缺血在炎症性肠病发病机制中的作用

炎症性肠病是一种以肠道慢性炎性反应为特征的疾病,主要包括溃疡性结肠炎和克罗恩病,其病因和发病机制尚不明确,可能有多种因素共同参与。临床上炎症性肠病和缺血性肠病之间存在诸多相似之处,此文就血管因素和肠道缺血在炎症性肠病发病机制中的作用作一综述。     

防御素与炎症性肠病

防御素是一组存在于动植物界的抗微生物阳离子多肽,参与机体对微生物的防御作用。目前已经发现的人体内防御素有10种,分为α防御素和β防御素。炎症性肠病(IBD)的发病机制尚不明确,可能有多种因素共同参与。研究表明,宿主肠道菌群失调可能导致IBD,而防御素参与了肠道上皮细胞对肠腔内微生物的先天性防御机制。     

炎症性肠病结肠镜检查的评价

随着结肠镜对炎症性肠病镜下和活检病理形态改变的认识不断加深 ,它的使用价值也不断提高。Ｆｒ櫣ｈｍｏｒｇｅｎ总结过去 10年经验 ,发现对溃疡性结肠炎确诊率达 93.9% ,对克罗恩病达 77.3%。因此 ,近年来有倾向 ,结肠镜应列为诊断炎症性肠病的常规检查。结合我院过去 2 0年中炎症性肠病所见的形态改变 ,对其使用价值进行讨论。　　炎症性肠病在结肠镜下的形态 ,首先表现为分布方式和累及部位不同。溃疡性结肠炎呈连续性分布 ,并且疾病初期往往先累及直肠 ,逐渐向近端结肠蔓延 ,严重者累及整个结肠 ,仅有极少数倒灌性肠炎者可达回肠末端近…     

调节性T细胞在炎症性肠病中的作用

炎症性肠病（IBD）是一类病因和发病机制尚未完全明确的非特异性肠道炎性疾病。调节性T 细胞（Treg）有抑制自身免疫的功能,是维持肠道免疫稳态的重要因素。Treg细胞数量减少或功能异常均有可能导致IBD发生。此文就目前国内外关于Treg细胞在IBD中的作用机制及其指导治疗方面的研究现状作一综述。     

β防御素与炎症性肠病

防御素是一类具有抗微生物活性的小分子多肽,广泛存在于生物体内,按其分子结构特点,分为α、β和θ防御素三大类,参与机体对微生物的防御作用。此文综述β防御素的发现分布、基因表达调控及其抗微生物作用,探讨其与炎症性肠病的关系及应用前景。     

炎症性肠病的肠外表现和并发症

<正>克罗恩病(CD)和溃疡性结肠炎(UC)都属于炎症性肠病(IBD)。IBD肠外表现的病因可能涉及到多种因素,有时候IBD的肠外表现(IBD本身累及其他器官)与IBD继发的肠外并发症(如营养不良、慢性炎症、药物的不良反应等所致)比较难鉴别。一般而言,IBD的肠外表现与IBD的活动性一致,但有些可能与IBD的活动性不一样,例如原发性硬化性胆管炎和强直性脊柱炎。这些肠外表现的症状可     

miR-155在炎症性肠病中的免疫作用机制研究进展

炎症性肠病(inflammatory bowel disease, IBD)是一种原因未明的肠道非特异性炎症性疾病,其发病率逐年升高,对IBD的发病机制研究有待进一步深入,找到合适的治疗方法亟待解决.近期研究表明miR-155在IBD中的作用不可小觑,可通过Jarid2/notch1信号通路及促进2型巨噬细胞分化来调节TH17分化,并通过抑制细胞毒T淋巴细胞相关抗原4调节Treg、通过细胞信号传导的抑制因子1调节肠成纤维细胞和肌成纤维细胞以及通过调节DNA双链断裂沉积来影响肠道炎症,本文就mi R-155在IBD中的免疫作用机制作一综述.     

T淋巴细胞在炎症性肠病发生发展中的作用

炎症性肠病(inflammatory bowel disease,IBD)是一种常见的慢性胃肠道病,包括溃疡性结肠炎(ulcerative colitis,UC)和克罗恩病(Crohn's disease,CD)。前者是一种慢性非特异性结肠炎症,重者发生溃疡,病变主要累及结肠黏膜和黏膜下层;范围多自远段结肠开始,可逆行向近段发展,甚至     

P选择素与炎症性肠病

炎症性肠病(IBD)包括溃疡性结肠炎(UC)和克罗恩病(CD),目前认为血小板功能异常在其发病机制及发展过程中起着重要作用.P选择素是细胞黏附分子中选择素家族成员,介导血小板活化及炎症反应等.研究表明P选择素在炎症性肠病的病理过程中起重要作用.     

