炎症性肠病应用环孢菌素A治疗7例分析

<正> 炎症性肠病(IBD)包括溃疡性结肠炎(UC)和克罗恩病(CD),是以慢性反复性发作为特点的肠道炎症性疾病,前者仅累及结肠,后者整个胃肠道都可受累。两病在不同国家的发病率不同,西方国家的发病率较高,UC约为2/10~5～10/10~5,CD约在6/10~5～10/10~5,我国尚无权威的统计学数据,但发病率自60年代后逐渐增多,而且多为青壮年发病,并发症多且重,严重影响生活和劳动能力。 IBD的传统用药包括柳氮磺胺吡啶(SASP)或其     

炎症性肠病的药物治疗现状

炎症性肠病（inflammatory bowel disease,IBD）目前是消化系统疾病的研究热点之一,主要包括溃疡性结肠炎（ulcerative colitis,UC）和克罗恩病（Crohn''s disease,CD）,其发病机制尚未完全阐明,也尚无针对IBD的有效治疗药物。随着对IBD发病机制的深入研究,出现了一些新型药物和制剂。笔者就IBD及其药物治疗的研究现状作一简要综述。     

炎症性肠病治疗进展

炎症性肠病(Inflammatory bowel disease，IBD)是一组病因不明的慢性、反复发作性肠道非特异炎症性疾病，主要包括溃疡性结肠炎(ulcerative colitis，UC)和克罗恩病(Crohn’S disease，CD)，发病率在我国乃至亚洲地区呈增高趋势，日前的主要治疗方法是抗炎和调节免疫反应：近年来随着对IBD发病机制的深入研究，许多全新的治疗方法和新型的药物制剂开始应用于临床。现就IBD的治疗进展情况作一综述。     

炎症性肠病的生物治疗

炎症性肠病(inflammatory bowel disease,IBD)是胃肠道的慢性炎症,临床上主要表现为溃疡性结肠炎和克罗恩病,均由免疫调节紊乱所致。抗原激发的IBD是特异的慢性炎症。IBD患者肠上皮屏障功能存在缺陷,容许细菌种植,通过抗原递呈细胞(主要是黏膜树突状细胞和巨噬细胞),将     

儿童炎症性肠病的药物治疗

炎症性肠病(IBD)是慢性复发性肠道非特异性炎症.近年来,亚非国家IBD的发病率也呈上升趋势.儿童克罗恩病(CD)和溃疡性结肠炎(UC)的治疗反应个体差异很大.本文介绍氨基水杨酸类药物、糖皮质激素、免疫抑制药物、生物制剂及微生态制剂等在儿童IBD治疗中的应用,以及不同药物在诱导缓解和维持缓解中的作用,并探讨"下台阶"疗法在儿童IBD中的应用概念.     

炎症性肠病的药物治疗

1什么是炎症性肠病？ 炎症性肠病（inflammatory bowel diseases,IBD）是一种特殊的慢性肠道炎症性疾病,主要包括克罗恩病和溃疡性结肠炎。克罗恩病可发生于消化道任何部位,为慢性、反复发作的肠壁全层性炎症,常见于回肠末端和结肠。溃疡性结肠炎为发生于结肠的弥漫性、浅表性、局限于黏膜层的炎症,常见于直肠和乙状结肠。     

炎症性肠病发病机制与治疗研究进展

传统的炎症性肠病(Inflammory Bowel Disease，IBD)的治疗，着眼于控制炎症和调节免疫紊乱，以有效控制疾病发作和维持缓解。尽管常用的三大类药物，水杨酸类、类固醇激素和免疫抑制剂的研究均有很大的发展，并仍为IBD治疗的主药，但对克罗恩病(CD)与溃疡性结肠炎(UC)的缓解率分别仅70％与80％左右，即便是最佳的维持缓解方案也仅能使复发率降低50%左右，CD与UC分别约有2／3与1／3的病例最终需手术治疗。因此，患者的生活质量仍然受到一定影响。随着IBD发病机制的深入研究，特别是近10多年来在环境因素、遗传因素与免疫反应异常等方面研究的重大进展，使IBD治疗从概念到具体措施都发生了深刻变化。     

