溃疡性结肠炎的中医病因病机探讨

中医学认为多种致病因素,外感六淫、饮食不节、情志失调、禀赋不足等均可通过损伤脾胃功能而引发溃疡性结肠炎,通过探讨诸致病因素与脾胃功能失调间的关系,剖析溃疡性结肠炎的中医病因病机,有助于深入了解溃疡性结肠炎的发病机制和发病规律,提高中医药治疗溃疡性结肠炎的临床疗效。     

溃疡性结肠炎的浅析

目的探讨溃疡性结肠炎的病因及治疗方法。方法对近10年的来溃疡性结肠炎的病因研究和治疗方法进行研究、分析,总结。结果通过研究发现,溃疡性结肠炎的病因目前尚不明确,与多种因素相关,治疗主要以药物治疗为主,严重者采用手术治疗。结论溃疡性结肠炎的病因及治疗方法还需要进一步探讨。     

溃疡性结肠炎的药物治疗

溃疡性结肠炎的药物治疗张军，谢庆荣（山东沂水中心医院２７６４００）慢性溃疡性结肠炎简称溃疡性结肠炎（ＵＣ），是一种原因不明的炎症性疾病。发病可能与免疫、感染、遗传、过敏及神经因素有关。临床以反复发作、迁延不愈的腹痛腹泻、粘液或脓血便为特征，无特效治疗...     

溃疡性结肠炎的药物治疗进展

溃疡性结肠炎(UC) 为多发性难治病，发病机制复杂,是多因素、多环节相互作用的结果。该文作者对其治疗药物氨基水杨酸类、肾上腺皮质激素类、中药、抗菌药、免疫抑制药等的适应证、疗效和不良反应等方面进行了评价。UC的治疗多采用肠道给药，能增加药物与病变部位的接触面积且可降低不良反应。     

美沙拉嗪联合中药治疗溃疡性结肠炎36例临床分析

溃疡性结肠炎发病机制复杂,是多因素、多环节相互作用的结果,以腹泻、粘液脓血便、腹痛为主要症状。病情轻重不等,反复发作,缠绵难愈,近2年来我们采用美沙拉嗪联合中医治疗溃疡性结肠炎36例,取得满意疗效,报告如下。     

氟哌噻吨美利曲辛联合美沙拉嗪治疗溃疡性结肠炎

<正>溃疡性结肠炎是一种慢性肠道非特异性炎症,它主要累及结肠黏膜和黏膜下层,发病从远端结肠,逆行向近端蔓延,可逐渐累及整个结肠,呈连续性分布,同时可伴有肠外的表现。目前溃疡性结肠炎的发病机制尚不清楚,多与免疫机制有关。但近年来临床发现,该病的发生与精神心理因素有着极大的关系,且精神因素又直接参与了该病的复发。2000年以来我院采取在原抗溃疡性结肠炎治疗的同时,加用氟哌噻吨美利曲辛(黛力新),获得较为满意的结果。     

激素加锡类散、甲硝唑治疗溃疡性结肠炎23例分析

疡性结肠炎的病因尚未完全明确,近年来关于发病机制的研究集中在免疫机制,并认为和遗传因素有关,感染、精神因素等与本病发病也有一定的关系.所以治疗较困难,我们从1992年～2001年采用激素加锡类散、甲硝唑治疗23例溃疡性结肠炎取得了较好的疗效.报告如下:     

基于中医整体观探讨溃疡性结肠炎合并消化性溃疡的作用机制及治疗思路

近年来发现临床中溃疡性结肠炎合并消化性溃疡的患者逐年增多,这些不仅严重影响患者的生活及工作质量,也是临床诊治的难点。溃疡性结肠炎合并消化性溃疡的发病机制不明,溃疡性结肠炎是一种自身免疫性疾病,但有研究表明两者的发生在病因学上有着相似的病因基础和共同影响因素。本文试从中医整体观,运用五脏一体观和形神一体观,较大程度解释两者的相关性并为临床诊治提供思路,并针对溃疡性结肠炎与消化性溃疡相似的发病高危因素采取相应预防治疗措施,并探讨其积极的临床意义。     

美沙拉嗪与枯草杆菌二联活菌肠溶胶囊联用治疗溃疡性结肠炎疗效探讨

<正>溃疡性结肠炎作为一种肠道慢性非特异性病变,患者主要表现为反复发作腹痛、腹泻及黏液脓血便等,炎症多侵犯结肠、直肠黏膜及黏膜下层[1]。我国溃疡性结肠炎发病率呈逐年增高趋势;其发病机制还未完全阐明,美沙拉嗪被认为是治疗溃疡性结肠炎首选药物,同时近年来随着肠道微环境稳     

