Journal of the Canadian Association of Gastroenterology最新文献

Background and aim: The history of colonization and its ongoing impact poses significant health disparities among Indigenous communities. We aimed to centre the voices and stories of Indigenous patients and family advocates (IPFAs-Indigenous patients living with inflammatory bowel disease [IBD] and family members of Indigenous individuals with IBD) engaged in patient-oriented research projects and who are part of the IBD among Indigenous Peoples Research Team (IBD-IPRT).

Methods: IPFAs and Indigenous and non-Indigenous researchers of the IBD-IPRT followed a storytelling research methodology to let IPFAs share their stories as research team members. Four IPFAs documented their experiences as IBD patients, advocates, and research partners. The stories were analyzed for themes. The identified themes were collaboratively verified with the IPFAs.

Results: The full stories shared by the IPFAs were transcribed and presented in this paper. Following a background analysis of themes in the 4 narratives, we were also able to identify 4 key themes that could be relevant to improving patient-oriented research initiatives: (1) health promotion, (2) leadership and voice, (3) community engagement, and (4) disease awareness and access to care. Trust building, strong relationships, and effective partnerships are core components for conducting patient-oriented research with Indigenous community members.

Conclusions: Indigenous patient engagement in health research is crucial to ensure that lived experiences, knowledge, and cultural values are adequately adopted to improve research outcomes. Centering IPFAs in IBD research can promote cultural awareness and actionable recommendations to improve health outcomes for individuals with IBD and their families and caregivers.

With the prevalence of inflammatory bowel diseases (IBD) continuing to rise in Canada and globally, developing improved therapeutics that successfully treat greater percentages of patients with reduced complications is paramount. A better understanding of pertinent immune pathways in IBD will improve our ability to both successfully dampen inflammation and promote gut healing, beyond just inhibiting specific immune proteins; success of combination therapies supports this approach. Interferons (IFNs) are key cytokines that protect mucosal barrier surfaces, and their roles in regulating gut homeostasis and inflammation differ between the three IFN families (type I, II, and III). Interestingly, the gut microbiota and microbial metabolites impact IFN-signaling, yet how this system is impacted in IBD remains unclear. In this review, we discuss the current knowledge of how gut microbiota directly or indirectly impact IFN levels/responses, and what is known about IFNs differentially regulating gut homeostasis and inflammation in animal models or patients with IBD.

Background: The rising incidence of inflammatory bowel diseases (IBD), including Crohn's disease (CD) and ulcerative colitis (UC), specifically in the developing world, suggests an important environmental effect. Amongst environmental influences, dietary factors, particularly the adoption of a westernized diet, have been specifically noticed. In contrast, the Mediterranean diet (MED), characterized by high intake of fruits, vegetables, whole grains, legumes, nuts, olive oil, and moderate consumption of animal and ultra processed foods, has shown potential positive effects in IBD.

Methods: Here we conducted a narrative review focusing on the evidence regarding the role of MED in IBD prevention and management.

Results: Epidemiological studies suggest inverse association of MED with CD development. Furthermore, adherence to MED has been associated with clinical improvement in active CD and maintenance of lower levels of inflammatory markers in UC, along with improved quality of life and lower mortality rates in IBD patients. Mechanistically, MED promotes a diverse and beneficial gut microbiota, possesses anti-inflammatory properties through polyphenols and dietary fats, and may modulate oxidative stress. In clinical practice, MED may be adapted to diverse disease phenotypes and cultural preferences, and is a sustainable, easy to maintain dietary approach.

Conclusion: Current evidence may support the integration of MED into clinical practice in IBD care. In future research, the efficacy of MED in specific IBD phenotypes should be assessed.

