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炎症性肠病中黏膜糖蛋白合成异常与吸烟无关。

Abnormal mucosal glycoprotein synthesis in inflammatory bowel diseases is not related to cigarette smoking.

作者信息

Ryder S D, Raouf A H, Parker N, Walker R J, Rhodes J M

机构信息

University Department of Medicine, University of Liverpool, UK.

出版信息

Digestion. 1995;56(5):370-6. doi: 10.1159/000201261.

Abstract

Patients with ulcerative colitis are usually non- or ex-smokers in contrast to Crohn's disease where smoking is common. Abnormalities of quantity and quality of intestinal mucus have been postulated in the pathogenesis of these diseases. It is possible that smoking habit may exert its effects via changes in mucus in inflammatory bowel disease. We have therefore studied incorporation of N-acetylglucosamine into synthesized colonic mucin in explants from 85 controls with normal colonoscopic appearances and histology, including 27 smokers and 58 nonsmokers, 36 patients with ulcerative colitis and 19 with ileocolonic Crohn's disease over 24 h in tissue culture. Incorporation of N-acetylglucosamine into normal explants was 31.3 +/- (SD) 7.1 dpm/microgram biopsy protein, incorporation was increased in patients with active Crohn's disease (mean 41.2 +/- (SD) 10.4 dpm/microgram biopsy protein, p = 0.003), decreased in inactive ulcerative colitis (mean 24.1 +/- 7.8 dpm/microgram biopsy protein, p = 0.0006) but normal in active ulcerative colitis (mean 35.0 +/- 13.8 dpm/microgram biopsy protein, p = 0.44). No significant relationship was found between cigarette smoking habits and mucus synthesis in controls with normal mucosa (nonsmokers, n = 58, mean 31.0 +/- (SD) 7.52 dpm/microgram biopsy protein; smokers, n = 27, mean 31.8 +/- (SD) 6.1 dpm/microgram biopsy protein, p = 0.9). This study shows that mucus glycoprotein synthesis is reduced in inactive ulcerative colitis, rising to normal levels in active disease and that synthesis is increased in Crohn's disease. There is no effect of smoking on mucus synthesis by control biopsies suggesting that the differences seen in inflammatory bowel disease are not related to cigarette smoking.

摘要

与吸烟常见的克罗恩病不同,溃疡性结肠炎患者通常不吸烟或已戒烟。这些疾病的发病机制中已假定存在肠道黏液数量和质量的异常。吸烟习惯可能通过炎症性肠病中黏液的变化发挥作用。因此,我们研究了在组织培养中,85例结肠镜检查外观和组织学正常的对照者(包括27名吸烟者和58名非吸烟者)、36例溃疡性结肠炎患者和19例回结肠克罗恩病患者的外植体中N-乙酰葡糖胺掺入合成结肠黏蛋白的情况,持续24小时。N-乙酰葡糖胺掺入正常外植体的量为31.3±(标准差)7.1 dpm/微克活检蛋白,活动性克罗恩病患者的掺入量增加(平均41.2±(标准差)10.4 dpm/微克活检蛋白,p = 0.003),非活动性溃疡性结肠炎患者的掺入量减少(平均24.1±7.8 dpm/微克活检蛋白,p = 0.0006),而活动性溃疡性结肠炎患者的掺入量正常(平均35.0±13.8 dpm/微克活检蛋白,p = 0.44)。在黏膜正常的对照者中,吸烟习惯与黏液合成之间未发现显著关系(非吸烟者,n = 58,平均31.0±(标准差)7.52 dpm/微克活检蛋白;吸烟者,n = 27,平均31.8±(标准差)6.1 dpm/微克活检蛋白,p = 0.9)。这项研究表明,非活动性溃疡性结肠炎中黏液糖蛋白合成减少,在活动性疾病中升至正常水平,而克罗恩病中合成增加。吸烟对对照活检组织的黏液合成没有影响,这表明在炎症性肠病中观察到的差异与吸烟无关。

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