IBD药物治疗进展

引言:炎症性肠病(inflammatory bowel disease,IBD)是一组病因尚未完全清楚的慢性、非特异性肠道炎症性疾病,包括溃疡性结肠炎( ulcerative colitis,UC)和克罗恩病(Crohn's disease,CD).IBD在西方国家相当常见,但近20年来,随着人们生活方式的改变和诊断水平的提高,IBD的发病率在我国逐年上升.UC主要累及结肠黏膜和黏膜下层,范围从远段结肠开始,可逆向近段发展,可累及全结肠和末端结肠,呈连续性分布.     

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炎症性肠病(inflammatory bowel diseases,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(ulcerative colitis,UC)和克罗恩病(Crohn's disease,CD).前者又称非特异性溃疡性结肠炎,是一种原因不明的直肠和结肠炎症,病变主要限于大肠黏膜与黏膜下层.临床主要表现为腹泻、腹痛和黏液脓血便,多呈反复发作慢性过程.后者为一种慢性肉芽肿性炎症,病变可累及胃肠道各部位,而以末段回肠及其邻近结肠为主,多呈节段性、非对称性分布.临床主要表现为腹痛、腹泻、瘘管、肛门及肛周病变和不同程度的肠外表现.     

对炎症性肠病诊断治疗规范的建议

炎症性肠病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)。前者是一种慢性非特异性的结肠炎症 ,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 ,甚至累及全结肠及末段回肠 ,呈连续性分布。临床主要表现为腹泻、腹痛、黏液脓血便。后者病变可累及胃肠道各部位 ,而以末段回肠及其邻近结肠为主 ,为一种慢性肉芽肿性炎症 ,多呈节段性、非对称性分布。临床主要表现为腹痛、腹泻、瘘管、肛门病变和不同程度的全身症状。中华医学会消化病学分会曾先后…     

对炎症性肠病诊断治疗规范的建议

炎症性肠病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 (Ｃｒｏｈｎ病 ,ＣＤ)。前者是一种慢性非特异性的结肠炎症 ,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 ,甚至累及全结肠及末段回肠 ,呈连续性分布。临床主要表现为腹泻、腹痛、黏液脓血便。后者病变可累及胃肠道各部位 ,而以末段回肠及其邻近结肠为主 ,为一种慢性肉芽肿性炎症 ,多呈节段性、非对称性分布。临床主要表现为腹痛、腹泻、瘘管、肛门病变和不同程度的全身症状。中华医学会消化…     

肠道菌群及其代谢物与溃疡性结肠炎的关系

溃疡性结肠炎(ulcerative colitis,UC)是一种慢性非特异性结肠和直肠炎性疾病,属于炎症性肠病(inflammatory bowel disease,IBD)中的一种。病变主要局限于大肠黏膜和黏膜下层,通常涉及直肠和乙状结肠,也可延伸至整个结肠。病程漫长,常反复发作,严重影响患者的生活质量[1]。流行病学调查发现,UC见于任何年龄,但初发以20~30岁多见,男女比例为1.0:1~1.3:1。     

中国炎症性肠病的诊断

炎症性肠病(IBD)是一种病因及发病机制尚不十分清楚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).UC是一种慢性非特异性结肠炎症,病变主要累及结肠黏膜层和黏膜下层;CD是一种胃肠道的慢性肉芽肿性炎性疾病,病变可累及消化道各部位,以末端回肠及邻近结肠最为常见,病变为穿壁性炎症,呈节段性、非对称性分布.     