炎症性肠病的治疗药物研究进展

摘要：炎症性肠病是一种慢性肠道炎症性疾病,包括溃疡性结肠炎和克罗恩病,易导致严重的消化吸收障碍,病情反复,需终身治疗,严重影响患者的生活及心理健康。传统的治疗药物主要有氨基水杨酸制剂、糖皮质激素、免疫抑制药等。随着对其发病机制研究的不断深入,针对发病机制而开发的新兴药物有TNF-α抑制药、抗黏附生物制剂、白细胞介素（IL）-12/IL-23抑制药,以及一系列的小分子药物,如Janus激酶（JAK）抑制药、鞘氨醇-1-磷酸受体调节药、磷酸二酯酶4抑制药等。此外,非药物治疗和辅助治疗也在逐渐显示其独特的优势。本文针对炎症性肠病治疗药物的研究进展进行综述,以期为临床治疗方案和药物研发提供依据。     

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(Idiopathicinflammatory bowel disease),包括溃疡性结肠炎(Ulcerative colitis,UC)和克罗恩病(Crohn’s dis-ease,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。IBD的病因和发病机制尚不完全清楚,目前认为主要与免疫功能异常和炎症介质生成增多相关。若阻断或抑制免疫反应和特异性受体的作用、减少或抑制前列腺素、白三烯、血小板激活因子(PAF)及某些细胞因子等,均可使病情有所缓解。IBD常用的治疗药物为氨基…     

Drug therapy of inflammatory bowel disease

The drugs that are effective in inflammatory bowel disease (IBD) act by inhibiting the chronic unregulated intestinal inflammation in these patients. The mainstays of the drug therapy of IBD are a variety of formulations of 5-aminosalicylic acid (5-ASA), the conventional and newer low bioavailability glucocorticoids, the nitroimidazole antibiotic metronidazole, and certain immunomodulating agents. Increased understanding of the mechanisms of inflammation in IBD has permitted the development of effective designer drugs. These agents are products of the biotechnology industry and include antibodies to tumor necrosis factor (TNF)-alpha, antisense oligonucleotides and recombinant human interleukin (IL)-10. In addition, a number of other agents such as nicotine and n-3 fatty acids are useful in certain patients. This review first focuses on the pharmacology and mechanism of action of these drugs in IBD, followed by an approach to the treatment of patients with ulcerative colitis (UC) and Crohns disease (CD). The recommendations consider type and activity of IBD and are based largely on data from controlled trials and systematic reviews in the IBD literature.     

帕金森病的药物治疗

帕金森病(PD)的多种治疗药物是针对运动症状的治疗,而PD非运动症状可降低患者生活质量,甚至可加重PD患者的运动症状和功能残疾,其治疗也不容忽视.本文综述PD运动症状的药物治疗原则,以及各类药物的临床使用及其疗效评价,同时汇总多种非运动症状的药物治疗研究.     

帕金森病治疗药物的临床应用进展

帕金森病的临床治疗药物目前主要为对症治疗药物,有左旋多巴、多巴胺受体激动剂、单胺氧化酶B抑制剂、儿茶酚胺-O-甲基转移酶抑制剂等,其中雷沙吉兰、普拉克索、恩托卡朋等治疗效果良好.同时,神经保护性药物也是当前的研究热点.本文综述帕金森病治疗药物的临床应用进展.     

