炎症性肠病的发病机制新解

近年来，我国炎症性肠病发病率有逐渐升高的趋势，克罗恩病(CD)和溃汤性结肠炎(UC)青年患者比例远多于二十年前。据研究，这两种病与遗传、环境(食物、肠茵)及免疫因素有关，遗传、环境和免疫因素的相互作用可导致肠粘膜免疫反应过度活跃，造成肠道组织炎症和损伤。     

炎症性肠病发病机制新进展

炎症性肠病(inflammatory bowel disease,IBD)包括克罗恩病(Crohn’s disease,CD)和溃疡性结肠炎(ulcerative colitis,UC),其病因和发病机制仍不清楚,目前大多学者认为持续肠道感染、肠黏膜屏障缺损、肠黏膜免疫调节异常、遗传和环境等因素共同参与了疾病发生过程[1-4]。本文将阐述IBD免疫病理学发病机制     

炎症性肠病的发病机制及临床诊治研究进展

炎症性肠病（IBD）是一组病因不明的慢性肠道炎症性疾病,包括溃疡性结肠炎（UC）和克罗恩病（CD）,两者组织损伤的基本病理过程相似,但可能由于致病因素及发病具体环节不同其组织损害的表现不同。现将近年来IBD的发病机制及临床诊治研究进展作一综述。     

炎症性肠病病因与发病机制的研究进展

炎症性肠病（inflammatory bowel disease,BD)的病因不清，发病机制复杂。随着其发病率的上升，对其病因及可能的机制的研究也在不断深入。目前认为IBD是免疫性疾病，其发病与环境、遗传及免疫因素关系密切。     

炎症性肠病发病机制的研究进展

对炎症性肠病（IBD）的研究已有多年,但其确切病因尚不清楚.近年来,有关IBD发病机制方面的研究更新了一些观点.2001年发现了第一个克罗恩病（CD）易感基因CARD15/NOD2,从而使对IBD发病机制的研究集中在遗传学方面[1].     

难治性炎症性肠病发病的相关机制

难治性炎症性肠病发病机制尚不明确,目前多认为其发生与糖皮质类固醇激素(GC)依赖与抵抗、多耐药基因表达、巯嘌呤甲基转移酶(TPMT)活性相关,免疫异常、感染、精神心理因素及患者依从性等影响着疾病的发生发展,此文就其发病机制的研究进展作一综述.     

炎症性肠病发病机制的微生物因素

炎症性肠病(IBD)的病因和发病机制尚不明确,肠道微生物与IBD发病关系密切,IBD患者肠道菌群存在失调,有证据表明,正常人群的肠黏膜免疫系统对肠道正常菌群存在耐受,而某些具有IBD遗传易感性人群的肠黏膜免疫系统对其肠道菌群失去耐受,肠道茵群参与了 IBD的发病．肠道细菌及其产物能刺激肠黏膜免疫系统,诱发这些具有IBD遗传易感性人群肠黏膜免疫系统功能紊乱,产生异常的免疫反应．不过,探究肠道细菌与IBD发病之间的关系,尚需要进一步的临床和实验研究．     

炎症性肠病的病因及发病机制

炎症性肠病（IBD）的病因与发病机制至今仍未完全明确，目前认为它是多种因素相互作用引起，主要与遗传、免疫、感染、环境及精神等因素有关。     

炎症性肠病动物模型分类及其与发病机制关系的研究进展

炎症性肠病动物模型已被广泛用于研究人类炎症性肠病的病因及发病机制，研究发现CD4^ T细胞在炎症性肠病免疫发病机制中起重要作用，Thl细胞因子IFN-γ和TNF-α介导炎症的病理变化类似于人类克罗恩病；Th2细胞因子IL-4介导的炎症病理特征类似于人类溃疡性结肠炎。肠道菌群的存在及肠上皮细胞的屏障功能缺陷在诱发肠道炎症病理过程中也起着一定作用。     

炎症性肠病动物模型分类及其与发病机制关系的研究进展

炎症性肠病动物模型已被广泛用于研究人类炎症性肠病的病因及发病机制,研究发现CD_4~+T细胞在炎症性肠病免疫发病机制中起重要作用,Th1细胞因子IFN-γ和TNF-α介导炎症的病理变化类似于人类克罗恩病;Th2细胞因子IL-4介导的炎症病理特征类似于人类溃疡性结肠炎。肠道菌群的存在及肠上皮细胞的屏障功能缺陷在诱发肠道炎症病理过程中也起着一定作用。     

Th17细胞在炎症性肠病发病机制作用的研究进展

炎症性肠病的病因和发病机制尚未完全明确。最近的研究表明,Th17细胞及与其相关的细胞因子、Th细胞亚群所导致的炎症过程在炎症性肠病的发生发展中起重要作用。本文就Th17的分化调控机制及Th17与其相关的细胞因子、Th细胞亚群在炎症性肠病的发病机制中的作用作一概述。     

Colorectal cancer in inflammatory bowel disease:The risk,pathogenesis,prevention and diagnosis

Patients with inflammatory bowel disease(IBD)are at increased risk for developing colorectal cancer(CRC),although the overall incidence of IBD-associated CRC has been diminishing in recent decades in western countries.As demonstrated in previous studies,the risk of CRC in IBD increases with longer duration,extent of colitis,a familial history of CRC,coexistent primary sclerosing cholangitis,and the degree of inflammation.The pathogenesis of CRC in IBD is poorly understood.Similar to sporadic CRC,IBD-associated CRC is a consequence of sequential episodes of genomic alteration.Multiple inter-related pathways,including immune response by mucosal inflammatory mediators,oxidative stress,and intestinal microbiota,are also involved the pathogenesis of IBD-associated CRC.Continuing colonic inflammation appears to be a factor in the development of CRC;therefore,anti-inflammatory agents such as5-aminosalicylate compounds and immune modulators have been considered as potential chemopreventive agents.Colonoscopic surveillance is widely accepted as being effective in reducing the risk of IBD-associated CRC,although no clear evidence has confirmed that surveillance colonoscopy prolongs survival in patients with extensive colitis.The traditional recommendation has been quadrantic random biopsies throughout the entire colon;however,several guidelines now have endorsed chromoendoscopy with a target biopsy because of increasing diagnostic yields and reduced workloads for endoscopists and pathologists.New technologies such as narrow band imaging,confocal endomicroscopy,and autofluorescence imaging have not yet been confirmed as surveillance strategies in IBD.     

