肠内营养治疗在炎症性肠病中的应用
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摘要
炎症性肠病(inflammatory bowel disease, IBD)是一类病因尚未完全明确的慢性非特异性肠道炎症性疾病。近年来,基础与临床研究进展揭示了膳食在IBD发病机制中的重要作用,其主要通过影响肠道黏膜免疫系统与菌群增加IBD易感性。营养不良是IBD患者常见的临床表现,而饮食疗法,尤其是肠内营养支持治疗可诱导和维持缓解、有效改善患者营养状况,在IBD的治疗中具有重要意义。不合理的膳食结构常是引起疾病复发的重要因素,因此需适时和恰当地应用肠内营养,进行个体化治疗。
Inflammatory bowel disease(IBD) is a group of chronic disorders, whose etiology has not yet been fully elucidated. The mucosal immune system and the microbiota in the intestinal tract have been implicated in the pathogenesis of IBD, and both of these can be influenced by diet. Recent advances in basic and clinical science have demonstrated that diet plays a key role in the pathogenesis of IBD. Malnutrition is one the main clinical manifestations of IBD, and dietary therapies such as enteral nutrition has demonstrated efficacy for induction and maintenance of remission, as well as improvement in nutritional status. It is widely accepted that nutritional support therapy is an essential treatment for IBD, however, certain foods might increase the likelihood of a flare, therefore, timely and appropriate use of individualized enteral nutrition therapy is needed.
Inflammatory bowel disease(IBD) is a group of chronic disorders, whose etiology has not yet been fully elucidated. The mucosal immune system and the microbiota in the intestinal tract have been implicated in the pathogenesis of IBD, and both of these can be influenced by diet. Recent advances in basic and clinical science have demonstrated that diet plays a key role in the pathogenesis of IBD. Malnutrition is one the main clinical manifestations of IBD, and dietary therapies such as enteral nutrition has demonstrated efficacy for induction and maintenance of remission, as well as improvement in nutritional status. It is widely accepted that nutritional support therapy is an essential treatment for IBD, however, certain foods might increase the likelihood of a flare, therefore, timely and appropriate use of individualized enteral nutrition therapy is needed.
引文
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[33] Johnson T, Macdonald S,Hill S M,et al. Treatment of active Crohn's disease in children using partial enteral nutrition with liquid formula:a randomised controlled trial[J]. Gut,2006,55(3):356-361.
[34] González-Huix F,Fernández-Baftares F, Esteve-Comas M,et al.Enteral versus parenteral nutrition as adjunct therapy in acute ulcerative colitis[J]. Am J Gastroenterol, 1993,88(2):227-232.
[35] Hanai H,Iida T,Takeuchi K,et al. Nutritional therapy versus 6-mercaptopurine as maintenance therapy in patients with Crohn's disease[J]. Dig Liver Dis,2012,44(8):649-654.
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[37] Papada E, Kaliora A C, Gioxari A, et al. Anti-inflammatory effect of elemental diets with different fat composition in experimental colitis[J].Br J Nutr,2014,111(7):1213-1220.
[38] Kono H,Fujii H,Ogiku M,et al. Enteral diets enriched with medium-chain triglycerides and N-3 fatty acids prevent chemically induced experimental colitis in rats[J]. Transl Res,2010,156(5):282-291.
[39] Singh V,Yeoh B S, Walker R E,et al. Microbiota fermentationNLRP3 axis shapes the impact of dietary fibres on intestinal inflammation[J]. Gut,2019. DOI:10.1136/gutjnl-2018-316250.
[2] Huang H,Fang M, Jostins L, et al. Fine-mapping inflammatory bowel disease loci to single-variant resolution[J]. Nature,2017,547(7662):173-178.
[3] Peters L A,Perrigoue J,Mortha A,et al. A functional genomics predictive network model identifies regulators of inflammatory bowel disease[J]. Nat Genet,2017,49(10):1437-1449.
