The dynamics of gastritis

Abstract

The dynamics of gastritis remain a topic of intense investigation. The results of these investigations have increased our knowledge concerning the development of preneoplastic lesions and cancer of the stomach and given us insight with regard to the interactions among bacterial colonization, chronic inflammation, and carcinogenesis in other organs. The past year has presented us with further data showing that the progression of chronic gastritis to gland loss and gastric cancer is related to the severity of inflammation, which is influenced by the characteristics of the bacterial strain, host genetics, and hypochlorhydria. In contrast, Helicobacter pylori eradication leads to a rapid disappearance of neutrophils in the gastric mucosa. Chronic inflammation with mononuclear cells also improves upon eradication, but at a much slower rate, usually not leading to normalization within the first year after therapy. Whether H. pylori eradication can thus prevent new development of atrophy and metaplasia as well, or lead to regression of pre-existing lesions, has been the topic of many studies by now. Unfortunately, most of these studies have suffered from their case design, limited sample size, and short follow-up. Therefore, the conflict in outcome of these case studies comes as no surprise. The few prospective, randomized, controlled studies, however, strongly confirm that H. pylori eradication leads to healing of gastritis, which can at least halt further development of atrophy and metaplasia. Whether these lesions can truly regress remains to be proven.