浅析益生菌在炎症性肠病中的临床应用

炎症性肠病(inflammatory disease,IBD)主要包括溃疡性结肠炎(Culcerative colitis,UC)和克罗恩病(Crohn disease,CD),是一种病因和发病机制尚未明确的慢性肠道炎症性疾病,其特点是复发与缓解交替出现,诊断主要依据临床病史和影像学、内镜和病理学检查[1].     

硫化氢在炎症性肠病中的作用研究进展

<正>炎症性肠病(inflammatory bowel disease,IBD)是以腹痛、腹泻为主要症状的非特异性慢性肠道炎症性疾病的总称。主要包括溃疡性结肠炎(ulcerative colitis,UC)和克罗恩病(Crohn’s disease,CD)等。该病发病率逐年升高,易复发且可并发其他多种疾病,严重影响患者生活质量。IBD病因与发病机制至今仍未完全明确,但普遍认为是遗传、环境及免疫等多种因素综合作用的结果。硫化氢(hydrogen sulfide,H₂S)是一种有毒气体,在体内参与包括肠道生理病理状态在内的多种生理过程。本文将就近年来H₂S及其在IBD中的研究进展加以综述。     

树突状细胞在炎症性肠病中的作用

炎症性肠病可能是遗传和环境因素共同作用导致肠道黏膜对肠道正常菌群免疫反应失常而引起的慢性非特异性炎症。树突状细胞在抗原富集的肠道环境中起着调节免疫应答的重要作用,既能启动免疫应答,又能诱导免疫耐受。这种调节功能缺陷可能导致炎症性肠病。本文就相关方面的研究进展进行综述。     

微小RNA在炎症性肠病诊断与治疗中的作用

炎症性肠病(IBD),主要包括克罗恩病和溃疡性结肠炎,是由胃肠道慢性炎性引起的,但具体的发病机制尚未阐明。微小RNA(miRNA)是进化中高度保守的非编码RNA,在转录后水平参与了人体内多种基因的调控。许多miRNA已被发现参与IBD的发生、发展,并且可能用作生物学标志及治疗靶点。本文就miRNA在IBD中的作用及在诊断与治疗中的作用进行综述。     

炎症性肠病的治疗

1　药物治疗1 1　口服氨基水杨酸制剂　柳氮磺胺吡啶 (ＳＡＳＰ)治疗炎症性肠病 (ＩＢＤ)已有多年。口服 4～ 6ｇ/ｄ ,可使 64%～ 77%患者产生良好的效果。临床及内镜检查缓解后 ,一般以 2 ｇ/ｄ维持治疗至少 1年。如病情复发 ,仍需加大至 4 ｇ/ｄ。严重病例可加用或改用糖皮质类固醇。ＳＡＳＰ的不良反应较多 ,主要有药物热、皮疹、食欲减退、贫血及中性粒细胞缺乏等 ,其发生率与用药剂量有关。近年来采用 5 -氨基水杨酸 (5 -ＡＳＡ)治疗ＩＢＤ。 5 -ＡＳＡ是ＳＡＳＰ在结肠分解后产生的发挥治疗作用的成分 ;但 5 -ＡＳＡ口服后容易吸收 ,…     

炎症性肠病

背景 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）。营养不良在IBD患者，尤其是CD患者中多见。根据疾病严重程度不同，65％-78％的CD患者和18％-62％的UC患者有体重下降。25％-80％的CD患者和26％-50％的UC患者存在低蛋白血症。半数CD患者存在贫血，可能继发于营养不良，而80％的UC患者存在贫血，主要原因为血液丢失。腹泻所致电解质丢失在CD和UC中均常见。     

益生菌在功能性肠病中的应用

微生态制剂也称微生态调节剂,是指含活菌、死菌、菌体组分和产物或是仅含活菌和死菌的微生物制剂,包括益生菌(probiotcs)、益生元(prebiotics)、合生元(synbiotics)三大类,具有调整微生态、保持微生态平衡、提高宿主健康水平的作用.益生菌由含足够数量的非致病性的特定活菌组成,通过改善宿主黏膜表面的微生物菌群来保持微生态平衡.临床常用的益生菌是乳酸杆菌、双歧杆菌、肠球菌和芽孢杆菌.     