[4] Ananthakrishnan A N,Khalili H,Konijeti G G,et al. A prospective study of long-term intake of dietary fiber and risk of Crohn's disease and ulcerative colitis[J]. Gastroenterology, 2013, 145(5):970-977.
[5] Racine A,Carbonnel F,Chan S S,et al. Dietary patterns and risk of inflammatory bowel disease in Europe:results from the EPIC study[J]. Inflamm Bowel Dis,2016,22(2):345-354.
[6] Ananthakrishnan A N,Khalili H,Konijeti G G,et al. Long-term intake of dietary fat and risk of ulcerative colitis and Crohn's disease[J].Gut,2014,63(5):776-784.
[7] Wallace J L,Vong L,McKnight W,et al. Endogenous and exogenous hydrogen sulfide promotes resolution of colitis in rats[J].Gastroenterology,2009,137(2):569-578.
[8] Werner T, Wagner S J,Martinez I,et al. Depletion of luminal iron alters the gut microbiota and prevents Crohn's disease-like ileitis[J]. Gut,2011,60(3):325-333.
[9] Ananthakrishnan A N,Khalili H,Song M,et al. Zinc intake and risk of Crohn's disease and ulcerative colitis:a prospective cohort study[J]. Int J Epidemiol,2015,44(6):1995-2005.
[10] Lewis J D,Abreu M T. Diet as a trigger or therapy for inflammatory bowel diseases[J]. Gastroenterology, 2017, 152(2):398-414.
[11] Gassull M A,Cabr6 E. Nutrition in inflammatory bowel disease[J]. Curr Opin Clin Nutr Metab Care,2001,4(6):561-569.
[12] Wu S,Zhang Y G,Lu R,et al. Intestinal epithelial vitamin D receptor deletion leads to defective autophagy in colitis[J]. Gut,2015,64(7):1082-1094.
[13] Reich K M,Fedorak R N,Madsen K,et al. Vitamin D improves inflammatory bowel disease outcomes:basic science and clinical review[J]. World J Gastroenterol,2014,20(17):4934-4947.
[14] Zhang H,Wu H,Liu L,et al. 1,25-dihydroxyvitamin D_3 regulates the development of chronic colitis by modulating both T helper(Th)1and Th17 activation[J].APMIS,2015,123(6):490-501.
[15] Xiao S,Jin H,Liu S,et al. Retinoic acid increases Foxp3'regulatory T cells and inhibits development of Th17 cells by enhancing TGF-β-driven Smad3 signaling and inhibiting IL-6 and IL-23 receptor expression[J]. J Immunol, 2008, 181(4):2277-2284.
[16] Mielke L A,Jones S A,Raverdeau M,et al. Retinoic acid expression associates with enhanced IL-22 production byγδT cells and innate lymphoid cells and attenuation of intestinal inflammation[J]. J Exp Med,2013,210(6):1117-1124.
[17] Reinisch W,Staun M,Bhandari S,et al. State of the iron:how to diagnose and efficiently treat iron deficiency anemia in inflammatory bowel disease[J]. J Crohns Colitis,2013,7(6);429-440.
[18] Bergamaschi G,Di Sabatino A,Albertini R,et al. Prevalence and pathogenesis of anemia in inflammatory bowel disease. Influence of anti-tumor necrosis factor-alpha treatment[J]. Haematologica,2010,95(2):199-205.
[19] Jowett S L,Seal C J,Pearce M S,et al. Influence of dietary factors on the clinical course of ulcerative colitis:a prospective cohort study[J].Gut,2004,53(10):1479-1484.
[20] Tanaka M,Iwao Y,Sasaki S,et al. Moderate dietary temperance effectively prevents relapse of Crohn disease:a prospective study of patients in remission[J]. Gastroenterol Nurs,2007,30(3):202-210.
[21] Guerreiro C S,Ferreira P,Tavares L,et al. Fatty acids,IL6,and TNFa polymorphisms:an example of nutrigenetics in Crohn's disease[J]. Am J Gastroenterol,2009,104(9):2241-2249.
