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In the western world a sharp rise in the incidence of inflammatory bowel disease (IBD) has been observedsince the early 1950s. The increase in the incidence of ulcerative colitis preceded the increase in the incidenceof Crohn's disease by about 10 - 15 years. In high incidence areas, a female preponderance at a young age isobserved in Crohn's disease, whereas in ulcerative colitis male incidence is still high at older ages. IBD ismore common in the western world than in eastern areas and, in both the United States and Europe, a north-south gradient has been reported, with IBD more common in the north than in the south. There are alsoindications that in typically low-incidence areas, more cases are being seen lately. Rates for Japan suggestthat this Asian population is now affected with approximately equal frequency as western populations withregard to ulcerative colitis; Crohn's disease in contrast is still less common. The prevalence of Crohn'sdisease in the Chinese populations in Hong Kong and Singapore appears to be increasing, and more cases havealso been observed lately in central China. This could be due to a greater awareness and better availability ofhealth care and/or improved study methods. However, it may also be a real increase, reflecting changingenvironmental factors. Both genetic factors and environment are thought tO be important in developing IBD,the observed increase during the past decennia is probably due to environmental factors since genetic make-upcannot change that quickly. Smoking is the only consistent risk factor in case-control studies, but does notseem to explain the observed changes in incidence and age and gender distribution in the two diseases,nutrition and life-style factors changed to a great extent during the period in which the rising incidence ofIBD has been reported. Following the temporal trends in these areas and using case-control settings in apopulation based manner during the coming years should prove to be of great interest, as this might shedsome light on the role of environmental factors in the etiology of IBD.
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The current established drugs used to treat inflammatory bowel disease include glucocorticoids includingnewer agent budesonide, sulfasalazine and 5-ASA compounds such as Asacol, Pentasa, Dipentum andBalsalazide and immunomodulatory agents such as azathioprine, and 6-mercaptopurine. Additional drugswhich have been found to be useful, particularly in refractory cases of Crohn's disease including fistulizingtype of Crohn's disease, include cyclosporine A, methotrexate, humanized antibody against TNFa(cA2),FK506, IL-10, IL-11 and Probiotics. Various agents, whether used alone or in combination, have to betailored for each patient and none is ideal. Exciting new developments directed against proinflammatorypathways, cytokines, free oxygen radicals and cell surface related immune targets are areas of intense recentinvestigations and many novel therapeutic agents are expected to be available in the near future for medicaltreatment of inflammatory bowel disease.
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重视炎症性肠病的规范化诊断与治疗
近年来,我国炎症性肠病(IBD)[包括溃疡性结肠炎(UC)和克罗恩病(CD)]报告病例数急增,3年前,基于多家医院病例统计推测,其患病率分别为11.6/10万和1.4/10万,且可能有被低估之虞[1].
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合理使用免疫抑制剂以提高炎症性肠病的疗效
在炎症性肠病(IBD)药物治疗中,免疫抑制剂[常用的如硫唑嘌呤(AZA)和6-巯基嘌呤(6-MP)]主要用于糖皮质激素(简称为激素)治疗无效或激素依赖的患者,合理使用可提高疗效并大限度地减少药物不良反应的发生.免疫抑制剂用于IBD的治疗,近20年来在国外已广泛推广并不断有深入的研究,但在我国应用的经验和临床研究尚少.
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关注脊柱关节炎的关节外表现
脊柱关节炎( SpA)是一组慢性炎症性风湿性疾病,具有特定的病理生理、临床、影像学和遗传学特征,主要包括强直性脊柱炎(AS)、反应性关节炎( ReA)、炎性肠病性关节炎(arthropathy of inflammatory bowel disease)、银屑病关节炎(PsA)、未分化脊柱关节病和幼年脊柱关节炎,整体人群患病率为0.5%~1.9%[1].这类疾病的主要临床特征包括炎性腰背痛、以下肢关节为主的非对称性的寡关节炎、附着点炎以及特殊器官受累如前葡萄膜炎、银屑病皮疹、慢性炎性肠病、主动脉根部病变和心脏传导异常.近年来随着各种新型药物,特别是生物制剂的出现,SpA的治疗有了迅速的发展,TNFα抑制剂对SpA的脊柱炎和外周关节炎具有很好的疗效,对葡萄膜炎、银屑病皮疹及炎症性肠病( IBD)也有肯定的疗效.但近10年的临床经验也发现,不同的TNFα抑制剂在治疗SpA时,不同的临床表现对治疗的反应并不完全相同,其大的差异体现在关节外表现和并发症上[2].现着重介绍SpA患者关节外表现及临床治疗选择,以帮助临床医师更好的认识疾病全貌,并使患者获益更大.
