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Helicobacter pylori and Nonmalignant Diseases
Author(s) -
Ierardi Enzo,
Goni Elisabetta,
Losurdo Giuseppe,
Di Mario Francesco
Publication year - 2014
Publication title -
helicobacter
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.206
H-Index - 79
eISSN - 1523-5378
pISSN - 1083-4389
DOI - 10.1111/hel.12157
Subject(s) - helicobacter pylori , medicine , gerd , gastroenterology , aspirin , disease , ghrelin , gastric acid , endocrine system , peptic , gastritis , zollinger ellison syndrome , peptic ulcer , stomach , hormone , reflux
Peptic ulcer bleeding and recurrence rate are strongly linked to Helicobacter pylori infection even if nonsteroidal anti‐inflammatory drugs ( NSAID s) 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 NSAID s 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.