Bonderup Ole K, Hansen Jesper B, Madsen Poul, Vestergaard Vibeke, Fallingborg Jan, Teglbjaerg Peter S
Department of Medicine, Randers Hospital, Randers, Denmark.
Eur J Gastroenterol Hepatol. 2006 Oct;18(10):1095-9. doi: 10.1097/01.meg.0000231747.83760.bd.
In collagenous colitis, the production of nitric oxide in the colon is found to be 50 to 100-fold higher than in healthy controls. The role of nitric oxide in collagenous colitis is debated and it has been suggested that nitric oxide has a causative role in diarrhoea. The aim of this study was to examine the possible effect of budesonide treatment on the level of inducible nitric oxide synthase mRNA.
In 20 patients with collagenous colitis, clinical activity was assessed by registration of the daily stool frequency and stool weight. Sigmoidoscopy was performed and biopsies for histological examination and one biopsy for determination of inducible nitric oxide synthase mRNA was obtained in 16 patients.
Budesonide treatment was followed by a significant reduction of inducible nitric oxide synthase mRNA (P<0.01) whereas no change was observed after placebo treatment. Significant correlations between inducible nitric oxide synthase mRNA and the grade of inflammation (rho=0.47; P<0.01), the daily stool weight (rho=0.51; P<0.005) and the daily stool frequency (rho=0.49; P<0.005) were observed. No significant association was observed between inducible nitric oxide synthase mRNA and the thickness of the collagen layer.
In patients with collagenous colitis, treatment with budesonide results in a reduction of inducible nitric oxide synthase mRNA. The level of inducible nitric oxide synthase mRNA in colonic mucosa correlates with the inflammatory and clinical activity. The results support that nitric oxide is a central factor in the pathogenesis of collagenous colitis.
在胶原性结肠炎中，发现结肠中一氧化氮的产生比健康对照者高50至100倍。一氧化氮在胶原性结肠炎中的作用存在争议，有人认为一氧化氮在腹泻中起致病作用。本研究的目的是检验布地奈德治疗对诱导型一氧化氮合酶mRNA水平的可能影响。
对20例胶原性结肠炎患者，通过记录每日大便频率和大便重量来评估临床活动度。对16例患者进行了乙状结肠镜检查，并取活检进行组织学检查，另取一块活检组织用于测定诱导型一氧化氮合酶mRNA。
布地奈德治疗后诱导型一氧化氮合酶mRNA显著降低（P<0.01），而安慰剂治疗后未观察到变化。观察到诱导型一氧化氮合酶mRNA与炎症程度（rho=0.47；P<0.01）、每日大便重量（rho=0.51；P<0.005）和每日大便频率（rho=0.49；P<0.005）之间存在显著相关性。未观察到诱导型一氧化氮合酶mRNA与胶原层厚度之间存在显著关联。
在胶原性结肠炎患者中，布地奈德治疗可使诱导型一氧化氮合酶mRNA降低。结肠黏膜中诱导型一氧化氮合酶mRNA水平与炎症和临床活动度相关。结果支持一氧化氮是胶原性结肠炎发病机制中的一个核心因素。
