Irritable bowel syndrome is the most frequent functional disorder of the digestive system. Patients with irritable bowel syndrome have motor disorders not only in the colon, but also in other parts of the digestive tract such as the oesophagus and small intestine; however, it is not known whether the stomach is also involved. We used a radiolabelled mixed solid-liquid meal (technetium-99m for the solid component, indium-111 for the liquid component) to study gastric emptying of solids (GES), liquids (GEL) and indigestible solids (GER) in 50 patients diagnosed as having irritable bowel syndrome (30 with predominant constipation and 20 with predominant diarrhoea). GER was measured by counting the number of indigestible solids remaining in the stomach 4 h after they were swallowed. In patients with irritable bowel syndrome, GES and GEL were slower than in control subjects (P<0.05). GER was normal in all patients except for two women. Thirty-two patients (64%) showed delayed GES, 29 (58%) delayed GEL, and 2 (4%) delayed GER. Among patients with irritable bowel syndrome, GES was slower in those with predominant constipation than in those with predominant diarrhoea (P<0.05); GEL and GER were similar in both groups. Gastroparesis was found in a large proportion of patients with irritable bowel syndrome, suggesting the presence of a more generalised motor disorder of the gut.
Evidence of postprandial 'physiologic gastroparesis' was found in women, although no differences were found between men and women in gastric motility during fasting. The rate of emptying was not related to changes in plasma concentrations of sex hormones during the menstrual cycle.
Gastric emptying of a solid meal and of 10 indigestible radiopaque solids was measured with scintigraphic and radiological techniques in 50 healthy volunteers (controls), 41 patients with insulin-dependent diabetes mellitus, and 50 patients with functional dyspepsia. Gastroparesis was found in 51% of our diabetic patients and 74% of our patients with dyspepsia. The values of Tlag, T1/2 and the percentage of isotope remaining in the stomach at 105 min were 14.9 min, 59.4 min and 25.3% in control subjects; 21.4 min, 88.1 min, and 46.9% in diabetic patients (P < 0.05 vs the control group); and 23.2 min, 114.6 min, and 58.7% in dyspeptic patients (P < 0.05 vs the control group). Whereas all healthy volunteers emptied all 10 indigestible solids in less than 4 hr, only 51% and 32% of diabetics and dyspeptics, respectively, achieved this emptying time (P < 0.01). Their respective values of T1/2 were 81 min, 212 min, and 203 min (P < 0.01 for diabetics and dyspeptics vs controls). We found no correlation between the findings for gastric emptying of digestible and indigestible solids. We conclude that gastroparesis affecting digestive and interdigestive motility is present in a high percentage of diabetics and functional dyspeptics and that conscientious evaluation of gastroparesis in both groups requires studies designed specifically to characterize each type of motility.
European general practitioners and gastroenterologists have produced recommendations that emphasize education of the patient, a positive symptom-based diagnosis, diet and lifestyle advice, psychological support and a critical analysis of current specific psychological and pharmacological treatments.
Cyclic GMP plays an important role in maintaining homeostasis in the gastric mucosa. NSAIDs damage the mucosa by mechanisms that may be mediated by alterations in the intragastric concentration of cyclic GMP. To test this hypothesis we studied the effects of the oral administration of acetylsalicylic acid (100, 300, and 500 mg/kg), piroxicam (5, 10, and 20 mg/kg) and sodium diclofenac (10, 25, 50, and 100 mg/kg), and of their interaction with zaprinast (5 mg/kg) and IBMX (10 mg/kg), on intragastric concentrations of cyclic GMP and the gastric erosive index in rats. All determinations were done 3 hr after the NSAID was given. All NSAIDs induced dose-dependent decreases in mucosal concentrations of cyclic GMP, which correlated inversely with the surface area showing mucosal injury. In contrast, cyclic GMP concentrations remained normal, and no intragastric damage was seen in rats given zaprinast (cyclic GMP-specific phosphodiesterase inhibitor) or IBMX (non-specific phosphodiesterase inhibitor) or in combination with NSAIDs. These findings are in line with the hypothesis that cyclic GMP is involved in the biochemical mechanisms of NSAID-induced gastric injury.
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