营养与炎症性肠病

营养和炎症性肠病的发病机制及治疗有密切的关系,深入研究两者的关系对临床有重要的意义。此文对饮食中的营养成分是否和发病有关、如何营养支持等问题作一简要概述。     

Extraintestinal manifestations in inflammatory bowel disease

Inflammatory bowel diseases (IBD) can be really considered to be systemic diseases since they are often associated with extraintestinal manifestations, complications, and other autoimmune disorders. Indeed, physicians who care for patients with ulcerative colitis and Crohn's disease, the two major forms of IBD, face a new clinical challenge every day, worsened by the very frequent rate of extraintestinal complications. The goal of this review is to provide an overview and an update on the extraintestinal complications occurring in IBD. Indeed, this paper highlights how virtually almost every organ system can be involved, principally eyes, skin, joints, kidneys, liver and biliary tracts, and vasculature (or vascular system) are the most common sites of systemic IBD and their involvement is dependent on different mechanisms.     

Pharmacogenetics in inflammatory bowel disease

Pharmacogenetics is the study of the association between variability in drug response and (or) drug toxicity and polymorphisms in genes. The goal of this field of science is to adapt drugs to a patient's specific genetic background and therefore make them more efficacious and safe. In this article we describe the variants in genes that influence either the efficacy or toxicity of common drugs used in the treatment of inflammatory bowel diseases (IBD), ulcerative colitis (UC), and Crohn's disease (CD) including sulfasalazine and mesalazine, azathioprine (AZA) and 6-mercaptopurine (6-MP), methotrexate (MIX), glucocorticosteroids (CSs) and infliximab. Furthermore, difficulties with pharmacogenetic studies in general and more specifically in IBD are described. Although pharmacogenetics is a promising field that already contributed to a better understanding of some of the underlying mechanisms of action of drugs used in IBD, the only discovery translated until now into daily practice is the relation between thiopurine S-methyltransferase (TPMT) gene polymorphisms and hematological toxicity of thiopurine treatment. In the future it is necessary to organize studies in well characterized patient cohorts who have been uniformly treated and systematically evaluated in order to quantitate drug response more objectively. An effort should be made to collect genomic DNA from all patients enrolled in clinical drug trials after appropriate informed consent for pharmacogenetic studies.     

Pediatric inflammatory bowel disease

Inflammatory bowel disease is an important cause of gastrointestinal pathology in children and adolescents. The incidence of pediatric inflammatory bowel disease is increasing; therefore, it is important for the clinician to be aware of the presentation of this disease in the pediatric population. Laboratory tests, radiology studies, and endoscopic procedures are helpful in diagnosing inflammatory bowel disease and differentiating between Crohn's disease and ulcerative colitis. Once diagnosed, the goal of medical management is to induce remission of disease while minimizing the side effects of the medication. Specific attention needs to be paid to achieving normal growth in this susceptible population. Surgical management is usually indicated for failure of medical management, complication, or malignancy. Algorithms for diagnostic evaluation and treatment of pediatric inflammatory bowel disease are presented. The specific psychosocial issues facing these patients are also discussed in this review as are the future goals of research in the complex problem of pediatric inflammatory bowel disease.     

Risk of cardiovascular disease in inflammatory bowel disease

Abundant scientific evidence supporting an association between inflammatory bowel disease(IBD) and venous thromboembolic events, caused by an IBD related hypercoagulability, is acknowledged and thromboprophylactic treatment strategies are now implemented in the management of IBD patients. In contrary, the risk of arterial thromboembolic disease, as ischemic heart disease, cerebrovascular events, and mesenteric ischemia in patients with IBD remains uncertain and the magnitude of a potentially increased risk is continuously debated, with ambiguous risk estimates among studies. The evident role of inflammation in the pathogenesis of atherosclerosis forms the basis of a biological plausible link; the chronic systemic inflammation in IBD patients increases the risk of atherosclerosis and thereby the risk of thrombotic events. Further, studies have shown that the burden of traditional risk factors for atherosclerosis, such as obesity, diabetes mellitus, and dyslipidemia is lower in IBD populations, thus further strengthen the role of non-traditional risk factors, as chronic inflammation in the linking of the two disease entities. Likewise, mortality from cardiovascular disease in IBD remains questioned. The aim of the current review is to give an up-date on the existing evidence of the possible association between IBD and cardiovascular disease and to discuss traditional and non-traditional risk factors.     

