Duodenogastric bile reflux and gastrointestinal motility in pathogenesis of functional dyspepsia. Role of cholecystectomy.

To establish the pathogenic role of duodenogastric reflux in dyspeptic symptoms we have compared the clinical features, gastrointestinal motility, and rates of duodenogastric bile reflux in 12 cholecistectomized dyspeptic patients, 12 dyspeptic patients with intact gallbladder, and 12 healthy controls. Specific symptoms were scored for severity and frequency. Gastrointestinal manometry was performed during 3 hr of fasting and 2 hr postprandially. Simultaneously, samples of duodenal and gastric contents were obtained sequentially for quantification of bile acids. Results show that symptom global severity (9.6 +/- 0.4 vs 8.8 +/- 0.7) and frequency (9.9 +/- 0.8 vs 9.0 +/- 0.5) were similar in both dyspeptic groups; only abdominal pain was milder in cholecystectomized patients (1.9 +/- 0.1 vs 2.6 +/- 0.2; P < 0.05). Fasting gastric bile acid concentrations were higher in cholecystectomized patients (P < 0.05) and antral postcibal motility lower (P < 0.05) than in the groups. No relation among gastric hypomotility, duodenogastric bile reflux, and symptom scores was detected. We concluded that patients with functional dyspepsia and a prior cholecystectomy have clinical features similar to those with gallbladders, but some physiological features are dissimilar: antral motility is decreased and duodenogastric bile reflux is increased. Thus, a uniform clinical expression of various pathophysiological disturbances constitutes the basis of functional dyspepsia.

Does Helicobacter pylori infection increase gastric sensitivity in functional dyspepsia?

The role of Helicobacter pylori infection in the pathogenesis of functional dyspepsia is debated. It is known that a substantial fraction of dyspeptic patients manifest a low discomfort threshold to gastric distension. This study investigated the symptomatic pattern in 27 H pylori positive and 23 H pylori negative patients with chronic functional dyspepsia, and potential relations between infection and gastric hyperalgesia. Specific symptoms (pain, nausea, vomiting, bloating/fullness, early satiety) were scored from 0 to 3 for severity and frequency (global symptom scores: 0-15). The mechanical and perceptive responses to gastric accommodation were evaluated with an electronic barostat that produced graded isobaric distensions from 0 to 20 mm Hg in 2 mm Hg steps up to 600 ml. Gastric compliance (volume/pressure relation) and perception (rating scale: 0-10) were quantified. Standard gastrointestinal manometry and recorded phasic pressure activity at eight separate sites during fasting and postprandially were also assessed. H pylori positive and H pylori negative patients manifested similar severity and frequency of specific symptoms and global symptom scores (mean (SEM)) (severity: 9.5 (2.0) v 9.0 (2.1); frequency: 10.8 (2.0) v 9.7 (2.2)). No differences were seen either in gastric compliance (53 (4) ml/mm Hg v 43 (3) ml/mm Hg) or in gastric perception of distension (slope: 0.50 (0.05) v 0.53 (0.06)). Postprandial antral motility was significantly decreased in H pylori positive patients (two hours motility index: 10.4 (0.6) v 12.6 (0.5); p < 0.05). It is concluded that H pylori infected patients with functional dyspepsia present no distinctive symptoms by comparison with H pylori negative counterparts and H pylori infection is associated with diminished postprandial antral motility but it does not increase perception of gastric distension.