• N J Talley.
• Division of Gastroenterology, Mayo Medical School, Rochester, Minnesota 55902.
• Aliment. Pharmacol. Ther. 1991 Jan 1; 5 Suppl 1: 145-62.

AbstractDyspepsia can be defined as the presence of upper abdominal pain or discomfort; other symptoms referable to the proximal gastrointestinal tract, such as nausea, early satiety, and bloating, may also be present. Symptoms may or may not be meal related. To be termed chronic, dyspepsia should have been present for three months or longer. Over half the patients who present with chronic dyspepsia have no evidence of peptic ulceration, other focal lesions, or systemic disease and are diagnosed as having non-ulcer (or functional) dyspepsia. Non-ulcer dyspepsia is a heterogeneous syndrome. It has been proposed that this entity can be subdivided into a number of symptomatic clusters or groupings that suggest possible underlying pathogenetic mechanisms. These groupings include ulcer-like dyspepsia (typical symptoms of peptic ulcer are present), dysmotility (stasis)-like dyspepsia (symptoms include nausea, early satiety, bloating, and belching that suggest gastric stasis or small intestinal dysmotility), and reflux-like dyspepsia (heartburn or acid regurgitation accompanies upper abdominal pain or discomfort). The aetiology of non-ulcer dyspepsia is not established, although it is likely a multifactorial disorder. Motility abnormalities may be important in a subset of dyspepsia patients but probably do not explain the symptoms in the majority. Epidemiological studies have not convincingly demonstrated an association between Helicobacter pylori and non-ulcer dyspepsia. Other potential aetiological mechanisms, such as increased gastric acid secretion, psychological factors, life-event stress, and dietary factors, have not been established as causes of non-ulcer dyspepsia. Management of non-ulcer dyspepsia is difficult because its pathogenesis is poorly understood and is confounded because of a high placebo response rate. Until more data are available, it seems reasonable that treatment regimens target the clinical groupings described above. Antacids are no more effective than placebo in non-ulcer dyspepsia, although a subgroup of non-ulcer dyspepsia patients with reflux-like or ulcer-like symptoms may respond to H2-receptor antagonists. However, there is no significant benefit of these agents over placebo in many cases. Bismuth has been shown to be superior to placebo in patients with H. pylori in a number of studies, but these trials had several shortcomings and others have reported conflicting findings. Sucralfate was demonstrated in one study to be superior to placebo, but this finding was not confirmed by another group of investigators. Prokinetic drugs appear to be efficacious, and may be most useful in patients with dysmotility-like and reflux-like dyspepsia.

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