Role of cytokines in inflammatory bowel disease

Inflammatory bowel disease （IBD）, which includes Crohn’s disease （CD） and ulcerative colitis （UC）, rep- resents a group of chronic disorders characterized by inflammation of the gastrointestinal tract, typically with a relapsing and remitting clinical course. Mucosal mac- rophages play an important role in the mucosal im- mune system, and an increase in the number of newly recruited monocytes and activated macrophages has been noted in the inflamed gut of patients with IBD. Activated macrophages are thought to be major con- tributors to the production of inflammatory cytokines in the gut, and imbalance of cytokines is contributing to the pathogenesis of IBD. The intestinal inflammation in IBD is controlled by a complex interplay of innate and adaptive immune mechanisms. Cytokines play a key role in IBD that determine T cell differentiation of Th1, Th2, T regulatory and newly described Th17 cells. Cytokines levels in time and space orchestrate the development, recurrence and exacerbation of the inflammatory process in IBD. Therefore, several cyto- kine therapies have been developed and tested for the treatment of IBD patients.     

High incidence of inflammatory bowel disease in The Netherlands

PURPOSE: To gain recent epidemiologic information about inflammatory bowel disease in The Netherlands, a prospective study over four years (1991–1995) was performed. METHODS: The incidence of inflammatory bowel disease and its subgroups was examined using standardized reports of newly diagnosed patients. A separate study compared the Inflammatory Bowel Disease Registration and computerized diagnostic files of a subgroup of general practitioners with the aim of estimating completeness of case ascertainment. RESULTS: The following mean incidence rates (per 100,000 inhabitants and year) were found: 6.9 (95 percent confidence interval, 5.9–7.9) for Crohn's disease, 10 (95 percent confidence interval, 8.7–11.2) for ulcerative colitis (23 percent of these with ulcerative proctitis), and 1.1 (95 percent confidence interval, 0.7–1.5) for indeterminate colitis. In the age category 20 to 29 years, the incidence rate of Crohn's disease with small-bowel involvement was higher in females than in males. In extended ulcerative colitis, a male preponderance was observed in the older age groups. Estimated case ascertainment was 78 percent. CONCLUSIONS: Compared with recent studies in neighboring countries, the observed age and gender standardized incidence rates are high in the south of The Netherlands. Completeness of case ascertainment might have contributed to this observation; however, case ascertainment was low in ulcerative proctitis. In the study area, differences in age and gender standardized incidence rates and in disease localizations could be compatible with an influence of environmental risk factors.Supported by The Development Fund, University Hospital Maastricht, Byk BV, Zwanenburg, and Pharmacia BV, Woerden, The Netherlands. The European Collaborative Study of Inflammatory Bowel Disease has been assisted by a grant of the European Communities Brussels (DG XII-F-6).     

Antineutrophil cytoplasmic antibodies in inflammatory bowel disease

PURPOSE: Perinuclear antineutrophil cytoplasmic antibodies have been found consistently in patients with ulcerative colitis; however, their pathogenetic and clinical role is still uncertain. In this study we tested the prevalence of perinuclear antineutrophil cytoplasmic antibodies in a large population of patients with ulcerative colitis and Crohn's disease, with particular attention to the possible correlation with clinical features. METHODS: Perinuclear antineutrophil cytoplasmic antibody reactivity was investigated with indirect immunofluorescence in 279 patients with ulcerative colitis, 110 patients with Crohn's disease, and 252 unrelated healthy subjects. RESULTS: Perinuclear antineutrophil cytoplasmic antibodies were found in 84 of 279 patients with ulcerative colitis (30 percent), 10 of 110 patients with Crohn's disease (9 percent), and 2 of 252 healthy subjects (<1 percent;P<0.001), respectively. Perinuclear antineutrophil cytoplasmic antibodies were significantly more frequent in patients with ulcerative colitis with higher relapse rate (43vs. 27 percent;P<0.002), and patients with Crohn's disease with colitis (27vs. 2.5 percent;P<0.0003). Perinuclear antineutrophil cytoplasmic antibodies were also significantly less frequent in patients with ulcerative colitis in remission (18vs. 34 percent;P<0.0025). CONCLUSIONS: In this study we confirm the relative specific of perinuclear antineutrophil cytoplasmic antibodies, either for ulcerative colitis or for Crohn's disease involving the colon. Perinuclear antineutrophil cytoplasmic antibodies were more frequently found in patients with ulcerative colitis with a more aggressive clinical behavior; however, their presence had a limited value in identifying homogeneous subgroups of patients in our population.Presented in part at the Digestive Disease Week Meeting, San Francisco, California, May 19 to 22, 1996.     