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炎症性肠病93例临床分析
炎症性肠病(inflammatory bowel disease,IBD)一词专指病因未明的炎症性肠病(idiopathic inflammatory bowel disease),包括溃疡性结肠炎(ulcerative colitis,UC)和克罗恩病(Crohn′s disease,CD)[1].
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炎症性肠病的流行病学和自然史
1 流行病学特征炎症性肠病(IBD)是世界范围的疾病,在不同地域、不同人群中的发病率差异很大.了解IBD发病率在人群内部及不同人群的差异,能为寻找IBD的病因提供线索.1.1 地理分布 IBD分布具有显著的地理特点,在挪威、瑞士、美国等北半球国家多见,溃疡性结肠炎(UC)、克罗恩病(CD)的发病率分别为每年3~14.3/10万人、0.7~11.6/10万人,而在南半球国家少见,二者的发病率分别为每年2.0~6.3/10万人、0.9~3.1/10万人.亚、非洲国家IBD少见,据报道日本UC、CD的发病率分别为每年0.5/10万人、0.08/10万人.IBD发病率还存在城乡差别,在城市的发病率较农村高,这与人口过度拥挤、暴露于传染源以及生活方式等因素有关.
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炎症性肠病遗传因素的研究进展
炎症性肠病(IBD)包括溃疡性结肠炎(UC)和克罗恩病(CD),属慢性肠道非特异性炎性疾病.IBD病因不明,发病机制可能与遗传、环境及免疫等多种因素有关.
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炎症性肠疾病的治疗
炎症性肠疾病(IBD)包括溃疡性结肠炎(UC)和克罗恩病(CD),是一种原因不明的非特异性炎性肠道疾病.发病年龄多在10~40岁,目前在我国已由少见疾病转为常见疾病,其中以溃疡性结肠炎为多,是胃肠道疾病和慢性腹泻的主要原因,严重影响病人的身体健康,在诊治方面引起临床医生的高度重视.
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努力提高炎症性肠疾病的外科治疗水平
炎症性肠疾病(IBD)包括溃疡性结肠炎(UC)和克罗恩病(CD),未定型结肠炎(indeterminate colitis,IC)则介于两者之间.
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炎症性肠病慢性腹泻的药物治疗
炎症性肠病(Inflammatory bowel disease,IBD)一词专指病因未明的炎症性肠病(Idiopathic inflammatory bowel disease),包括溃疡性结肠炎(Ulcerative colitis,UC)和克罗恩病(Crohn's disease,CD),在欧洲、北美发病率较高,在我国IBD的发病有上升趋势,已成为慢性腹泻的主要原因之一.
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肠黏膜免疫与炎症性肠病研究现状
炎症性肠病(inflammatory bowel disease,IBD)是一组慢性肠道炎症性疾病,包括溃疡性结肠炎(ulcerative colitis,UC)和克罗恩病(Crohn's disease).近年来,在黏膜免疫研究方面特别是在IBD发生的免疫因素与治疗方法方面提出了一些新见解.
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克罗恩病的诊断与治疗进展
炎症性肠病(inflammatory bowel disease,IBD)广义上指的是由各种原因所引起的肠道炎症性疾病,包括各种感染及各种非感染性的肠道炎症;狭义上指的是特发性炎症性肠病(idiopathic inflammatory bowel disease),包括溃疡性结肠炎,克罗恩病及未定型结肠炎.克罗恩病(Crohn's disease,CD)以胃肠道慢性肉芽肿性炎症、末段回肠及邻近结肠常受累、病变多呈节段性和非连续性为特征.
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正确选择炎症性肠病实验研究的动物模型
炎症性肠病(inflammatory bowel disease,IBD)是一种反复发作的慢性非特异性肠道炎症性疾病,主要包括溃疡性结肠炎(ulcerative colitis,UC)和克罗恩病(Crohn's disease,CD),其确切病因和发病机制至今尚未阐明,治疗上也缺乏特异有效的药物[1,2].因此,为研究其病因和发病机制以及开发新的治疗药物,建立理想的、类似于人类IBD的动物模型就显得非常重要.
