Digestion · 2001
Gastric electrical activity and gastrointestinal hormones in dyspeptic patients.
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Riezzo G, Chiloiro M, Russo F, Clemente C, Di Matteo G, Guerra V, Di Leo A
Аннотация
AIMS: To explore the patterns of gastric electrical activity, gastric emptying and gastrointestinal hormones in dyspeptic patients and relate them to Helicobacter pylori status.
METHODS: Twenty-two patients with functional dyspepsia and 29 healthy volunteers underwent cutaneous electrogastrography and dynamic ultrasound before and after a test meal. All dyspeptic patients underwent endoscopy and biopsy; all subjects were examined for the presence of antibodies to H. pylori, and the plasma levels of gastrin, neurotensin, cholecystokinin, and pancreatic polypeptide were measured.
RESULTS: The area under the curve (AUC) of the normal slow wave percentage was lower in dyspeptic patients than controls (Kruskal-Wallis p = 0.016; Dunn's test: H. pylori-positive patients: 21,235.5 [19,101.0-22,688.8] vs. H. pylori-negative controls: 22,532.0 [20,133.0-23,755.0], p < 0.05). The AUC of the tachygastria percentage was higher in dyspeptic patients than controls (p = 0.0001; H. pylori-positive patients: 2,173.5 [325.8-3,055.3] vs. H. pylori-negative controls: 682.0 [118.5-1,902.4], p < 0.05; H. pylori-negative patients: 1,843.0 [1,107.0-4,277.0] vs. H. pylori-negative controls: 682.0 [118.5-1,902.4], p < 0.05). The AUC of gastrin was higher in H. pylori-positive than H. pylori-negative subjects (p = 0.0002; H. pylori-positive patients: 16,146.5 [11,368.8-33,141.7] vs. H. pylori-negative controls: 11,250.0 [5,674.0-17,448.0], p < 0.05; H. pylori-positive controls: 20,250.0 [12,070.0-64,430.0] vs. H. pylori-negative controls: 11,250.0 [5,674.0-17,448.0], p < 0.05). In the total group of dyspeptic patients and in the H. pylori-positive patients, a negative correlation was found between the AUC of neurotensin and the total score for postprandial fullness (dyspeptic patients r = -0.51, p = 0.01; H. pylori-positive patients r = -0.66, p = 0.02).
CONCLUSIONS: In dyspeptic patients, alterations in gastric electrical activity were not related to H. pylori infection. Nevertheless, H. pylori infection induces higher gastrin levels in both patients and asymptomatic subjects.
METHODS: Twenty-two patients with functional dyspepsia and 29 healthy volunteers underwent cutaneous electrogastrography and dynamic ultrasound before and after a test meal. All dyspeptic patients underwent endoscopy and biopsy; all subjects were examined for the presence of antibodies to H. pylori, and the plasma levels of gastrin, neurotensin, cholecystokinin, and pancreatic polypeptide were measured.
RESULTS: The area under the curve (AUC) of the normal slow wave percentage was lower in dyspeptic patients than controls (Kruskal-Wallis p = 0.016; Dunn's test: H. pylori-positive patients: 21,235.5 [19,101.0-22,688.8] vs. H. pylori-negative controls: 22,532.0 [20,133.0-23,755.0], p < 0.05). The AUC of the tachygastria percentage was higher in dyspeptic patients than controls (p = 0.0001; H. pylori-positive patients: 2,173.5 [325.8-3,055.3] vs. H. pylori-negative controls: 682.0 [118.5-1,902.4], p < 0.05; H. pylori-negative patients: 1,843.0 [1,107.0-4,277.0] vs. H. pylori-negative controls: 682.0 [118.5-1,902.4], p < 0.05). The AUC of gastrin was higher in H. pylori-positive than H. pylori-negative subjects (p = 0.0002; H. pylori-positive patients: 16,146.5 [11,368.8-33,141.7] vs. H. pylori-negative controls: 11,250.0 [5,674.0-17,448.0], p < 0.05; H. pylori-positive controls: 20,250.0 [12,070.0-64,430.0] vs. H. pylori-negative controls: 11,250.0 [5,674.0-17,448.0], p < 0.05). In the total group of dyspeptic patients and in the H. pylori-positive patients, a negative correlation was found between the AUC of neurotensin and the total score for postprandial fullness (dyspeptic patients r = -0.51, p = 0.01; H. pylori-positive patients r = -0.66, p = 0.02).
CONCLUSIONS: In dyspeptic patients, alterations in gastric electrical activity were not related to H. pylori infection. Nevertheless, H. pylori infection induces higher gastrin levels in both patients and asymptomatic subjects.