RESUMO
Until recently, diet as a therapeutic tool to treat inflammatory bowel disease (IBD) has not been proven effective. Nearly a century in the making we are in the grips of a revolution in diet therapies for IBD, driven by emerging data revealing diet as a key environmental factor associated with IBD susceptibility, and observational studies suggesting that dietary intake may play a role in the disease course of established IBD. This review summarizes the current evidence for diets trialed as induction and maintenance therapy for IBD. For Crohn's disease, exclusive enteral nutrition and the Crohn's disease exclusion diet with partial enteral nutrition are supported by emerging high-quality evidence as induction therapy, but are short-term approaches that are not feasible for prolonged use. Data on diet as maintenance therapy for Crohn's disease are conflicting, with some studies supporting fortification, and others suppression, of certain food components. For ulcerative colitis, data are not as robust for diet as induction and maintenance therapy; however, consistent themes are emerging, suggesting benefits for diets that are plant-based, high in fiber and low in animal protein. Further studies for both Crohn's disease and ulcerative colitis are eagerly awaited, which will allow specific recommendations to be made. Until this time, recommendations default to population based healthy eating guidelines.
RESUMO
BACKGROUND: Exclusive enteral nutrition (EEN) induces remission and mucosal healing in patients with Crohn's disease, but the mechanism of action remains unknown. AIM: To outline current understanding of the mechanisms of action of EEN. METHODS: From a comprehensive literature search, published data were critically examined in a narrative review. RESULTS: Multiple potential mechanisms of action have been identified. EEN optimises nutritional status. Differences in gut microbiota in terms of overall diversity and taxonomic community structure are observed between responders and non-responders to EEN. Therapy with EEN alters microbial metabolites (including faecal short-chain fatty acids, amino acids, branched-chain amino acids and sulphide) and faecal pH. Epithelial effects and restoration of barrier function, as well as changes in mucosal cytokine profiles and T-cell subsets are observed in responders to EEN. The impact of inclusion or exclusion of specific dietary components may be of importance, but putative detrimental components are found in many formulas. A major challenge in interpreting these findings is that they often contradict or change in opposite directions to what is considered 'beneficial'. It is difficult to differentiate between the observations following EEN being driven by EEN per se and those associated with resolving inflammation. CONCLUSIONS: The mechanisms of action of EEN are likely to involve a complex interplay between host mucosal immune response and luminal environment, but the identity of key factors remains poorly understood. A better definition of pathogenic factors may aid in developing more targeted dietary treatment and provide insights into the pathogenesis of Crohn's disease.
Assuntos
Doença de Crohn , Humanos , Doença de Crohn/terapia , Nutrição Enteral , Fezes , Mucosa , Dieta , Indução de RemissãoRESUMO
Objective: To evaluate clinical outcomes, patterns of use, tolerance and nutritional outcomes of exclusive enteral nutrition (EEN) in adults with Crohn's disease and to compare initiation in the inpatient compared with ambulatory care setting. Design/method: Adults with Crohn's disease who received EEN at a single centre over 2.5 years were identified and outcomes assessed via examination of patient records. Results: EEN was initiated in 60 patients (23 as an outpatient) who had objective evidence of active disease. Of 49 in whom the goal was induction of remission, 28 completed EEN and 24 achieved clinical remission/response. Twenty-one withdrew prematurely, due to intolerance in 15 and disease factors in 6. Of 11 with a planned intervention, 6 fulfilled the goal of downstaging disease while two were intolerant. Completion of the prescribed therapy was associated with self-reported adherence to EEN and with improvements in disease activity scores and biochemical markers. Malnutrition halved (40% to 20%) and intentional weight loss (median 5.1 kg) was achieved in six obese patients. The major reason for intolerance was the inability to accept total avoidance of non-formula food. There were no differences in any outcomes according to the location of initiation of therapy. Conclusion: Positive outcomes occur in 70% of adult patients with Crohn's disease tolerating EEN and 81% in those who are able to completely adhere to EEN, without compromise of nutritional status. Similar success occurs when initiated as an inpatient or outpatient. Failure to tolerate EEN is the major hurdle to its use.
RESUMO
Historically, dietitians played a minor part in the management of inflammatory bowel disease (IBD), including Crohn's disease and ulcerative colitis. Patients were commonly referred for consequences of uncontrolled disease, such as malnutrition and bowel obstruction risk. Today, dietitians are fundamental members of the multidisciplinary IBD team, from educating on the role of diet at diagnosis and throughout the lifespan of a patient with IBD to guiding primary induction therapy. This aspect is reflected in published guidelines for IBD management, which previously placed diet as only a minor factor, but now have diet-specific publications. This Review describes a four-step approach in a dietitian's assessment and management of diet in patients with IBD: (1) identifying and correcting nutritional gaps and dietary imbalances; (2) considering diet to treat active disease with the use of exclusive enteral nutrition (EEN) or emerging diets that could replace EEN; (3) using therapeutic diets to control existing complications of IBD, such as reduced fibre to prevent bowel obstruction in stricturing disease or a fermentable oligosaccharides, disaccharides, monosaccharides and polyols diet to manage co-existing functional gut symptoms; and (4) considering the role of diet in preventing IBD development in high-risk populations.