肠黏膜通透性改变与炎症性肠病关系的研究进展

<正>炎症性肠病(inflammatory bowel disease,IBD)是一种累及回肠、直肠、结肠的慢性复发性炎症性肠道疾病,包括溃疡性结肠炎(ulcerative colitis,UC)和克罗恩病(crohn’s disease,CD)。目前认为其发病机制与免疫因素、遗传因素和环境因素等有关。持续10年以上和病变范围较大的IBD增加癌变的风险[1]。近年来,肠黏膜屏障功能损伤被认为是炎症性肠病发病机制中的主要因素,成为被关注的焦     

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）。前者是一种慢性非特异性结肠炎症，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，甚至累及全结肠和末段回肠，呈连续性分布；临床主要表现为腹泻、腹痛和黏液脓血便。后者为一种慢性肉芽肿性炎症，病变可累及胃肠道各部位，[第一段]     

炎症性肠病与微生态制剂

炎症性肠病(inflammatory bowel disease,IBD)是一种病因尚不清楚的慢性肠道炎症性肠病,包括溃疡性结肠炎(ulcera-tive colitis,UC)和克罗恩病(Crohn’s disease,CD)两大类。其发病机制至今仍不清楚,遗传易感性、黏膜免疫和肠道微生态环境三者的相互作用被认为可能参与IBD的发病。目前的治疗包括传统治疗和生物制剂,药物治疗包括5大类型,分别是抗炎药物、免疫抑制剂、生物制剂、抗生素及症状缓解药物。微生物在IBD发病中的作用一直受到重视,本文就微生态制剂在炎症性肠病中的应用情况作一综述。     

肠道黏膜岩藻糖基化与炎症性肠病研究进展

炎症性肠病(inflammatory bowel disease, IBD)是一种病因不明、异常免疫介导的肠道慢性及复发性炎症性疾病.肠道黏膜岩藻糖基化是在岩藻糖基转移酶的调控下,将岩藻糖转移到肠道黏膜蛋白质侧链上形成岩藻糖苷键的过程.肠道黏膜岩藻糖基化在IBD中的作用机制尚未完全探明,本文就肠道黏膜岩藻糖基化与IBD研究进展作一综述.     

State of knowledge of helminth fauna of freshwater fishes of Poland

A total 89 fish and lamprey species has been recorded from Polish freshwater habitats. Twenty-seven of them (30.3%) have not been surveyed for parasitic helminthes. Some of the latter fishes are either rare or not easily accessible. Other live only in specific habitats in scattered localities. An important obstacle for studying parasite faunas of some fishes may be their status on an endangered species. Among the non-surveyed fishes, are those which have been relatively recently introduced to Poland or migrated there on their own. The present paper attempts to review all hitherto not studied helminthologically fish species, their habitats, localities and current protection status.     

高血压降压治疗目标的再认识

根据传统的高血压水平的定义,1993年WHO高血压治疗指南提出血压控制目标为<140/90mm Hg(1mm Hg=0.133kPa),但是并非所有患者都必须将血压降至同一水平,而应根据患者情况进行个体化治疗。Framingham进行的一项长达10～12年的心血管事件研究发现,第5年后,正常上限血压[收缩压(SBP     

Lack of correlation of degree of villous atrophy with severity of clinical presentation of coeliac disease

BACKGROUND AND AIM: Both the clinical presentation and the degree of mucosal damage in coeliac disease vary greatly. In view of conflicting information as to whether the mode of presentation correlates with the degree of villous atrophy, we reviewed a large cohort of patients with coeliac disease. PATIENTS AND METHODS: We correlated mode of presentation (classical, diarrhoea predominant or atypical/silent) with histology of duodenal biopsies and examined their trends over time. RESULTS: The cohort consisted of 499 adults, mean age 44.1 years, 68% females. The majority had silent coeliac disease (56%) and total villous atrophy (65%). There was no correlation of mode of presentation with the degree of villous atrophy (p=0.25). Sixty-eight percent of females and 58% of males had a severe villous atrophy (p=0.052). There was a significant trend over time for a greater proportion of patients presenting as atypical/silent coeliac disease and having partial villous atrophy, though the majority still had total villous atrophy. CONCLUSIONS: Among our patients the degree of villous atrophy in duodenal biopsies did not correlate with the mode of presentation, indicating that factors other than the degree of villous atrophy must account for diarrhoea in coeliac disease.