ABSTRACT Hypermobility spectrum disorders (HSD) and hypermobility Ehlers–Danlos syndrome (hEDS) are frequently associated with gastrointestinal symptoms, although the underlying mechanisms remain unclear. This study aimed to compare antroduodenal motility in patients with and without HSD/hEDS. We included 239 patients (50 HSD/hEDS and 189 non‐HSD/hEDS) with gastrointestinal symptoms undergoing antroduodenal manometry (ADM). The prevalence of antroduodenal dysmotility was not different between both groups, but enteric dysmotility was less common in the HSD/hEDS group (13% vs. 34%, p = 0.006). Delayed gastric emptying rates were similar, suggesting that delayed gastric emptying is more relevant for patients with HSD/hEDS and gastrointestinal symptoms.

This article is linked to Aliu et al papers. To view these articles, visit https://doi.org/10.1111/apt.17988 and https://doi.org/10.1111/apt.18161

BACKGROUND Gastric peroral endoscopic pyloromyotomy (G-POEM) is a promising therapeutic modality for refractory gastroparesis (GP). However, as characteristics of suitable patients for G-POEM remain unclear, antro-duodenal manometry (ADM) has been suggested to provide objective parameters for patient selection. The aim of the present study was to identify ADM parameters as predictors for treatment response after G-POEM in refractory GP. METHODS Refractory GP patients who underwent a G-POEM between 2017 and 2022 were included. The following ADM parameters were mainly scored: antral hypomotility, pylorospasm, and the presence of neuropathic enteric patterns. Treatment response was defined as a GCSI-score decrease of ≥1 point 12 months after G-POEM. Explorative analyses were performed on potential predictors of response using logistic regression analysis. KEY RESULTS Sixty patients (52 women, mean age 52 ± 14 years.) with refractory GP (33 idiopathic, 16 diabetic, 11 postsurgical) were included. Clinical response data were available for 52 patients. In 8 out of 60 patients, it was not feasible to advance the catheter beyond the pylorus. Abnormal ADM was found in 46/60 patients (77%). Antral hypomotility and pylorospasm were found in respectively 33% and 12% of patients. At least one neuropathic enteric dysmotility pattern was found in 58% of patients. No differences were found when comparing baseline ADM parameters between clinical response groups at 12 months follow-up. Following explorative analyses, no ADM parameters were identified to predict clinical response 12 months after G-POEM. CONCLUSIONS AND INFERENCES No ADM parameters were identified as predictors of clinical response after G-POEM in refractory GP patients. Additionally, a high percentage of abnormal ADM tracings was found, in particular with relation to enteric dysmotility, while only a low percentage of patients showed antral hypomotility or pylorospasm.

This article is linked to Aliu et al papers. To view these articles, visit https://doi.org/10.1111/apt.17988 and https://doi.org/10.1111/apt.18027.

OBJECTIVE To investigate the biological mechanisms underlying the associations of psychological stress and intestinal inflammation in inflammatory bowel disease (IBD). DESIGN Experimental mouse models and large human cohorts have been used. METHOD Consecutive mouse models with chemically induced colitis were used to investigate biological pathways though which psychological stress leads to gut inflammation. These results were validated in three human cohorts with patients with IBD. RESULTS Stress induced elevated levels of glucocorticoids drive the generation of an inflammatory subset of enteric glia cells. These enteric glia cells produce the protein CSF1, that promotes monocyte accumulation in the intestinal mucosa and TNF-mediated intestinal inflammation. CONCLUSION A pivotal role for the enteric nervous system (ENS) has been discovered in mediating the aggravating effect of psychological stress on intestinal inflammation.

Persistent gastrointestinal symptoms are prevalent in adult patients with inflammatory bowel disease (IBD), even when endoscopic remission is reached. These symptoms can have profound negative effects on the quality of life of affected patients and can be difficult to treat. They may be caused by IBD‐related complications or comorbid disorders, but they can also be explained by irritable bowel syndrome (IBS)‐like symptoms.

This article is linked to Janssen et al papers. To view these articles, visit https://doi.org/10.1111/apt.17718 and https://doi.org/10.1111/apt.17745