The results show that IBD patients have significant sleep disturbance even when their disease is not active. This problem might affect quality of life, gastrointestinal symptoms and coping ability, and might potentially modify disease severity or increase risk of flare-up. Regardless of the primary or secondary origin of this problem, sleep disturbance should be addressed in the clinical management of patients with IBD.

Infliximab is not superior to placebo in preventing clinical recurrence after CD-related resection. However, infliximab does reduce endoscopic recurrence. ClinicalTrials.gov ID NCT01190839.

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Reactive oxygen metabolites are potent inflammatory mediators that may be involved in tissue injury in inflammatory bowel disease. To evaluate their role in inflammatory bowel disease, we investigated the effects oflowering the activities of reactive oxygen metabolites in experimental colitis induced by intracolonic administration of acetic acid in rats. Intracolonic administration of5% acetic acid caused severe inflammation (mean (SEM) inflammatory score was 24*3 (0.7) of a maximum score of 32). Acetic acid at 2-5% produced moderate inflammation (score= 17 (1.4) v 4-0 (0.5) in control rats). This lower dose was used for subsequent experiments. Specific superoxide anion scavenger methoxypolyethylene glycol:superoxide dismutase, and reactive oxygen metabolites scavenger, sulfasalazine, significantly decreased the severity of inflammation (s'cores: 8 (4.4) and 9-8 (2.2) respectively). The xanthine oxidase inhibitors, tungsten and pterin aldehyde, failed to improve inflammation but another xanthine oxidase inhibitor, aliopurinol, a compound with known superoxide anion scavenging effect, did limit the inflammation (10(2)). Inhibition ofhydroxyl radicalproduction by deferoxamine orlowering hydroxyl radical values by a scavenger, dimethyl sulfoxide, did not affect the severity of inflammation. These data suggest: (1) that reactive oxygen metabolites play an important role in experimental colitis, (2) that the xanthine oxidase pathway is not a major source of reactive oxygen metabolites in colitis, and (3) that tissue injury in experimental colitis is not caused by generation of hydroxyl radicals.

Alcohol consumption is a potential trigger for flare in Inflammatory Bowel Disease (IBD) flare because of alcohol’s pro-oxidant effects and its deleterious effects on gut barrier function. The association with alcohol consumption and IBD flare is unclear. To test this hypothesis, we evaluated the pattern of alcohol consumption and its self-reported effect on gastrointestinal (GI) symptoms in patients with IBD. We recruited 129 consecutive patients: 52 patients with Crohn’s Disease, 38 patients with Ulcerative Colitis, and 39 patients with Irritable Bowel Syndrome (IBS). All participants completed a validated questionnaire on disease activity, the CDAI or UCAI respectively, validated questionnaires to quantify alcohol consumption by NIAAA criteria, and two structured questionnaires we designed to access patients’ perception of the effect of alcohol on their GI symptoms and on overall GI symptom severity. The pattern of current, light, moderate, and heavy alcohol consumption in inactive IBD was similar to the general US population. Specifically, 56 of 90 (62%) of inactive IBD patients were current drinkers, compared to 61% in the general US population. Of current drinkers, 75% of IBD (N=42), and 43% of IBS (N=9) reported a worsening of GI symptoms with alcohol consumption (p=0.01); however, overall GI symptom severity did not differ when compared to quantity of alcohol consumed. Patients with inactive IBD drink alcohol in quantities similar to the general population. Current drinkers with inactive IBD are more likely to report worsening of GI symptoms with alcohol than current drinkers with IBS.

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Article first published online 29 April 2015.

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