title: Distal procto-colitis, natural cytotoxicity, and essential fatty acids.
abstract: OBJECTIVE
  Recently, it has been postulated that patients with ulcerative colitis have altered natural cytotoxicity, in particular natural killer (NK) and lymphokine-activated killer (LAK) cell activities. These cellular mechanisms have been postulated to play an etiological role in the pathogenesis of the disease process. We have shown previously that the essential fatty acids (EFA) eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) specifically inhibit natural cytotoxicity. Our aim was to evaluate the role of omega-3 EFA in the modulation of natural cytotoxicity and disease activity in patients with distal procto-colitis.
  
  
  METHODS
  In this pilot study patients were randomized into two groups. Each patient received either fish oil extract (EPA, 3.2 g, and DHA, 2.4 g) (n = 9) or sunflower oil (placebo) (n = 9) daily in a double-blind manner for 6 months. Monthly assessments of disease activity (clinical and sigmoidoscopic scores) and histological evaluation of mucosal biopsies were carried out. Also, the circulating levels and activities of NK and LAK cells, using flow cytometric analysis (CD16+ CD56+) and in vitro 51 chromium release assays (K562), respectively, were monitored.
  
  
  RESULTS
  After 6 months' supplementation with EFA, there was improvement in the clinical activity compared with pretreatment evaluation. There was significant reduction in the sigmoidoscopic and histological scores in the EFA group compared with the placebo group. Essential fatty acid supplementation for 6 months also induced significant reduction in the circulating numbers of CD16+ and CD56+ cells and the cytotoxic activity of NK cells, compared with the placebo group.
  
  
  CONCLUSIONS
  This pilot study has demonstrated that omega-3 fatty acids can suppress natural cytotoxicity and reduce disease activity in patients with distal procto-colitis. These findings suggest a therapeutic strategy for managing patients with inflammatory bowel disease.
authors.affiliation: Department of Surgery, University of Aberdeen, United Kingdom.
authors.forename: Y Z
authors.initials: YZ
authors.lastname: Almallah
authors.forename: S
authors.initials: S
authors.lastname: Richardson
authors.forename: T
authors.initials: T
authors.lastname: O'Hanrahan
authors.forename: N A
authors.initials: NA
authors.lastname: Mowat
authors.forename: P W
authors.initials: PW
authors.lastname: Brunt
authors.forename: T S
authors.initials: TS
authors.lastname: Sinclair
authors.forename: S
authors.initials: S
authors.lastname: Ewen
authors.forename: S D
authors.initials: SD
authors.lastname: Heys
authors.forename: O
authors.initials: O
authors.lastname: Eremin
mesh_terms: D000328:Adult; D000368:Aged; D003093:Colitis, Ulcerative / Q000276:immunology* / Q000473:pathology; D003602:Cytotoxicity, Immunologic / Q000187:drug effects*; D004281:Docosahexaenoic Acids / Q000494:pharmacology; D004311:Double-Blind Method; D015118:Eicosapentaenoic Acid / Q000494:pharmacology; D005228:Fatty Acids, Essential / Q000494:pharmacology*; D005260:Female; D005434:Flow Cytometry; D006801:Humans; D015979:Killer Cells, Lymphokine-Activated / Q000276:immunology*; D007694:Killer Cells, Natural / Q000276:immunology*; D008297:Male; D008875:Middle Aged; D010865:Pilot Projects; D011349:Proctitis / Q000276:immunology* / Q000473:pathology
chemical_list: D005228:Fatty Acids, Essential; D004281:Docosahexaenoic Acids; D015118:Eicosapentaenoic Acid