Biologic therapy for inflammatory bowel disease

Despite all of the advances in our understanding of the pathophysiology of inflammatory bowel disease (IBD), we still do not know its cause. Some of the most recently available data are discussed in this review; however, this field is changing rapidly and it is increasingly becoming accepted that immunogenetics play an important role in the predisposition, modulation and perpetuation of IBD. The role of intestinal milieu, and enteric flora in particular, appears to be of greater significance than previously thought. This complex interplay of genetic, microbial and environmental factors culminates in a sustained activation of the mucosal immune and non-immune response, probably facilitated by defects in the intestinal epithelial barrier and mucosal immune system, resulting in active inflammation and tissue destruction. Under normal situations, the intestinal mucosa is in a state of 'controlled' inflammation regulated by a delicate balance of proinflammatory (tumour necrosis factor [TNF]-alpha, interferon [IFN]-gamma, interleukin [IL]-1, IL-6, IL-12) and anti-inflammatory cytokines (IL-4, IL-10, IL-11). The mucosal immune system is the central effector of intestinal inflammation and injury, with cytokines playing a central role in modulating inflammation. Cytokines may, therefore, be a logical target for IBD therapy using specific cytokine inhibitors. Biotechnology agents targeted against TNF, leukocyte adhesion, T-helper cell (T(h))-1 polarisation, T-cell activation or nuclear factor (NF)-kappaB, and other miscellaneous therapies are being evaluated as potential therapies for IBD. In this context, infliximab is currently the only biologic agent approved for the treatment of inflammatory and fistulising Crohn's disease. Other anti-TNF biologic agents have emerged, including CDP 571, certolizumab pegol (CDP 870), etanercept, onercept and adalimumab. However, ongoing research continues to generate new biologic agents targeted at specific pathogenic mechanisms involved in the inflammatory process. Lymphocyte-endothelial interactions mediated by adhesion molecules are important in leukocyte migration and recruitment to sites of inflammation, and selective blockade of these adhesion molecules is a novel and promising strategy to treat Crohn's disease. Therapeutic agents that inhibit leukocyte trafficking include natalizumab, MLN-02 and alicaforsen (ISIS 2302). Other agents being investigated for the treatment of Crohn's disease include inhibitors of T-cell activation, peroxisome proliferator-activated receptors, proinflammatory cytokine receptors and T(h)1 polarisation, and growth hormone and growth factors. Agents being investigated for treatment of ulcerative colitis include many of those mentioned for Crohn's disease. More controlled clinical trials are currently being conducted, exploring the safety and efficacy of old and new biologic agents, and the search certainly will open new and exciting perspectives on the development of therapies for IBD.     

炎性肠病的基因疗法

炎性肠病(inflammatory bowel disease,IBD)包括溃疡性结肠炎(ulcerative colitis,UC)和克罗恩病(Crohn's disease,CD),其致病原因尚不清楚。目前常用的药物治疗伴有明显不良反应而且无法完全治愈疾病。最近几年IBD基因治疗引起关注。通过抑制炎症因子基因以及上调免疫调节因子基因表达来恢复肠道细胞因子的平衡是一种有前途的治疗IBD的方法。本文简要介绍几个可以用于IBD基因治疗的分子(如TNF-α、IL-10、NF-κB和IL-22等)以及它们相应的动物临床试验结果和未来展望。     

Optimum therapy for acute pelvic inflammatory disease

Neisseria gonorrhoeae is responsible for about one-third to one-half of cases of acute pelvic inflammatory disease (PID), although there is considerable geographical variation. Chlamydia trachomatis is also an important aetiological agent, and is currently isolated 4 times more commonly from the cervix than the gonococcus. However, it is now clear that acute PID is polymicrobial in aetiology. Even when N. gonorrhoeae and/or C. trachomatis are isolated from the endocervix, anaerobes such as Bacteroides fragilis, Peptococcus and Peptostreptococcus and aerobes, especially the Enterobacteriaceae such as E. coli, are also frequently isolated. Bacterial synergism, coinfection with the gonococcus and C. trachomatis and the involvement of multiple other micro-organisms including aerobes and anaerobes and antibiotic resistance make the selection of an optimal antibiotic regimen difficult. The Centers for Disease Control (CDC) recommendations first proposed in 1982 and revised in 1985 emphasise broad spectrum antimicrobial therapy including coverage of C. trachomatis. In September 1989, the CDC revised its recommendation for the treatment of acute PID. Current recommendations include the use of newer third generation cephalosporins such as ceftriaxone, ceftizoxime and cefotaxime which give excellent coverage of the gonococcus and the Enterobacteriaceae. It is still important to include doxycycline or a tetracycline to cover C. trachomatis. For patients with advanced disease or a tubo-ovarian abscess, clindamycin plus gentamicin has been the regimen of choice. Aztreonam, a new monobactam, has several advantages over gentamicin including less toxicity, more dependable blood levels and good coverage of N. gonorrhoeae and the Enterobacteriaceae.     

炎症性肠疾病的微生态调节治疗

炎症性肠病包括溃疡性结肠炎、克罗恩病等,表现为肠黏膜免疫系统对肠内共生细菌产生异常反应的一类慢性肠道疾病,有明显家族聚集性但病因不明,肠道与其共栖微生物的稳态平衡一旦破坏即可发病。不同遗传个体对有害菌、无害菌或益生菌等肠内共生菌呈现不同的反应性,而肠内共生菌对肠道卫生以及天然免疫和获得免疫间的互动具有重要作用。