STAT蛋白在炎症性肠病发病机制中的作用

炎症性肠病主要包括溃疡性结肠炎和克罗恩病,是肠道慢性非特异性炎症性疾病,病因尚不十分明确,近年来认为STAT蛋白,尤其是STAT3和STAT1通过细胞因子和JAK途径在炎症性肠病的发病机制中发挥重要作用,而SOCS家族参与STAT信号通路的负向调控.     

炎症性肠病合并贫血的研究进展

贫血是炎症性肠病(IBD)患者常见的并发症之一,会导致生活质量下降,也可增加患者的住院频率。据报道IBD并发贫血的发病率为6～74[1]。IBD患者贫血的发病机制尚未完全明了,铁摄入与丢失的负平衡、慢性病所致贫血、VitB12和叶酸缺乏、药物介导、炎症因子、溶血等众多因素均可能参与贫血的发生。过去普遍认为贫血是IBD不可避免的伴随症状,往往重视度不够,但最近的观点强调,贫血是此类患者明确的治疗内容。     

炎症性肠病中药物性肝损伤的研究进展

炎症性肠病(inflammatory bowel disease,IBD)的治疗常使用氨基水杨酸制剂、免疫抑制剂、生物制剂等,这些药物均可能导致肝细胞损伤、胆汁淤积性肝炎,甚至暴发性肝衰竭。使用免疫抑制剂及生物制剂还可能激活潜在的肝炎病毒。除此之外,硫唑嘌呤还可能导致肝血管源性病变,如再生性结节。本文将概述治疗IBD的药物导致肝损伤的相关研究进展。     

Autoantibodies and an immune-based rat model of inflammatory bowel disease

The exact causes of inflammatory bowel disease(IBD)are not yet fully defined.From a vast body of literature,we know that the immune response has long been involved in the pathogenesis of IBD,including both ulcerative colitis and Crohn’s disease.A variety of specific alterations can lead to immune activation and inflammation directed to the colon,as revealed by some animal models.Current research has focused on the role of antibodies in downstream events and mechanisms of autoimmunity and inflammation.It is not well known whether the production of antibodies is a serologic consequence of IBD,or if it is a result of barrier dysfunction induced by inflammation.Here,we present a new hypothesis to distinguish the complex links between genetic susceptibility,barrier dysfunction,commensal and pathologic microbial factors and inflammatory response(especially autoantibodies)in the pathogenesis of IBD.To ascertain the hypothesis,we developed a pilot model with the concept of the presence of antibodies against enteric bacterial antigens in IBD.Results confirmed our hypothesis.Our hypothesis suggests the possibility of subcutaneous vaccination of animals with administration of all or specific enteric bacterial antigens.     

肠易激综合征与炎症性肠病相关性研究进展

肠激综合征和炎症性肠病是两类不同的疾病,但近年来的基础研究和临床观察发现,两者存在相互联系.这为今后两种疾病的诊断、治疗、随访提出了新的要求.也为胃肠道功能性疾病的研究提出了新的思路.此文主要就肠易激综合征和炎症性肠病在发病机制和临床表现上的异同作一阐述.     

MicroRNAs与炎症性肠病

炎症性肠病(IBD)的发病机制与免疫、炎症、损伤、遗传等因素密切相关。MicroRNAs是一类小的非编码RNA,其通过与靶基因3’UTR区结合,负向调控基因表达,在炎症性肠病的发病机制中发挥重要的作用。     

Clostridium difficile and inflammatory bowel disease: Role in pathogenesis and implications in treatment

Clostridium difficile(C.difficile)is the leading cause of antibiotic associated colitis and nosocomial diarrhea.Patients with inflammatory bowel disease(IBD)are at increased risk of developing C.difficile infection(CDI),have worse outcomes of CDI-including higher rates of colectomy and death,and experience higher rates of recurrence.However,it is still not clear whether C.difficile is a cause of IBD or a consequence of the inflammatory state in the intestinal environment.The burden of CDI has increased dramatically over the past decade,with severe outbreaks described in many countries,which have been attributed to a new and more virulent strain.A parallel rise in the incidence of CDI has been noted in patients with IBD.IBD patients with CDI tend be younger,have less prior antibiotic exposure,and most cases of CDI in these patients represent outpatient acquired infections.The clinical presentation of CDI in these patients can be unique-including diversion colitis,enteritis and pouchitis,and typical findings on colonoscopy are often absent.Due to the high prevalence of CDI in patients hospitalized with an IBD exacerbation,and the prognostic implications of CDI in these patients,it is recommended to test all IBD patients hospitalized with a disease flare for C.difficile.Treatment includes general measures such as supportive care and infection control measures.Antibiotic therapy with either oral metronidazole,vancomycin,or the novel antibiotic-fidaxomicin,should be initiated as soon as possible.Fecal macrobiota transplantation constitutes another optional treatment for severe/recurrent CDI.The aim of this paper is to review recent data on CDI in IBD:role in pathogenesis,diagnostic methods,optional treatments,and outcomes of these patients.