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重视炎症性肠病遗传易感性的研究
炎症性肠病(IBD)包括溃疡性结肠炎(UC)和克罗恩病(CD),是一组慢性肠道炎症性疾病,其病因尚未完全阐明,发病机制假设为由大量肠道细菌诱发的过度肠黏膜免疫反应,在具有遗传易感性的人群中导致肠黏膜损伤.
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对我国炎症性肠病诊断治疗规范的共识意见
炎症性肠病(IBD)是一种病因尚不十分清楚的慢性非特异性肠道炎症性疾病,包括溃疡性结肠炎(UC)和克罗恩病(CD).
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炎症性肠病的诊断标志
目前炎症性肠病(IBD)的诊断是基于临床、内镜、组织学和放射学检查的结果.终诊断为功能性肠道疾病的患者常因怀疑IBD而作广泛检查.寻找非侵入性IBD筛选方法的研究仍在进行中,其目的是要找到一种特异、敏感的标志或标志组合,以替代现有昂贵的侵入性诊断方法.对临床医师而言,另一个问题是预测复发和观察疾病活动程度时遇到的困难.本文就应用非侵入性诊断标志监测IBD活动性、鉴别克罗恩病(CD)和溃疡性结肠炎(UC)及区分IBD和肠功能紊乱方面的研究进展作一介绍.(牛凤丽摘译自Dubinsky MC, Seidman EG. Diagnostic markers of inflammatory bowel disease. Current Opinion in Gastroenterology, 2000, 16: 337~342.刘文忠校)
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炎症性肠病免疫治疗新方法
炎症性肠病(IBD)的病因尚不清楚,因此治疗不能直接针对病因,而只能集中于导致肠道粘膜慢性炎症的某些途径.IBD肠道粘膜损伤主要是由肠道免疫反应上调所致.目前治疗IBD的新型免疫药物发展迅速,其作用是在某些特异位点阻断致炎途径,现就这方面的研究进展作一介绍.(梁晓摘译自Heuschkel RB. New immunologic treatments for inflammatory bowel disease. Current Opinion in Gastroenterology, 2000, 16: 565~570.刘文忠校)
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对加强炎症性肠病临床研究的意见
受中华医学会消化病学分会委托,我们在成都承办了全国炎症性肠病(IBD)学术研讨会.这次会议检阅了近年来我国IBD研究现状;学习了当前国外IBD研究的先进经验;讨论了IBD诊断和治疗的规范以及今后科研的方向.会前的文献复习、会后有关诊断治疗规范的整理,对进一步加强IBD临床研究的问题进行认真思考.现提出几点粗浅的看法,供同道参考.
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AIM: Ulinastatin has been reported to be beneficial for maintenance of steroid-refractory inflammatory bowel disease (IBD), but the mechanism underlying remains uncertain. Leukocyte recruitment to inflammatory site plays an important role in the pathogenesis of IBD, analysis of leukocyte and endothelium interaction may provide new avenues for treatment of IBD. In this study, we evaluated the efficacy of Ulinastatin in dextran sulfate sodium (DSS) induced colitis rat model using intravital video microscopy. METHODS: Rats were given drinking water containing 3.5% (W/V) DSS for 10 days then 1% for 14 days. DSS induced colitis rats were treated Ulinastatin 3 000 unit*kg-1*d-1 via intraperitoneum during 1% DSS feeding. Controls received distilled water for 24 days. Body weight was determined for all groups. Colitis severity was assessed using histological scoring systems by H&E sections. Intravital microscopic techniques were used to quantitate leukocyte adhesion (LA), leukocyte emigration (LE) and venular protein leakage (VPL) in rat mesentery. RESULTS: DSS induced loss of body weight, whereas Ulinastatin-treated rat showed a significant increase in body weight. Histological analysis revealed improvement of colitis such as leukocyte infiltration, loss of goblet cells, transmural edema. DSS intake elicited increase in LA, LE, and VPL compared to control group. Ulinstatin significantly reversed the increase in LA, LE, and VPL induced by DSS. CONCLUSION: Administration of Ulinastatin effectively ameliorates experimental colitis by interfering with leukocyte recruitment, and may become a potential candidate for control of inflammation of IBD.