Helicobacter pylori: review of research findings.

Helicobacter pylori attracted widespread interest from gastroenterologists because of its potential aetiologic role in disorders of the upper gastrointestinal tract. Based on extensive microbiological studies, Campylobacter pylori was renamed Helicobacter pylori, and the organism represents a new genus of bacteria. It is generally accepted that H. pylori causes chronic, non-specific gastritis (type B gastritis). The inflammatory response occurs even though the bacterium does not penetrate the gastric epithelium; it is found on the surface of and adjacent to the epithelium. The clinical significance of histological gastritis is unknown. The bacterium is often found in asymptomatic subjects. In Caucasian adults, the prevalence of infection increases with increasing age. Higher rates of infection are found in blacks and Hispanics than would be expected for their age. Whether these different rates are the result of racial or socioeconomic factors is not known. It is theorized, but not proven, that high rates of infection with H. pylori at an early age may explain the high incidence of gastric carcinoma found in Hispanic populations. H. pylori is found in almost every patient with duodenal ulcer disease, although no direct evidence for a causal relationship exists. Indirect evidence is based on the findings that if H. pylori infection is eradicated, ulcer recurrence is less likely (up to one year of follow-up). A small percentage of patients have a relapse despite eradication of the organism, suggesting a role for other factors in duodenal ulcer disease. The role of H. pylori in gastric ulcer disease is unknown. Seventy to eighty per cent of patients with gastric ulcer have evidence of H. pylori infection, and preliminary data seem to support the existence of two distinct aetiologic groups: those with gastric ulcers related to H. pylori infection and those with gastric ulcers related to use of non-steroidal anti-inflammatory drugs. The role of H. pylori in non-ulcer dyspepsia is unknown. Some clinicians believe that H. pylori causes non-ulcer dyspepsia and treat these patients for H. pylori infection. However, the data supporting this practice are poor. Treatment is only recommended for patients with resistant duodenal ulcers and patients who have frequent relapses of duodenal ulcers and who are willing to take triple-drug therapy (bismuth compounds, metronidazole, tetracycline) for the infection. As 95% of patients with duodenal ulcer have evidence of H. pylori infection, there is probably little need to confirm the diagnosis of H. pylori infection.