Peptic ulcer bleeding and recurrence rate are strongly linked to Helicobacter pylori
infection even if nonsteroidal anti-inflammatory drugs (
NSAIDs) play a relevant role in this setting. Further studies confirm that H. pylori eradication lowers the risk of recurrent
peptic ulcer bleeding. Therefore, a test-and-treat strategy appears to be mandatory for patients with a history of
ulcer bleeding and
NSAIDs and/or
aspirin use. Concerning
gastroesophageal reflux disease (
GERD), evidence clearly shows that H. pylori status has no effect on symptoms and treatment. Therefore, H. pylori treatment is not contraindicated in patients with
GERD. The exact role of H. pylori in functional
dyspepsia (FD) remains controversial. Novel possible mechanisms by which H. pylori may elicit dyspeptic symptoms include alterations of gastric motility, as well as endocrine and
acid-secretory abnormalities. Hunger sensations,
acid secretion, and gastrointestinal motility are regulated by
ghrelin, particularly produced by the gastric enteroendocrine cell compartment. The improvement of symptoms correlates with enhanced plasma
ghrelin levels. Apart from the need for more trials on this topic, these findings may give insight into the underlying pathophysiology of FD symptoms. Recent reports suggest that the presence of
bacterial DNA in the oral cavity may be relevant to its transmission. A potential protective role of H. pylori on
inflammatory bowel diseases needs to be better elucidated.