Canadian Association of Gastroenterology Clinical Practice Guideline for the Medical Management of Pediatric Luminal Crohn's Disease

Background & Aims: We aim to provide guidance for medical treatment of luminal Crohn's disease in children. Methods: We performed a systematic search of publication databases to identify studies of medical management of pediatric Crohn's disease. Quality of evidence and strength of recommendations were rated according to the GRADE (Grading of Recommendation Assessment, Development, and Evaluation) approach. We developed statements through an iterative online platform and then finalized and voted on them. Results: The consensus includes 25 statements focused on medical treatment options. Consensus was not reached, and no recommendations were made, for 14 additional statements, largely due to lack of evidence. The group suggested corticosteroid therapies (including budesonide for mild to moderate disease). The group suggested exclusive enteral nutrition for induction therapy and biologic tumor necrosis factor antagonists for induction and maintenance therapy at diagnosis or at early stages of severe disease, and for patients failed by steroid and immunosuppressant induction therapies. The group recommended against the use of oral 5-aminosalicylate for induction or maintenance therapy in patients with moderate disease, and recommended against thiopurines for induction therapy, corticosteroids for maintenance therapy, and cannabis in any role. The group was unable to clearly define the role of concomitant immunosuppressants during initiation therapy with a biologic agent, although thiopurine combinations are not recommended for male patients. No consensus was reached on the role of aminosalicylates in treatment of patients with mild disease, antibiotics or vedolizumab for induction or maintenance therapy, or methotrexate for induction therapy. Patients in clinical remission who are receiving immunomodulators should be assessed for mucosal healing within 1 year of treatment initiation. Conclusions: Evidence-based medical treatment of Crohn's disease in children is recommended, with thorough ongoing assessments to define treatment success

Dietary interventions for induction and maintenance of remission in inflammatory bowel disease

