NUTRITIONAL SUPPORT IN INFLAMMATORY BOWEL-DISEASE - CURRENT STATUS AND FUTURE-DIRECTIONS

被引:14
作者
GREENBERG, GR [1 ]
机构
[1] UNIV TORONTO,DEPT MED,TORONTO M5S 1A1,ONTARIO,CANADA
关键词
ENTERAL NUTRITION; INFLAMMATORY BOWEL DISEASE; PARENTERAL NUTRITION;
D O I
10.3109/00365529209095991
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
Malnutrition is a frequent occurrence in patients with acute inflammatory bowel disease. Total nutritional support provided either parentally (TPN) or enterally (TEN) has been advocated not only as an adjunct for improving nutrition but also as primary therapy. For patients with acute Crohn's disease, short-term rates of remission after TEN are equivalent to TPN. Coupled with certain advantages when compared with TPN, including simpler administration, fewer side effects, and preservation of the intestinal mucosal barrier, TEN may therefore be the preferred route for nutrient delivery. Controlled trials indicate equivalent or superior efficacy when enteral polymeric diets are compared with elemental diets for inducing remission in acute Crohn's disease. Moreover, when provided as an elemental diet, TEN is as effective as corticosteroids for achieving remission in acute Crohn's disease, but corticosteroids appear to be more effective than polymeric diets. Although the provision of nutritional support rather than bowel rest is the major factor contributing to symptomatic improvement, the optimal nutrient composition and the precise mechanisms whereby nutritional support achieves clinical remission remain to be clarified. In contrast to Crohn's disease, nutritional support is not effective for achieving remission in patients with ulcerative colitis. Thus, enteral nutritional support is an effective therapy for the short-term management of acute Crohn's disease. Whether long-term remission is equivalent to treatment with drugs or surgery requires prospective evaluation. Future avenues of investigation also include defining the optimal nutrient composition and the underlying mechanisms that achieve maximal nutritional repletion, promote mucosal cell renewal, and potentially directly retard production of inflammatory mediators.
引用
收藏
页码:117 / 122
页数:6
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