Helicobacter pylori: aggressor or innocent bystander?
Helicobacter pylori seeks gastric mucosa, whether found in the stomach, duodenum, or Barrett's esophagus. Definitive diagnosis can be secured by appropriate stains of mucosal biopsies and culture, but the rapid urease test, breath isotope studies, and serologic testing are also useful. The frequency of colonization increases with advancing age, but infection occurs earlier in underdeveloped countries. Although the reservoir is uncertain, water or food transmission seems likely. There is sufficient evidence to assign an etiologic role to the bacteria in the causation of type B antral gastritis. H. pylori is found in areas of gastric metaplasia within the duodenum and is associated with duodenitis. Although acute infection leads to hypochlorhydria, chronic colonization has little effect on acid secretion. Studies have thus far failed to establish a convincing relationship between H. pylori and nonulcer dyspepsia, although the bacteria may play a role in selected patients. H. pylori is found in association with most idiopathic gastric and duodenal ulcers, but it is unclear as to whether the bacteria plays a causative or permissive role. The organism has a predilection for intercellular spaces and the mucous layer, thus affording relative isolation from luminally active antibiotics. Monotherapy with bismuth preparations transiently eliminates the bacteria, but recolonization is rapid, probably due to regrowth of sequestered organisms. A combination of metronidazole, bismuth, and tetracycline (or amoxicillin) affords the best eradication rate, but the potential side effects of this program should be considered. The present therapy of duodenal ulcer disease is effective and without significant risk. Treatment of H. pylori should be reserved for those patients who relapse on adequate maintenance therapy. If a safe and effective antibiotic becomes available, more frequent testing and earlier treatment intervention may become more attractive. H. pylori is probably an "innocent bystander" for most patients, but the bacteria may sufficiently impair the defenses of the antral and duodenal mucosa to facilitate the development and relapse of ulcer disease in subsets of patients.
Clearfield
H R
HR
Division of Gastroenterology, Hahnemann University, Philadelphia, Pennsylvania.
D004386:Duodenum / Q000382:microbiology; D004415:Dyspepsia / Q000188:drug therapy / Q000209:etiology / Q000382:microbiology; D005744:Gastric Acid / Q000378:metabolism; D005756:Gastritis / Q000188:drug therapy / Q000382:microbiology* / Q000503:physiopathology; D016481:Helicobacter Infections / Q000150:complications* / Q000175:diagnosis / Q000188:drug therapy / Q000503:physiopathology; D016480:Helicobacter pylori; D006801:Humans; D010437:Peptic Ulcer / Q000188:drug therapy / Q000382:microbiology* / Q000503:physiopathology