Background Inflammatory bowel disease (IBD), comprised of Crohn's disease (CD) and ulcerative colitis (UC), is characterized by chronic mucosal inflammation, frequent hospitalizations, adverse health economics, and compromised quality of life. Diet has been hypothesised to influence IBD activity. Objectives To evaluate the efficacy and safety of dietary interventions on IBD outcomes. Search methods We searched the Cochrane IBD Group Specialized Register, CENTRAL, MEDLINE, Embase, Web of Science, Clinicaltrials.gov and the WHO ICTRP from inception to 31 January 2019. We also scanned reference lists of included studies, relevant reviews and guidelines. Selection criteria We included randomized controlled trials (RCTs) that compared the effects of dietary manipulations to other diets in participants with IBD. Studies that exclusively focused on enteral nutrition, oral nutrient supplementation, medical foods, probiotics, and parenteral nutrition were excluded. Data collection and analysis Two review authors independently performed study selection, extracted data and assessed bias using the risk of bias tool. We conducted meta‐analyses where possible using a random‐effects model and calculated the risk ratio (RR) and corresponding 95% confidence interval (CI) for dichotomous outcomes. We assessed the certainty of evidence using GRADE. Main results The review included 18 RCTs with 1878 participants. The studies assessed different dietary interventions for active CD (six studies), inactive CD (seven studies), active UC (one study) and inactive UC (four studies). Dietary interventions involved either the consumption of low amounts or complete exclusion of one or more food groups known to trigger IBD symptoms. There was limited scope for data pooling as the interventions and control diets were diverse. The studies were mostly inadequately powered. Fourteen studies were rated as high risk of bias. The other studies were rated as unclear risk of bias. The effect of high fiber, low refined carbohydrates, low microparticle diet, low calcium diet, symptoms‐guided diet and highly restricted organic diet on clinical remission in active CD is uncertain. At 4 weeks, remission was induced in: 100% (4/4) of participants in the low refined carbohydrates diet group compared to 0% (0/3) of participants in the control group (RR 7.20, 95% CI 0.53 to 97.83; 7 participants; 1 study; very low certainty evidence). At 16 weeks, 44% (23/52) of participants in the low microparticle diet achieved clinical remission compared to 25% (13/51) of control‐group participants (RR 3.13, 95% CI 0.22 to 43.84; 103 participants; 2 studies; I² = 73%; very low certainty evidence). Fifty per cent (16/32) of participants in the symptoms‐guided diet group achieved clinical remission compared to 0% (0/19) of control group participants (RR 20.00, 95% CI 1.27 to 315.40; 51 participants ; 1 study; very low certainty evidence) (follow‐up unclear). At 24 weeks, 50% (4/8) of participants in the highly restricted organic diet achieved clinical remission compared to 50% (5/10) of participants in the control group (RR 1.00, 95% CI 0.39 to 2.53; 18 participants; 1 study; very low certainty evidence). At 16 weeks, 37% (16/43) participants following a low calcium diet achieved clinical remission compared to 30% (12/40) in the control group (RR 1.24, 95% CI 0.67 to 2.29; 83 participants; 1 study; very low certainty evidence). The effect of low refined carbohydrate diets, symptoms‐guided diets and low red processed meat diets on relapse in inactive CD is uncertain. At 12 to 24 months, 67% (176/264) of participants in low refined carbohydrate diet relapsed compared to 64% (193/303) in the control group (RR 1.04, 95% CI 0.87 to 1.25; 567 participants; 3 studies; I² = 35%; low certainty evidence). At 6 to 24 months, 48% (24/50) of participants in the symptoms‐guided diet group relapsed compared to 83% (40/48) participants in the control diet (RR 0.53, 95% CI 0.28 to 1.01; 98 participants ; 2 studies; I² = 54%; low certainty evidence). At 48 weeks, 66% (63/96) of participants in the low red and processed meat diet group relapsed compared to 63% (75/118) of the control group (RR 1.03, 95% CI 0.85 to 1.26; 214 participants; 1 study; low certainty evidence). At 12 months, 0% (0/16) of participants on an exclusion diet comprised of low disaccharides / grains / saturated fats / red and processed meat experienced clinical relapse compared to 26% (10/38) of participants on a control group (RR 0.11, 95% CI 0.01 to 1.76; 54 participants; 1 study; very low certainty evidence). The effect of a symptoms‐guided diet on clinical remission in active UC is uncertain. At six weeks, 36% (4/11) of symptoms‐guided diet participants achieved remission compared to 0% (0/10) of usual diet participants (RR 8.25, 95% CI 0.50 to 136.33; 21 participants; 1 study; very low certainty evidence). The effect of the Alberta‐based anti‐inflammatory diet, the Carrageenan‐free diet or milk‐free diet on relapse rates in inactive UC is uncertain. At 6 months, 36% (5/14) of participants in the Alberta‐based anti‐inflammatory diet group relapsed compared to 29% (4/14) of participants in the control group (RR 1.25, 95% CI 0.42 to 3.70; 28 participants; 1 study; very low certainty evidence). Thirty per cent (3/10) of participants following the carrageenan‐free diet for 12 months relapsed compared to 60% (3/5) of the participants in the control group (RR 0.50, 95% CI 0.15 to 1.64; 15 participants; 1 study; very low certainty evidence). At 12 months, 59% (23/39) of milk free diet participants relapsed compared to 68% (26/38) of control diet participants (RR 0.83, 95% CI 0.60 to 1.15; 77 participants; 2 studies; I² = 0%; low certainty evidence). None of the included studies reported on diet‐related adverse events

The role of diet in the aetiopathogenesis of inflammatory bowel disease

Crohn’s disease and ulcerative colitis, collectively known as IBD, are chronic inflammatory disorders of the gastrointestinal tract. Although the aetiopathogenesis of IBD is largely unknown, it is widely thought that diet has a crucial role in the development and progression of IBD. Indeed, epidemiological and genetic association studies have identified a number of promising dietary and genetic risk factors for IBD. These preliminary studies have led to major interest in investigating the complex interaction between diet, host genetics, the gut microbiota and immune function in the pathogenesis of IBD. In this Review, we discuss the recent epidemiological, gene–environment interaction, microbiome and animal studies that have explored the relationship between diet and the risk of IBD. In addition, we highlight the limitations of these prior studies, in part by explaining their contradictory findings, and review future directions

Environmental risk factors in Crohn's disease and ulcerative colitis: an update.

International audienceRapid increase in Crohn's disease (CD) and ulcerative colitis (UC) incidence in developed countries, occurrence of CD in spouses and lack of complete concordance in monozygotic twins are strong arguments for the role of environmental factors in inflammatory bowel disease (IBD). Only two environmental factors have an established role in IBD. Smoking is a risk factor for CD and a protective factor for UC; appendectomy is a protective factor for UC. Many other environmental factors for IBD have been investigated. These are infectious agents, diet, drugs, stress and socio-economic factors. They are detailed in this paper. Among them, adherent invasive E. coli, infectious gastroenteritis, oral contraceptives and antibiotics could play a role in CD. To date, three theories integrate environmental factors to pathogenesis of IBD: hygiene, infection and cold chain. Much work remains to be done to identify risk factors for IBD. As exemplified by smoking, research of environmental risk factors of IBD is useful since it may lead to an improved disease course among patients and perhaps, to appropriate prevention among predisposed subjects. Further studies in this field are eagerly awaited

