Is the Only Good Helicobacter a Dead Helicobacter?

Background.Vast numbers of therapeutic studies of various drug regimens used for the cure of H. pylori infection have been published. However, many of these studies have been uncontrolled, included small numbers of patients, were published only as abstracts, differed widely in dosage sizes, schedules and durations and were of insufficient statistical power to make meaningful statements concerning their efficacy. Furthermore, there are no clear or universally accepted guidelines for the treatment of H. pylori infection. Thus, there remains profound confusion among practitioners on whom and how to treat.Objective.To critically review the currently available management strategies for H. pylori infection.Methods.Review of the literature.Results.Treatment of H. pylori requires the use of multiple drug regimens (triple therapy) which can be expensive and is often associated with side effects. Bad choice of treatments, poor patient counseling and compliance will lead to the emergence of resistant H. pylori strains. Resistance to H. pylori to metronidazole is already widespread and resistance to other antimicrobial agents is increasing. The resource/financial implications are not negligible.Conclusions.The introduction of kits that will enable the identification of pathogenic strains of H. pylori in the office setting may decrease the number of patients being given H. pylori eradication therapy, but much more evidence is needed to establish the practical value of such tests. In the meantime, as many clinicians adhere to the idea that the only good H. pylori is a dead H. pylori, the best practical policy option is education concerning the correct diagnostic methodology, correct choice of patients and the correct choice of treatment regimens. The discovery of Helicobacter pylori (H. pylori) has revolutionized our concepts of etiology, pathophysiology and treatment of many foregut diseases. Gastritis, gastric ulcer (GU), duodenal ulcer (DU), gastric cancer, MALT gastric lymphoma and other conditions are now regarded as being dependent on the colonization of the stomach by H. pylori. Many aspects of pathophysiology, such as the abnormalities of gastric acid secretion in duodenal ulcer disease, now for the first time fall into a logical and comprehensible pattern.