The role of Helicobacter pylori in peptic ulcer disease.
The pathophysiology of peptic ulcer disease (PUD) is often described as an imbalance between aggressive factors such as acid and pepsin and alterations in the mucosal protective mechanisms. Helicobacter pylori is a gram-negative organism that has been identified as a potential causative agent in the pathogenesis of PUD. The exact mechanism by which it contributes to mucosal damage is unknown. It is thought that the organism may disrupt the protective mucous layer, allowing the underlying epithelium to be injured by gastric acid. Significant evidence indicates that H. pylori is a major etiologic factor in type B gastritis. Data confirming its etiologic role in duodenal ulcer (DU) disease is not conclusive; however, eradication of the organism is associated with a reduction in the recurrence of DU. Optimum therapy to eradicate H. pylori has not been established, although several multidrug regimens have been evaluated. Treatment of H. pylori infection should be reserved for individuals in whom conventional therapy for DU is unsuccessful and those whose ulcers relapse during maintenance therapy.
Partipilo
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College of Pharmacy, University of Michigan, Ann Arbor.
Woster
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PS
D004359:Drug Therapy, Combination; D005744:Gastric Acid / Q000378:metabolism; D005753:Gastric Mucosa / Q000382:microbiology*; D016481:Helicobacter Infections / Q000188:drug therapy / Q000382:microbiology*; D016480:Helicobacter pylori; D006801:Humans; D009942:Organometallic Compounds / Q000627:therapeutic use; D010434:Pepsin A / Q000378:metabolism; D010437:Peptic Ulcer / Q000188:drug therapy / Q000382:microbiology* / Q000503:physiopathology; D014011:Tinidazole / Q000627:therapeutic use
D009942:Organometallic Compounds; D014011:Tinidazole; D010434:Pepsin A; C002791:bismuth tripotassium dicitrate