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Rectal Nitric Oxide (rectal + nitric_oxide)
Selected AbstractsEarly changes in rectal nitric oxide and mucosal inflammatory mediators in Crohn's colitis in response to infliximab treatmentALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 8 2007T. LJUNG SUMMARY Background Treatment with tumor necrosis factor-, 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-,, interleukin-1, and interferon-, 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-,, interleukin-1, and interferon-, and may serve as a quantitative biomarker of intestinal inflammation. [source] No evidence for a clear link between active intestinal inflammation and autism based on analyses of faecal calprotectin and rectal nitric oxideACTA PAEDIATRICA, Issue 7 2007Elisabeth Fernell Abstract Aim: Due to parental concern regarding the child's bowel habits and the ongoing discussion whether there might be an association between autism and intestinal inflammation, two inflammatory markers were analysed in a group of children with autism. Methods: Twenty-four consecutive children with autism (3,13 years) of unknown aetiology were investigated with respect to faecal calprotectin and rectal nitric oxide (NO). Results: One child who previously had a severe Clostridium difficile infection displayed raised levels of both these inflammatory markers and one child with extreme constipation for whom only calprotectin was possible to measure had raised levels. The remaining children displayed results that did not indicate an active inflammatory status in the intestine when the two inflammatory markers were combined. Conclusion: By the use of two independent markers of inflammatory reactions in the gut, i.e. rectal NO and faecal calprotectin we were not able to disclose evidence of a link between the autistic disorder and active intestinal inflammation. [source] | ||||||||||