Burke A, Lichtenstein G R, Rombeau J L
Department of Medicine, Hospital of the University of Pennsylvania, Philadelphia 19104, USA.
Baillieres Clin Gastroenterol. 1997 Mar;11(1):153-74. doi: 10.1016/s0950-3528(97)90059-2.
The role of diet in the aetiology and pathogenesis of ulcerative colitis (UC) remains uncertain. Impaired utilization by colonocytes of butyrate, a product of bacterial fermentation of dietary carbohydrates escaping digestion, may be important. Sulphur-fermenting bacteria may be involved in this impaired utilization. Oxidative stress probably mediates tissue injury but is probably not of causative importance. Patients with UC are prone to malnutrition and its detrimental effects. However, there is no role for total parenteral nutrition and bowel rest as primary therapy for UC. The maintenance of adequate nutrition is very important, particularly in the peri-operative patient. In the absence of massive bleeding, perforation, toxic megacolon or obstruction, enteral rather than parenteral nutrition should be the mode of choice. Nutrients may be beneficial as adjuvant therapy. Butyrate enemas have improved patients with otherwise recalcitrant distal colitis in small studies. Non-cellulose fibre supplements are of benefit in rats with experimental colitis. Eicosapentaenoic acid in fish oil has a steroid-sparing effect which, although modest, is important, particularly in terms of reducing the risk of osteoporosis, but it seems to have no role in the patient with inactive disease. gamma-Linolenic acid and anti-oxidants also are showing promise. Nutrients may also modify the increased risk of colorectal carcinoma. Oxidative stress can damage tissue DNA but there are no data published at present on possible protection from oral anti-oxidants. Butyrate protects against experimental carcinogenesis in rats with experimental colitis. Folate supplementation is weakly associated with decreased incidence of cancer in UC patients when assessed retrospectively. Vigilance should be maintained for increased micronutrient requirements and supplements given as appropriate. Calcium and low-dose vitamin D should be given to patients on long-term steroids and folate to those on sulphasalazine.
饮食在溃疡性结肠炎(UC)病因学和发病机制中的作用仍不明确。结肠细胞对丁酸盐(一种未被消化的膳食碳水化合物经细菌发酵产生的产物)利用受损可能很重要。硫发酵细菌可能参与了这种利用受损过程。氧化应激可能介导组织损伤,但可能并非病因学上的关键因素。UC患者易于出现营养不良及其有害影响。然而,全肠外营养和肠道休息作为UC的主要治疗方法并无作用。维持充足营养非常重要,尤其是对于围手术期患者。在没有大量出血、穿孔、中毒性巨结肠或梗阻的情况下,肠内营养而非肠外营养应作为首选方式。营养物质作为辅助治疗可能有益。在小型研究中,丁酸盐灌肠改善了患有其他方面顽固的远端结肠炎的患者。非纤维素纤维补充剂对实验性结肠炎大鼠有益。鱼油中的二十碳五烯酸具有激素节省作用,尽管作用适度,但很重要,特别是在降低骨质疏松风险方面,但它似乎对无活动期疾病的患者没有作用。γ-亚麻酸和抗氧化剂也显示出前景。营养物质还可能改变结直肠癌风险增加的情况。氧化应激可损伤组织DNA,但目前尚无关于口服抗氧化剂可能提供保护的数据。丁酸盐可预防实验性结肠炎大鼠的实验性致癌作用。回顾性评估时,补充叶酸与UC患者癌症发病率降低弱相关。应警惕微量营养素需求增加,并适当给予补充剂。长期使用类固醇的患者应给予钙和低剂量维生素D,服用柳氮磺胺吡啶的患者应给予叶酸。