirmary, Glasgow, Scotland.
D002452:Cell Count; D004381:Duodenal Ulcer / Q000378:metabolism / Q000382:microbiology / Q000473:pathology; D005744:Gastric Acid / Q000378:metabolism; D005748:Gastric Fundus / Q000378:metabolism / Q000382:microbiology / Q000473:pathology*; D005755:Gastrins / Q000378:metabolism; D005756:Gastritis / Q000378:metabolism / Q000382:microbiology / Q000473:pathology; D016481:Helicobacter Infections / Q000209:etiology / Q000378:metabolism / Q000473:pathology*; D016480:Helicobacter pylori; D006801:Humans; D011706:Pyloric Antrum / Q000378:metabolism / Q000382:microbiology / Q000473:pathology*; D012307:Risk Factors
D005755:Gastrins