Helicobacter pylori and nonmalignant diseases

Infection with Helicobacter pylori initially leads to superficial gastritis and usually progresses to chronic active gastritis. Although the vast majority of chronically infected subjects remain asymptomatic, somewhere between 10 % and 15% develop peptic ulcer disease. Most commonly, H. pylori infection is located in the gastric antrum, where it acts to inhibit somatostatin release and thus stimulate acid secretion, causing duodenal ulceration. Patients with pangastritis are predisposed to developing gastric ulceration. Although population-based studies show that patients with gastroesophageal reflux disease have a lower likelihood of H. pylori infection, there is no robust evidence suggesting that eradication of H. pylori leads to erosive esophagitis. Patients who lack endoscopic evidence of disease such as peptic ulceration (i.e., functional dyspepsia) experience a greater reduction in their dyspeptic symptoms following eradication of H. pylori as compared to placebo. The pathophysiology of H. pylori-mediated dyspepsia in these patients probably involves increased acid, decreased ghrelin, and altered gastric emptying. Eradication of H. pylori in patients with functional dyspepsia has the added benefit of preventing future peptic ulcer disease, especially in Asian populations. H. pylori has been weakly linked to various nonmalignant conditions ranging from halitosis to coronary heart disease. However, evidence in support of actively seeking and treating H. pylori exists only for idiopathic thrombocytopenic purpura and iron deficiency anemia. In epidemiological studies, H. pylori infection has been shown to be inversely associated with Crohn’s disease and asthma.