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Background & Aims: Differentiating patients with functional bowel disorders from those with inflammatory bowel disease (IBD) can be difficult. Rectal luminal levels of nitric oxide (NO) are greatly increased in IBD. To further evaluate this disease marker, we compared NO in patients with irritable bowel syndrome (IBS) with those found in patients with active IBD and in healthy control subjects., Methods: Rectal NO was measured with chemiluminescence technique by using a tonometric balloon method in 28 healthy volunteers, 39 patients with IBS, 86 with IBD (Crohn's disease and ulcerative colitis), and 12 patients with collagenous colitis. In addition, NO was measured before and after a 4-week treatment period in patients with active ulcerative colitis and repeatedly during 2 weeks in healthy volunteers., Results: NO was low in healthy control subjects (median, 45; 25th-75th percentile, 34-64 parts per billion [ppb]), and variations over time were small. In IBS patients NO was slightly increased (150, 53-200 ppb; P < .001), whereas patients with active IBD or collagenous colitis had greatly increased NO levels (3475, 575-8850 ppb, and 9950, 4475-19,750 ppb, respectively; P < .001). With a cutoff level of 250 ppb, NO had a sensitivity of 95% and a specificity of 91% in discriminating between active bowel inflammation and IBS. Rectal NO correlated with disease activity in IBD and collagenous colitis and decreased markedly in IBD patients responding to anti-inflammatory treatment., Conclusions: Rectal NO is a minimally invasive and rapid tool for discriminating between active bowel inflammation and IBS and a possibly useful add-on for monitoring patients with IBD.

Background: Luminal nitric oxide increases in ulcerative colitis and Crohn disease. The authors have previously used a minimally invasive method to demonstrate increased luminal nitric oxide in ulcerative colitis and Crohn disease of the colon. The aim of the current study was to determine whether this method could be applied to identify inflammatory activity in ulcerative colitis and Crohn disease in children., Methods: Thirty-six children (18 of whom had active disease) with inflammatory bowel disease localized to the colon were studied. The control group comprised 12 healthy children. To measure nitric oxide, a silicon catheter with an inflatable balloon was inserted into the rectum and inflated with 10 mL of nitric oxide-free air. After a 10-minute incubation time, the air was withdrawn and nitric oxide concentrations were immediately analyzed using a chemiluminescence technique., Results: Children with active ulcerative colitis and Crohn disease of the colon had greatly increased luminal nitric oxide concentrations in the rectum (8,840 +/- 5,120 and 15,170 +/- 4,757 parts per billion [ppb], respectively) compared with controls (77 +/- 17 ppb) (P < 0.001). Children with nonactive ulcerative colitis or Crohn disease displayed low concentrations of rectal nitric oxide (356 +/- 110 and 188 +/- 55 ppb, respectively), which was not different from that of healthy controls., Conclusion: Rectal nitric oxide measurement is a feasible and useful method for monitoring disease activity in inflammatory bowel disease, especially in children.

Background: The production of nitric oxide (NO) is increased in ulcerative colitis, as shown by bioassays of NO synthase activity in mucosal biopsy specimens. We wanted to develop a less invasive method for measurement of NO directly in the rectum in patients with inflammatory bowel disease (IBD)., Methods: We studied 10 patients with active ulcerative colitis, 6 with active Crohn's disease, 6 with non-active ulcerative colitis, and 24 controls without inflammation A tonometer balloon catheter was inserted in the rectum and inflated with 5 ml of NO-free air. After 15 min of incubation the sample was extracted, and the NO concentration was immediately analysed with a chemiluminescence technique., Results: Patients with active disease had greatly increased concentrations of NO in the rectum as compared with controls and patients with non-active disease., Conclusions: During inflammation in the large intestine increased amounts of NO are released from the mucosa. Measurements of NO directly in the rectum could be of help in further understanding the role of this gas in IBD. Moreover, it is tempting to speculate that this minimally invasive method could be clinically useful as a diagnostic tool and in monitoring the effect of therapy.

The production of nitric oxide (NO) is increased in active ulcerative colitis and in Crohn's disease. We have studied NO production in collagenous colitis (CC) and lymphocytic colitis (LC), both of which are inflammatory bowel disorders of unknown aetiology. NO levels were measured directly in gas sampled from the colon during colonoscopy. Plasma levels of NO metabolites (nitrate/nitrite) were also measured. Luminal NO levels were more than 100 times higher in patients with CC compared with controls. In addition, plasma levels of nitrate/nitrite were increased in the patients as compared with controls. Measurements of NO directly in the colon or its oxidation products in plasma may be a helpful tool in further understanding the role of NO in the pathophysiology of CC and LC. Moreover, it is tempting to speculate that these measurements could be clinically useful in the diagnosis and therapy monitoring of these two inflammatory bowel diseases.

Background Treatment with tumor necrosis factor-α monoclonal antibody (infliximab) reduces clinical activity and intestinal inflammation in Crohn’s disease. Aim To study the time-course of the effects of infliximab with reference to mucosal cytokine and inducible nitric oxide synthase expression. Methods Thirty-two patients with Crohn’s disease were treated with single dose infliximab (5 mg/kg). Disease activity was assessed days 1, 3, 7 and 28 using Harvey–Bradshaw index. Rectal nitric oxide levels were determined and rectal biopsies collected before treatment, 1 h after infusion and on days 3, 7 and 28. Immunohistochemical staining against inducible nitric oxide synthase, tumor necrosis factor-α, interleukin-1β and interferon-γ were performed. Results Clinical response was seen in 14 patients with down-regulation of global immunohistochemistry expression, reaching nadir day 3. Rectal nitric oxide was increased at baseline (3578 ± 1199 parts per billion, ppb) compared with controls (89 ± 13 ppb) ( P < 0.001). In patients with clinical response, rectal nitric oxide decreased from 3926 ± 1687 ppb to 1050 ± 428 ppb day 28 ( P < 0.05). Conclusions Down-regulation of mucosal inflammatory mediators occurs after infliximab. Rectal nitric oxide levels parallel down-regulation of inducible nitric oxide synthase, tumor necrosis factor-α, interleukin-1β and interferon-γ and may serve as a quantitative biomarker of intestinal inflammation. [ABSTRACT FROM AUTHOR]