[22] Ferreira P,Cravo M, Guerreiro C S,et al. Fat intake interacts with polymorphisms of Caspase9, FasLigand and PPARgamma apoptotic genes in modulating Crohn's disease activity[J]. Clin Nutr,2010,29(6):819-823.
[23] Reifen R,Matas Z,Zeidel L,et al. Iron supplementation may aggravate inflammatory status of colitis in a rat model[J]. Dig Dis Sci,2000,45(2):394-397.
[24] van der Logt E M,Blokzijl T,van der Meer R,et al. Westernized high-fat diet accelerates weight loss in dextran sulfate sodium-induced colitis in mice, which is further aggravated by supplementation of heme[J]. J Nutr Biochem,2013,24(6):1159-1165.
[25] de Silva A D,Tsironi E,Feakins R M,et al. Efficacy and tolerability of oral iron therapy ininflammatory bowel disease:a prospective, comparative trial[J]. Aliment Pharmacol Ther,2005,22(11-12):1097-1105.
[26] Lewis J, Chen E, Baldassano R, et al. Inflammation,antibiotics, and diet as environmental stressors of the gut microbiome in pediatric Crohn's disease[J]. Cell Host&Microbe,2015,18(4):489-500.
[27] Lee D,Baldassano R N,Otley A R,et al. Comparative effective-ness of nutritional and biological therapy in North American children with active Crohn's disease[J]. Inflamm Bowel Dis,2015,21(8):1786-1793.
[28] Levine A,Turner D,Pfeffer Gik T,et al. Comparison of outcomes parameters for induction of remission in new onset pediatric Crohn's disease:evaluation of the porto IBD group"growth relapse and outcomes with therapy"(GROWTH CD)study[J]. Inflamm Bowel Dis,2014,20(2):278-285.
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[30] Cohen-Dolev N,Sladek M, Hussey S,et al. Differences in outcomes over time with exclusive enteral nutrition compared with steroids in children with mild to moderate Crohn's disease:results from the GROWTH CD study[J]. J Crohns Colitis, 2018,12(3):306-312.
[31] Grover Z, Burgess C,Muir R,et al. Early mucosal healing with exclusive enteral nutrition is associated with improved outcomes in newly diagnosed children with luminal Crohn's disease[J]. J Crohns Colitis,2016,10(10):1159-1164.
[32] Ruemmele F M,Veres G,Kolho K L,et al. Consensus guidelines of ECCO/ESPGHAN on the medical management of pediatric Crohn's disease[J]. J Crohns Colitis,2014,8(10):1179-1207.
[33] Johnson T, Macdonald S,Hill S M,et al. Treatment of active Crohn's disease in children using partial enteral nutrition with liquid formula:a randomised controlled trial[J]. Gut,2006,55(3):356-361.
[34] González-Huix F,Fernández-Baftares F, Esteve-Comas M,et al.Enteral versus parenteral nutrition as adjunct therapy in acute ulcerative colitis[J]. Am J Gastroenterol, 1993,88(2):227-232.
[35] Hanai H,Iida T,Takeuchi K,et al. Nutritional therapy versus 6-mercaptopurine as maintenance therapy in patients with Crohn's disease[J]. Dig Liver Dis,2012,44(8):649-654.
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[37] Papada E, Kaliora A C, Gioxari A, et al. Anti-inflammatory effect of elemental diets with different fat composition in experimental colitis[J].Br J Nutr,2014,111(7):1213-1220.
[38] Kono H,Fujii H,Ogiku M,et al. Enteral diets enriched with medium-chain triglycerides and N-3 fatty acids prevent chemically induced experimental colitis in rats[J]. Transl Res,2010,156(5):282-291.
[39] Singh V,Yeoh B S, Walker R E,et al. Microbiota fermentationNLRP3 axis shapes the impact of dietary fibres on intestinal inflammation[J]. Gut,2019. DOI:10.1136/gutjnl-2018-316250.