Propriedades mecânicas, tribológicas e térmicas de nanocompósitos de PLLA com nanotubos de carbono de paredes múltiplas

Neste trabalho são estudados os efeitos da adição de nanotubos de carbono de parede múltipla (NCPM) em uma matriz de Poli(L-ácido láctico) (PLLA). Foras avaliadas duas rotas distintas de dispersão dos NCPM, uma utilizando agitação mecânica em solvente e a outra utilizando sonificação de alta energia em solvente. As propriedades mecânicas destes nanocompósitos foram avaliadas utilizando nanoindentação e microdureza vickers. Através da calorimetria exploratória diferencial foram determinadas as propriedades térmicas dos nanocompósitos (Tg, Tc, Tm e cristalinidade) obtidas. Por último, as propriedades tribológicas foram determinadas através de ensaios de deslizamento do tipo pino sobre disco, onde foram utilizadas diferentes cargas normais. As propriedades mecânicas e térmicas não foram significativamente afetadas pela adição do nanotubos, o que não se repetiu nas propriedades tribológicas, onde tanto o método de dispersão quanto a concentração de NCPM afetaram as propriedades. A micrografia das trilhas de desgaste sugere ainda que o mecanismo atuante foi modificado com a incorporação dos nanotubos, o mesmo pode ter acontecido nas amostras sonificadas

Meat intake is associated with a higher risk of ulcerative colitis in a large European prospective cohort study.

BACKGROUND AND AIMS: We aimed to investigate the association between protein intake and risk of inflammatory bowel disease (IBD) in the European Prospective Investigation into Cancer and Nutrition. METHODS: 413 593 participants from eight European countries were included. Dietary data were collected at baseline from validated food frequency questionnaires. Dietary data were calibrated to correct errors of measures related to each country-specific questionnaire. Associations between proteins (total, animal, and vegetable) or food sources of animal proteins, and IBD risk were estimated by Cox proportional hazard models. RESULTS: After a mean follow-up of 16 years, 177 patients with Crohn's disease (CD) and 418 with ulcerative colitis (UC), were identified. There was no association between total protein, animal, or vegetable protein intakes and CD or UC risks. Total meat and red meat intakes were associated with UC risk (HR for the 4 thvs. 1 st quartile = 1.40; 95% CI = 0.99-1.98; P-trend = 0.01; and 1.61; 95% CI = 1.10-2.36, P-trend = 0.007, respectively). There was no association between other food sources of animal protein (processed meat, fish, shellfish, eggs, poultry) and UC. We found no association between food sources of animal proteins and CD risk. CONCLUSION: Meat and red meat consumptions are associated with higher risks of UC. These results support dietary counseling of low meat intake in people at high-risk of IBD

Meat Intake Is Associated with a Higher Risk of Ulcerative Colitis in a Large European Prospective Cohort Studyø

BACKGROUND AND AIMS: We aimed to investigate the association between protein intake and risk of inflammatory bowel disease [IBD] in the European Prospective Investigation into Cancer and Nutrition. METHODS: A total of 413 593 participants from eight European countries were included. Dietary data were collected at baseline from validated food frequency questionnaires. Dietary data were calibrated to correct errors in measures related to each country-specific questionnaire. Associations between proteins [total, animal, and vegetable] or food sources of animal proteins, and IBD risk were estimated by Cox proportional hazard models. RESULTS: After a mean follow-up of 16 years, 177 patients with Crohn's disease [CD] and 418 with ulcerative colitis [UC], were identified. There was no association between total protein, animal protein, or vegetable protein intakes and CD or UC risks. Total meat and red meat intakes were associated with UC risk (hazard ratio [HR] for the 4th vs 1st quartile = 1.40, 95% confidence interval [CI] = 0.99-1.98, p-trend = 0.01; and 1.61, 95% CI = 1.10-2.36, p-trend = 0.007, respectively]. There was no association between other food sources of animal protein [processed meat, fish, shellfish, eggs, poultry] and UC. We found no association between food sources of animal proteins and CD risk. CONCLUSIONS: Meat and red meat consumptions are associated with higher risks of UC. These results support dietary counselling of low meat intake in people at high-risk of IBD