Since Helicobacter pylori (Hp) was first isolated in 1983, much work has been carried out on the pathogenic effects of this organism. Hp infection is common in humans and currently is the most important etiologic agent in the development of chronic active gastritis, gastric and duodenal ulcers, carcinoma and Maltlymphoma of the stomach. Moreover Hp infection has also been associated with various extradigestive diseases. At present, a role of Hp infection in dyspepsia is discussed. Dyspepsia is defined by persistence of pain, burning or discomfort localised to the upper abdomen; some authors include in dyspepsia symptoms such as belching, bloating, alitosis, nausea, postprandial repletion, vomiting and regurgitation. In absence of any underlying pathologies, such as peptic ulcer, gastroesophageal reflux, pancreatitis, biliary tract disease or others, dyspepsia is defined as functional or idiopathic dyspepsia. Functional dyspepsia may be distinct in ulcer, reflux or dysmotility -like dyspepsia and unspecified dyspepsia. Hp infection is common in dyspeptic patients and a role of this bacterium has been postulated mostly in ulcer-like dyspepsia. Mechanisms by when Hp induces dyspeptic symptoms are uncertain; bacterial cytotoxins, phlogosis mediators, activity of chronic gastritis Helicobacter-related and host immune response probably play an important role in pathogenesis of functional dyspepsia. However, dyspepsia is not present only in infected patients; therefore other pathogenic factors may be implicated in expression of dyspeptic symptoms in uninfected subjects, such as gastric dysmotility, modifications of gastric output or altered visceral sensibility, psychological factors, gastroesophageal reflux and irritable bowel.
|Number of pages||10|
|Publication status||Published - Jan 1999|
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