Journal of Neurogastroenterology and Motility最新文献

Background/aims: This study aims to evaluate the effects of acute codeine administration on primary and secondary esophageal peristalsis in patients with ineffective esophageal motility (IEM).

Methods: Eighteen IEM patients (8 women; mean age 37.8 years, range 23-64 years) were enrolled in the study. The patients underwent high-resolution manometry exams, consisting of 10 single wet swallows, multiple rapid swallows, and ten 20 mL rapid air injections to trigger secondary peristalsis. All participants completed 2 separate sessions, including acute administration of codeine (60 mg) and placebo, in a randomized order.

Results: Codeine significantly increased the distal contractile integral (566 ± 81 mmHg∙s∙cm vs 247 ± 36 mmHg∙s∙cm, P = 0.001) and shortened distal latency (5.7 ± 0.2 seconds vs 6.5 ± 0.1 seconds, P < 0.001) for primary peristalsis compared with these parameters after placebo treatment. The mean total break length decreased significantly after codeine treatment compared with the length after placebo (P = 0.003). Codeine significantly increased esophagogastric junction-contractile integral (P = 0.028) but did not change the 4-second integrated relaxation pressure (P = 0.794). Codeine significantly decreased the frequency of weak (P = 0.039) and failed contractions (P = 0.009), resulting in increased frequency of normal primary peristalsis (P < 0.136). No significant differences in the ratio of impaired multiple rapid swallows inhibition and parameters of secondary peristalsis were detected.

Conclusions: In IEM patients, acute administration of codeine increases contraction vigor and reduces distal latency of primary esophageal peristalsis, but has no effect on secondary peristalsis. Future studies are required to further elucidate clinical relevance of these findings, especially in the setting of gastroesophageal reflux disease with IEM.

Background/aims: The incidence of eosinophilic esophagitis (EoE) has been increasing recently. The role of regulatory T cells (Tregs) and correlations with other inflammatory cells in EoE remain unknown. We aim to clarify the role of Tregs and their correlations with inflammatory cells in EoE patients.

Methods: Biopsies from controls and EoE patients before and after treatments were analyzed. Eosinophil infiltration was evaluated by hematoxylin and eosin staining. Immunohistochemical staining was performed to examine infiltration of T cells, Tregs, and mast cells. Gene expressions of chemokines were evaluated by reverse transcription-quantitative polymerase chain reaction.

Results: Tregs and mast cells were increased in the esophageal epithelial layers of EoE patients. After treatments, Tregs and mast cells were decreased when histologic remission was achieved. Infiltration of Tregs correlated significantly with numbers of eosinophils and mast cells. Filaggrin mRNA was decreased in patients with EoE before treatment and upregulated after treatment, even when histologic remission was not achieved.

Conclusions: Tregs were increased in esophageal epithelium of patients with EoE, and correlated with mast cell infiltration.

Background/aims: Eating is the major synchronizer of gastrointestinal motility and secretions. The present study aims to evaluate the interplay between self-perceived constipation severity (CS) and colonic response to eating in constipated patients according to the phenotype.

Methods: We included 387 consecutive outpatients complaining of Rome IV chronic idiopathic constipation. Likert scales for CS, abdominal pain severity, bloating severity, depression and anxiety assessment, total and segmental colonic transit time (CTT), and colonic transit response to eating (CTRE) were performed in all patients.

Results: Of the 387 patients included (49.7 ± 16.4 years), 320 (83%) were female, 203 had irritable bowel syndrome with constipation (IBS-C), 184 as functional constipation (FC), and 283 had defecation disorders (DD). The female gender was characterized by increased bloating severity (P = 0.011) and decreased Bristol stool form (P = 0.002). In IBS-C and FC patients, CS was related with bloating severity (P < 0.001 in both groups) and total CTT (P = 0.007 in IBS-constipation, P = 0.040 in FC). In IBS-C patients, CS was also associated with abdominal pain severity (P = 0.003) and Bristol stool form (P = 0.004). In contrast, in FC, CS was only related to left CTRE (P = 0.006), and in patients with DD, CS was associated with total CTT (P < 0.001) and left CTRE (P = 0.002).

Conclusion: Colonic transit response to eating was not associated to CS in IBS-C patients, but left CTRE was associated with constipation severity in FC and DD patients.