• I D R Arnott, N Williams, H E Drummond, and S Ghosh.
• University Department of Medical Sciences, Western General Hospital, Edinburgh, UK. iarnott@ed.ac.uk
• Dig Liver Dis. 2002 Jun 1;34(6):424-9.

IntroductionSmoking in patients with Crohn's disease is associated with more frequent relapse. The mechanism responsible is unknown but a direct pro-inflammatory action on intestinal mucosa has been postulated. Mucosal inflammation in clinically inactive Crohn's disease predicts forthcoming relapse. Whole gut lavage fluid obtained after bowel cleansing with a polyethylene glycol electrolyte solution is an assessment of gut inflammation and immunity.AimTo assess whether whole gut lavage fluid interleukin-1beta and interleukin-8 differed between smokers and non-smokers with clinically inactive Crohn's disease.MethodsA total of 34 patients with inactive Crohn's disease (Crohn's disease activity index <150 and whole gut lavage fluid IgG concentration of <10 mg/ml) underwent whole gut lavage with interleukin-1beta and interleukin-8 analysed by enzyme-linked immunosorbent assay. Clinical details and blood markers of inflammation were collected.ResultsIn this series, 14 patients smoked (10 females, mean age 44.3+/-14.3 years), 20 did not (12 females, mean age 40.7+/-14.3). Surgical resection was more common in smokers (12/14 vs 8/20, p<0.008). Whole gut lavage fluid IgG was significantly lower in smokers (median 1.5 mg/ml (range 1.0-8.0 mg/ml) vs median 3.5 mg/ml (range 1.0-7.0 mg/ml), p<0.05). Whole gut lavage fluid interleukin-1beta was also lower in smokers [median 14.5 pg/ml (range 2-72 pg/ml) vs 26 pg/ml (range 7-1700 pg/ml)], p<0.03.ConclusionMarkers of mucosal inflammation in inactive Crohn's disease are lower in smokers than non-smokers. This is against the hypothesis that nicotine exerts a direct pro-inflammatory action via interleukin-1beta and interleukin-8. Further research is required to elucidate the exact mechanisms involved.

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