益生菌在功能性肠病中的应用

微生态制剂也称微生态调节剂，是指含活菌、死菌、菌体组分和产物或是仅含活菌和死菌的微生物制剂，包括益生菌（probiotics）、益生元（prebiotics）、合生元（synbiotics）三大类，具有调整微生态、保持微生态平衡、提高宿主健康水平的作用。益生菌由含足够数量的非致病性的特定活菌组成，通过改善宿主黏膜表面的微生物菌群来保持微生态平衡。临床常用的益生菌是乳酸杆菌、双歧杆菌、肠球菌和芽孢杆菌。     

益生菌对实验性炎症性肠病的肠屏障与微生态影响研究进展

炎症性肠病(IBD)的病因至今未明.近10年来,随着多种IBD动物模型的陆续开发,使得对益生菌治疗作用的研究得以广泛开展.诸多实验研究表明,益生菌对多种IBD动物模型的炎性症状均有明显地改善作用,益生菌的这种作用可能与其抑制肠道致病菌、增强肠屏障功能、调节肠道黏膜免疫反应、降解肠道内在或外来的致病抗原等有关.     

Role of microecology in chronic inflammatory bowel diseases

Inflammatory bowel diseases (IBD) are chronic conditions of unknown etiology. Current therapy mitigates the severity of acute bouts of mucosal inflammation but an eradication therapy is lacking. Growing incidence of IBD is associated with social development. Epidemiology suggests a relationship between the establishment of the individual gut flora and the risk of developing IBD. Patients show an impaired tolerance towards commensal bacteria of the resident flora. Unrestrained activation of the intestinal immune system against some commensal bacteria appears to be responsible for the characteristic relapsing course of these diseases. Wide-spectrum antibiotic therapy reduces bacterial load and mitigates intestinal inflammation in human IBD and in animal models. Current research aims at the identification of probiotics for bacterial antagonism therapies. Probiotics are living microorganisms which upon ingestion in certain numbers exert health benefits beyond inherent basic nutrition. Colonization with a Lactobacillus reuteri strain can prevent the development of colitis in genetically susceptible mice. Other studies have used a bacterium genetically engineered to secrete the antiinflammatory cytokine IL-10 and demonstrated a therapeutic effect in animal models of colitis. Moreover, some probiotics may naturally exhibit antiinflammatory properties when interacting with the human gut mucosa. Prebiotics such as inulin have also been shown to prevent colonic inflammation in animal models. Preliminary clinical trials with probiotics in IBD are encouraging. Probiotics offer a valuable tool for the prevention and control of inflammatory bowel diseases.     

Role of intestinal flora in inflammatory bowel disease and probiotics place in their management

The pathogenic role of certain microorganism of intestinal flora has been demonstrated in experimental colitis in animals and strongly suspected in inflammatory bowel disease in human, especially in Crohn's disease and pouchitis. Probiotics are living non pathogenic microorganisms that, upon oral ingestion exert benefits on human health by modulating enteric flora or by stimulation of local immune system. The aim of this article is to remind the role of intestinal flora in inflammatory bowel disease, the mechanism of inflammation induced by this flora and to review through the literature, the different clinical studies performed with probiotics in human.     