While the aetiology of inflammatory bowel disease (IBD) has been linked to genetic susceptibility coupled with environmental factors, the underlying molecular mechanisms remain unclear. Among the environmental factors, diet and the gut microbiota have been implicated as drivers of immune dysregulation in IBD. Indeed, epidemiologic studies have highlighted that the increase in incidence of IBD parallels the increase in dietary intake of omega-6 (n-6) polyunsaturated fatty acids (PUFAs) and the change in balance of intake of n-6 to n-3 fatty acids. Experimental evidence suggests that the increase in n-6 PUFA intake increases cell membrane arachidonic acid, which is accompanied by the production of pro-inflammatory mediators as well as increased oxidative stress; together, this contributes to the development of chronic inflammation. However, it is also increasingly clear that some of the n-6 PUFA-derived mediators exert beneficial effects depending on the settings and timing of ingestion. In contrast to n-6, when n-3 PUFA eicosapentaenoic acid and docosahexaenoic acid are incorporated into the cell membrane and are metabolized into less pro-inflammatory eicosanoids, as well as strong specialized pro-resolving mediators, which play a role in inflammation cessation. With a focus on preclinical models, we explore the relationship between dietary lipid, the gut microbiome, and intestinal inflammation.

Background: Interest in patient and public involvement in research has grown. Medical, health, and social care research has demonstrated several benefits of patient and public engagement, such as empowering user input and reducing attrition rates in clinical trials. To date, no study has reviewed patient engagement in inflammatory bowel disease (IBD). We aimed to describe the benefits, challenges, and best practices of patient engagement in IBD research.

Methods: We performed a systematic search on MEDLINE, EMBASE, and Cochrane for all clinical IBD research studies in which patients were involved in the research process (1946- 2023). Patient input was considered in: (1) study design, (2) study execution, (3) research dissemination, and/or (4) other domains not specified here. Two authors independently screened and extracted data on type of engaged person(s), format of engagement, author-reported benefits, recommendations, and challenges. For each study, we reported the level of patient engagement and study adherence to standardized reporting guidelines.

Results: After screening 9,355 articles, we included 51 for final analysis. IBD patients were most frequently engaged in study design. Patient engagement in IBD research improved recruitment rates and promoted the creation of user-friendly quality-of-life tools. Selection bias and recruitment difficulties were common challenges in the application of patient engagement. Authors recommended continuous patient involvement to address emerging priorities and cognitive interviewing to improve questionnaire clarity.

Conclusions: Patient engagement represents an important step in promoting patient-centred care. According to study authors, implementing cognitive interviewing techniques, continuous patient involvement, and standardized reporting guidelines may improve future iterations of engagement in IBD.

Functional dyspepsia (FD) is a highly prevalent disorder. Upper endoscopy is normal, and according to the Rome IV criteria, there is no established pathology. Data accumulated over the last 15 years has challenged the notion FD is free of relevant pathology, and in particular, increased duodenal eosinophils have been observed. Intestinal eosinophils play important roles in microbial defence, immune regulation, tissue regeneration and remodelling, and maintaining tissue homeostasis and metabolism; degranulation of eosinophils releases toxic granule products (e.g., major basic protein, eosinophil-derived neurotoxin) which can damage nerves. Normal cut-offs for eosinophil infiltration into the duodenum histologically are less than five eosinophils per high power field (<25 per five high power fields). In clinical practice there is evidence that pathologically increased intestinal eosinophils may often be overlooked. In a meta-analysis duodenal eosinophils were significantly increased in FD although there was substantial heterogeneity; degranulation of duodenal eosinophils was also significantly higher in FD without significant heterogeneity. In addition, increased duodenal permeability, systemic immune activation, and an altered mucosa-associated duodenal microbiome have been identified that may help explain why symptoms arise, often occur after food with exposure to food antigens, and typically fluctuate. Several potentially reversible risk factors for FD have now been identified. We evaluate the current evidence linking duodenal microinflammation and immune activation with FD and disorders of gut-brain interactions that overlap with FD. We propose a two-hit disease model for eosinophilic functional dyspepsia (EoFD) with management implications.