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Lipid treatment of inflammatory bowel disease.
Curr Opin Clin Nutr Metab Care 1999; 2(2):117-20CO

Abstract

The aetiology of inflammatory bowel disease remains unclear. Local mediators such as arachidonic acid metabolites and peptide mediators (cytokines) appear to contribute to the disease process. The successful administration of neutralizing antibodies against TNF-alpha has confirmed a pathophysiological role for this cytokine in Crohn's disease. Established therapy of inflammatory bowel disease with 5-aminosalicylic acid compounds has been shown to reduce local leukotriene B4 formation by inhibiting lipoxygenases. This therapeutic mechanism formed one rationale for examining the effect of n-3 fatty acids, which also inhibit leukotriene B4 formation, on the course of these diseases. In the first study, published in 1989, we found no beneficial effects of n-3 fatty acids in patients with Crohn's disease; however, there was clinical improvement, just falling short of significance, in patients with ulcerative colitis. Since then two uncontrolled and five controlled studies have further investigated the therapeutic effect of n-3 fatty acids in patients with ulcerative colitis. The size of the patient population in the controlled studies ranged from 10 to 96 patients in the largest study. Two of these studies showed a significant improvement in clinical activity and a steroid-sparing effect, respectively. Another study found only a trend towards improvement and one trial, which also included a treatment group receiving evening primrose oil, found no beneficial effect in the 16 patients receiving n-3 fatty acids. A large, 2 year trial of n-3 fatty acids in patients with ulcerative colitis off steroids, which was recently completed at the Universities of Munich and Mainz, showed a delay of the first episode of relapse, but no reduction in the cumulative relapse rate at 2 years. Controversial results have been published for Crohn's disease. A new enteric-coated formulation reportedly increased the proportion of patients in remission where as another trial using a conventional preparation found no significant effect.

Authors+Show Affiliations

Division of Clinical Pharmacology, Medizinische Klinik, Klinikum Innenstadt, University of Munich, Germany. stefanendres@lrz.uni-muenchen.deNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Review

Language

eng

PubMed ID

10453341

Citation

Endres, S, et al. "Lipid Treatment of Inflammatory Bowel Disease." Current Opinion in Clinical Nutrition and Metabolic Care, vol. 2, no. 2, 1999, pp. 117-20.
Endres S, Lorenz R, Loeschke K. Lipid treatment of inflammatory bowel disease. Curr Opin Clin Nutr Metab Care. 1999;2(2):117-20.
Endres, S., Lorenz, R., & Loeschke, K. (1999). Lipid treatment of inflammatory bowel disease. Current Opinion in Clinical Nutrition and Metabolic Care, 2(2), pp. 117-20.
Endres S, Lorenz R, Loeschke K. Lipid Treatment of Inflammatory Bowel Disease. Curr Opin Clin Nutr Metab Care. 1999;2(2):117-20. PubMed PMID: 10453341.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Lipid treatment of inflammatory bowel disease. AU - Endres,S, AU - Lorenz,R, AU - Loeschke,K, PY - 1999/8/24/pubmed PY - 1999/8/24/medline PY - 1999/8/24/entrez SP - 117 EP - 20 JF - Current opinion in clinical nutrition and metabolic care JO - Curr Opin Clin Nutr Metab Care VL - 2 IS - 2 N2 - The aetiology of inflammatory bowel disease remains unclear. Local mediators such as arachidonic acid metabolites and peptide mediators (cytokines) appear to contribute to the disease process. The successful administration of neutralizing antibodies against TNF-alpha has confirmed a pathophysiological role for this cytokine in Crohn's disease. Established therapy of inflammatory bowel disease with 5-aminosalicylic acid compounds has been shown to reduce local leukotriene B4 formation by inhibiting lipoxygenases. This therapeutic mechanism formed one rationale for examining the effect of n-3 fatty acids, which also inhibit leukotriene B4 formation, on the course of these diseases. In the first study, published in 1989, we found no beneficial effects of n-3 fatty acids in patients with Crohn's disease; however, there was clinical improvement, just falling short of significance, in patients with ulcerative colitis. Since then two uncontrolled and five controlled studies have further investigated the therapeutic effect of n-3 fatty acids in patients with ulcerative colitis. The size of the patient population in the controlled studies ranged from 10 to 96 patients in the largest study. Two of these studies showed a significant improvement in clinical activity and a steroid-sparing effect, respectively. Another study found only a trend towards improvement and one trial, which also included a treatment group receiving evening primrose oil, found no beneficial effect in the 16 patients receiving n-3 fatty acids. A large, 2 year trial of n-3 fatty acids in patients with ulcerative colitis off steroids, which was recently completed at the Universities of Munich and Mainz, showed a delay of the first episode of relapse, but no reduction in the cumulative relapse rate at 2 years. Controversial results have been published for Crohn's disease. A new enteric-coated formulation reportedly increased the proportion of patients in remission where as another trial using a conventional preparation found no significant effect. SN - 1363-1950 UR - https://www.unboundmedicine.com/medline/citation/10453341/Lipid_treatment_of_inflammatory_bowel_disease_ L2 - http://dx.doi.org/10.1097/00075197-199903000-00004 DB - PRIME DP - Unbound Medicine ER -