Prebiotics in inflammatory bowel diseases

In genetically susceptible individuals, an altered mucosal immune response against some commensal bacteria of the gut ecosystem appears to be the principal mechanism leading to intestinal lesions in inflammatory bowel disease (IBD). The information currently available does not provide an exact explanation about the origin of this important dysfunction of the interaction between host and commensal bacteria, but an altered microbial composition has been detected in the gut ecosystem of patients with Crohn's disease or ulcerative colitis. Prebiotics are food ingredients not digested nor absorbed in the upper intestinal tract that are fermented by intestinal bacteria in a selective way promoting changes in the gut ecosystem. Experimental and human studies have shown that inulin and oligofructose stimulate saccharolysis in the colonic lumen and favour the growth of indigenous lactobacilli and bifidobacteria. These effects are associated with reduced mucosal inflammation in animal models of IBD. Strong experimental evidence supports the hypothesis that inulin and oligofructose can offer an opportunity to prevent or mitigate intestinal inflammatory lesions in human Crohn's disease, ulcerative colitis, and pouchitis. Encouraging results have been obtained in preliminary clinical trials.     

Etiopathogenesis of inflammatory bowel diseases

The pathogenesis of IBD is only partly understood; various environmental and host (e.g. genetic-, epithelial-, immune and non-immune) factors are involved. It is a multifactorial polygenic disease with probable genetic heterogeneity, some genes are associated with IBD itself, while others increase the risk of ulcerative colitis (UC) or Crohn's disease (CD) or are associated with disease location and/or behaviour. The role of environmental factors, in particular, enteric antigens, smoking and non-steroid anti-inflammatory drug use has been well established. However uptil now no proof of a role of any unique pathogenic bacteria or special dietary and/or psychosocial factor has been identified. In this hypothesis, the disease may develop in a genetically predisposed host as a consequence of disregulated immune response to environmental, in particular, enteric antigens, resulting in a continuous immune-mediated inflammation (in CD predominantly Th-1, in UC a modified Th-2 mechanisms are involved) and not in tolerance. As a consequence, the permeability of mucosa and the antigen challenge increases, in contrast, the disregulated immune response is unable to downregulate the inflammatory process. This will result in a continuous inflammation and tissue damage. The pathogenesis of CD is thought to be mainly an antigen driven, T-lymphocyte dependent process, while in UC the role of epithelial factors and activated granulocytes are essential.     

Redox homeostasis in inflammatory bowel diseases

Janus faced oxygen radicals are secondary messengers of intracellular signal transduction pathways but also cytotoxic agents of cells. Activation of signal transduction proteins on mild oxidant stress and metal elements are still not clearly understood. Oxygen free radicals may have several functions in the expression of cytokines associated with inflammatory bowel disease. The molecular mechanism between activation, and inhibition participants of signal transduction are delicately controlled. Antioxidant-prooxidant balance of the cells can be traced back to the concentration of free-SH and its oxidised form,-S-S-. Healthy erythrocytes and plasma are rich in antioxidants, but their type of protection, differs significantly. The balance of free radicals and antioxidants is disturbed in inflammatory bowel disease. The antioxidant defence mechanism depends on concentration of metal elements, which determines enzyme activities. It seems that nutritional supplementation and adequate therapy restore the ion homeostasis, although, Zn overdose may cause disturbance in iron metabolism and consequently may influence erythrocyte functions.     

Promotion of a favorable gut flora in inflammatory bowel disease

Recent evidence suggests that the composition of colonic flora plays a role in intestinal inflammation in inflammatory bowel disease (IBO). This review examines the evidence that altering the concentrations of colonic bacteria might benefit patients with this condition.     

Hematologic aspects of inflammatory bowel diseases

Anaemia, thrombocytosis are common secondary changes in inflammatory bowel disease (IBD), reflecting the clinical severity of the IBD cases, too. On the other hand, increased platelet function, fibrinolytic abnormalities, hypercoagulation of IBD patients predispose to thromboembolic events, and they may as well contribute to the local microcirculatory alterations leading to IBD itself. Reduced FXIII levels have been observed in IBD, which seems to be correlated with mucosal repair and might have therapeutic importance, too. Genetic thrombophilia received much attention recently, however, much less is known how frequent they are in IBD, what their clinical significance is, do they modify the clinical course itself. A short, concise review about links between haematology and IBD is given.