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. 1999 Jan;44(1):55-64.
doi: 10.1136/gut.44.1.55.

Gastric accommodation in non-ulcer dyspepsia and the roles of Helicobacter pylori infection and vagal function

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Gastric accommodation in non-ulcer dyspepsia and the roles of Helicobacter pylori infection and vagal function

M Thumshirn et al. Gut. 1999 Jan.

Abstract

Background: The pathophysiological mechanisms in non-ulcer dyspepsia are incompletely understood.

Aims: To compare gastric motor and sensory functions in Helicobacter pylori positive or negative patients with non-ulcer dyspepsia.

Patients: Seventeen patients with non-ulcer dyspepsia and 16 asymptomatic controls.

Methods: The following were evaluated: gastrointestinal symptoms; gastric emptying and orocaecal transit of solids; abdominal vagal function; gastric compliance; fasting and postprandial gastric tone and phasic contractions; symptoms during ingestion of cold water and during the distension of an intragastric bag; and somatic sensitivity and personality profile (Minnesota Multiphasic Personality Inventory, MMPI).

Results: Gastric accommodation was reduced in H pylori negative dyspeptics relative to controls; the degree of accommodation was unrelated to H pylori status in dyspeptics. Increased postprandial gastric sensation was more frequent among H pylori positive patients (4/5 H pylori positive versus 4/12 H pylori negative patients). Intragastric meal distribution and orocaecal transit were normal; gastric emptying at four hours was abnormal in 4/17 patients. Vagal dysfunction was rare. Eight of 17 patients had somatisation or depression on MMPI.

Conclusion: Impaired gastric accommodation is frequent in non-ulcer dyspepsia and seems to be unrelated to vagal efferent dysfunction. H pylori infection does not seem to influence gastric accommodation, but is associated with heightened sensitivity in dyspeptics. Therapeutic approaches that restore normal postprandial accommodation and gastric sensitivity should be tested in non-ulcer dyspepsia.

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Figures

Figure 1
Figure 1
Experimental design for measurement of gastric compliance, tone, and sensation using a barostatically controlled polyethylene bag in the proximal stomach.
Figure 2
Figure 2
Gastric residual data at four hours. The shaded area shows normal ranges in our laboratory.23 NUD, non-ulcer dyspepsia.
Figure 3
Figure 3
Individual accommodation data for all groups studied. NUD, non-ulcer dyspepsia.
Figure 4
Figure 4
Representative tracings of gastric relaxation (accommodation) induced by meal ingestion. NUD, non-ulcer dyspepsia.
Figure 5
Figure 5
Aggregate sensation scores during fasting, early, and late postprandial periods in response to 4, 8, and 12 mm Hg distensions above baseline operating pressure. NUD, non-ulcer dyspepsia. *p⩽0.01 versus asymptomatic controls; †p<0.017 versus asymptomatic controls.
Figure 6
Figure 6
Distribution of impaired accommodation, delayed gastric emptying, gastric hypersensitivity, and abnormal reports on MMPI in patients with non-ulcer dyspepsia with and without H pylori infection.

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