Patients with Crohn’s disease have more dyspeptic symptoms than the general population, even when there is no evidence of inflammatory activity [2, 9, 18, 19]. Disorders in gastrointestinal motility have been observed in patients and in experimental models of Crohn’s diseases [4–8]. However, the association between gastric dysmotility and the presence of dyspeptic symptoms in these patients had not been previously investigated. Our study demonstrated that there was a delay in gastric emptying in inactive Crohn’s disease patients when compared with healthy individuals, and this gastric motility disorder seems to be associated with the presence of dyspeptic symptoms. In addition, we found a significant association between delayed gastric emptying and vomiting, even without any evidence of gastrointestinal obstruction.
Our results show that patients with inactive Crohn’s disease had significantly prolonged gastric emptying half time and lag time measured by 13C-OABT compared with healthy controls, which is in accordance with results published elsewhere [6, 8]. Annese et al. demonstrated that gastric emptying, measured by a scintigraphic study, was slowed in patients with nonobstructive Crohn’s disease . In addition, Keller et al. demonstrated that patients with Crohn’s disease had delayed gastric emptying, measured by a standardized 13C-octanoic acid breath test, and suggested that this disorder might partly be caused by excessive cholecystokinin (CCK) release . The delayed gastric emptying in inactive Crohn’s disease could be due to a decrease in the antroduodenal contraction rate, as described by Annese et al. in 1997, which showed that in the fed state, the inactive Crohn’s disease patients had antrum hypomotility characterized by a decrease in the number of contractions . Another possible explanation for these findings could be an increase in gastric compliance in these patients. However, at present and to the best of our knowledge, there are no studies available concerning gastric compliance in patients with Crohn’s diseases. The role of the intestinal inflammatory process in upper motility was evaluated by Schepper et al. who showed delayed gastric emptying in experimental models of acute colitis , which could be another explanation for the presence of gastric motility disorders away from the inflammatory site. However, despite the fact that our patients had no clinical evidence of intestinal inflammatory activity, as shown by very low CDAI scores, we cannot rule out the possibility of the presence of a mild level of inflammation in these patients.
Our results showed that Crohn’s diseases patients with dyspeptic symptoms had the t 1/2 time more prolonged than the patients without dyspeptic symptoms. However, there was no statistical difference in the t lag between the two subgroups. Then, we can infer that Crohn’s disease patients do not have major disturbances in gastric accommodation. The association between dyspeptic symptoms and delayed gastric emptying has been studied in other conditions, such as functional dyspepsia, and it has been found that only 23-26% of functional dyspeptic patients had delayed gastric emptying [20, 21]. We herein observed delayed gastric emptying in 40% of the patients with Crohn’s disease and dyspeptic symptoms. There may be other pathophysiological mechanisms involved in the genesis of dyspeptic symptoms in Crohn’s disease such as visceral hypersensitivity, impaired accommodation and disturbed antral-duodenum contractility . In accordance, Faure and Giguère already showed that in children with Crohn’s disease in remission suffering from chronic functional abdominal pain, the rectal sensory threshold for pain, measured by barostat, was significantly lower compared to normal subjects ; if this is true for visceral hypersensitivity, this might be a possible explanation for the presence of dyspeptic symptoms in our patients.
We found that Crohn’s disease patients without dyspepsia used more often immunosuppressant drugs (azathioprine-6MP) than patients with dyspepsia (p=0.04). This finding could indicate a more complete mucosal healing in these patients, which could not be expressed by a difference in CDAI scores between these two subgroups.
We observed that the particular symptom of vomiting was significantly associated with delayed solid emptying (Figure 3). In regards to dyspeptic symptoms, is important to note that our findings are in accordance with the observations by Sarnelli et al. who showed an association of delayed solid meal emptying rate with vomiting in patients with functional dyspepsia . Despite the major differences between the studies, the presence of similar associations between the vomiting symptom and delayed gastric emptying confirms the strength of the possible link between pathophysiological mechanism and symptom complex; in the case of Crohn’s disease patients, duodenal obstruction could be a possible explanation for this association. Duodenal obstruction is not a rare condition, yet none of our patients displayed radiological or endoscopic evidence of it. Also, delayed gastric emptying has been previously demonstrated in patients with nonobstructive Crohn’s disease . Besides, there were no differences between the two subgroups of patients with respect to the presence of obstruction or previous abdominal surgery.
Upper endoscopy performed in dyspeptic Crohn’s disease patients presented normal or minor endoscopic findings such as enanthematous gastritis. No significant differences in H. pylori infection were detected in Crohn’s disease patients with or without dyspeptic symptoms. The precise mechanisms of dyspeptic symptoms in patients with inactive Crohn’s disease are still unknown, but our findings suggest that impaired gastric emptying, clinically traduced as gastroparesis, could explain at least part of these symptoms.