Venous thromboembolism with inflammatory bowel disease

Venous thrombosis and thromboembolism appear to be increased in patients with inflammatory bowel disease. Although several acquired and genetic risk factors are known, about half that develop a thromboembolic event have no identifiable risk factor. Control of the inflammatory process is thought to be the key factor in risk reduction for thrombotic events. Prophylactic use of anticoagulants is not universally recommended, but possible use should be reviewed in an individual patient after evaluation of the risks, such as hemorrhage, compared to potential benefits. Particular consideration should be given if there has been a prior thrombotic event, if hospitalization will require surgery, or if an underlying coagulation disorder is present.     

Use of mycophenolate mofetil in inflammatory bowel disease

AIM： To assess the efficacy and safety of mycophenolate mofetil （MMF） prospectively in inflammatory bowel disease （IBD） patients intolerant or refractory to conventional medical therapy.
METHODS： Crohn＇s disease （CD） or ulcerative colitis/ IBD unclassified （UC/IBDU） patients intolerant or refractory to conventional medical therapy received MMF （500-2000 mg bid）. Clinical response was assessed by the Harvey Bradshaw index （HBI） or colitis activity index （CAI） after 2, 6 and 12 mo of therapy, as were steroid usage and adverse effects.
RESULTS： Fourteen patients （9 CD/5 UC/IBDU; 8M/6F; mean age 50.4 years, range 28-67 years） were treated and prospectively assessed for their response to oral MMF. Of the 11 patients who were not in remission on commencing MMF, 7/11 （63.6%） achieved remission by 8 wk. All 3 patients in remission on commencing MMF maintained their remission. Ten patients were still on MMF at 6 mo with 9/14 （64.3%） in remission, while of 12 patients followed for 12 mo, 8 were in remission without dose escalation （66.7%）. Three patients were withdrawn from the MMF due to drug intolerance. There were no serious adverse events attributed due to the medication.
CONCLUSION： MMF demonstrated efficacy in the management of difficult IBD. MMF appeared safe, well tolerated and efficacious for both short and long-term therapy, without the need for dose escalation. Further evaluation of MMF comparing it to conventional immunosuppressants is required.     

Osteoporosis in adult Sri Lankan inflammatory bowel disease patients

AIM： To determine if inflammatory bowel disease （IBD） is a risk factor for osteoporosis in adult Sri Lankans. METHODS： We identified eligible subjects from among consecutive patients diagnosed with IBD who attended our outpatient clinic. We included only patients aged between 20 and 70 years. Patients who were pregnant, had significant comorbidity, or were on calcium supplements or treatment for osteoporosis within the past 6 mo, were excluded. Healthy, ageand sex-matched controls were also recruited, in a control to patient ratio of 3：1. Both groups were screened for osteoporosis using peripheral dual energy X-ray absorptiometry scanning. RESULTS： The study population consisted of 111 IBD patients （male：female = 43：68; mean age 42.5 years） and 333 controls （male：female = 129：204; mean age 43.8 years）. The occurrence of osteoporosis among IBD patients （13.5%） was significantly higher than among controls （4.5%） （P = 0.001）. The frequency of osteoporosis was not significantly different between ulcerative colitis （14.45%） and Crohn＇s disease （10.7%）. However, on multivariate analysis, only age （P = 0.001）, menopause （P = 0.024） and use of systemic steroids （P 〈 0.001） were found to be associated independently with the occurrence of osteoporosis, while IBD, severity of disease, number of relapses, duration of illness or treatment other than systemic steroids were not. CONCLUSION： IBD does not appear to be an independent risk factor for the occurrence of osteoporosis in this population. However, the use of systemic steroids was a risk factor.