溃疡性结肠炎的药物治疗

<正> 溃疡性结肠炎是一种原因不明的慢性结肠炎,病变主要限于结肠的粘膜,表现为炎症或溃疡,多累及直肠和远端结肠,但可向近端扩展,以至遍及整个结肠。其发病机理目前还不十分清楚,主要与感染、自身免疫、精神、过敏反应等因素有关。溃疡性结肠炎的治疗包括一般治疗、药物治疗及手术治疗。目前对于溃疡性结肠炎的药物治疗主要包括5-氨基水杨酸制剂、皮质类固醇制剂、免疫抑制剂、抗生素及中药制剂。其药物的选择主要根据患者的疾病严重程度及对药物的耐受性而定,轻度主要选择5-氨基水杨酸制剂,中度在5-氨基水杨酸     

The role of TNFalpha in ulcerative colitis

Standard of care for ulcerative colitis involves long-term pharmacotherapy or colectomy. Approximately 20% to 30% of patients eventually require a colectomy because patients either do not respond or cannot tolerate the currently available pharmacotherapies. Advances in our knowledge of the pathophysiology of ulcerative colitis have highlighted the importance of cytokines such as tumor necrosis factor alpha (TNFalpha) in the inflammatory process. TNFalpha is a proinflammatory mediator that plays an integral role in the pathogenesis of inflammatory bowel disease. In addition, mounting evidence indicates a genetic association between TNFalpha and ulcerative colitis. Furthermore, increased TNFalpha levels have been demonstrated in studies of patients with ulcerative colitis. TNFalpha is likely an important component in the pathophysiology of ulcerative colitis, and thus agents targeting TNFalpha in ulcerative colitis have been studied. Recent randomized controlled trials have confirmed that biologic anti-TNFalpha therapy is effective in ulcerative colitis. Soluble TNFalpha receptors or biologic agents that suppress or inhibit TNFalpha production may also show therapeutic promise.     

Tumor necrosis factor alpha in ulcerative colitis and diverticular disease associated colitis

Conventional treatment of moderate-severe ulcerative colitis (UC) has resulted in only a limited therapeutic benefit. Advancing knowledge of UC pathogenesis and recent advances in biotechnology have led to the development of biological agents that selectively target individual inflammatory pathways. In particular, the role of tumor necrosis factor alpha (TNF-alpha) in UC pathogenesis has been clarified by serological and immunohistochemical studies in humans and by experimental models. Clinical efficacy of anti-TNF-alpha therapy with infliximab has been assessed in two large controlled trials, showing a good compromise between therapeutic gain and safety. The aim of this review is to provide an insight into the role of TNF-alpha and anti-TNF-alpha therapy in patients with UC and diverticular disease associated colitis.     

Immunosuppressive and biologic therapy for ulcerative colitis

Introduction: Recent insight into the pathogenesis of ulcerative colitis have led to the development of new treatment options. A better understanding of IBD pathophysiology has progressively led to a more frequent use of immunosuppressants and biologics.

Areas covered: The use of the conventional immunomodulators, such as azathioprine, 6-mercaptopurine, methotrexate, cyclosporine and tacrolimus, and anti-TNF-α agents, such as infliximab and adalimumab, in the treatment of ulcerative colitis are reviewed. Moreover, the ongoing studies evaluating the efficacy of emerging immunosuppressants in treating patients with ulcerative colitis are discussed. An effort is made to explore some critical areas in which early and more diffuse use of these agents may be advocated.

Expert opinion: Ulcerative colitis is a chronic condition mainly affecting young people in their more productive age, and determining high indirect costs to the patient and to society. Thus, there is a need for optimizing and renewing our traditional therapeutic approach to UC, and new therapies beyond conventional treatment options possibly aiming to change the poor clinical course of many patients with ulcerative colitis. Keeping in mind this potentially new therapeutic scenario, there are some critical areas in which early and more diffuse use of conventional and emerging new immunomodulators is advocated.     

Dapagliflozin,an SGLT2 inhibitor,ameliorates acetic acid-induced colitis in rats by targeting NFκB/AMPK/NLRP3 axis

Inflammopharmacology - The development of effective treatment strategies has been hindered by the complex pathogenesis of ulcerative colitis (UC). UC patients treated with current therapeutic...     

Genetics and ulcerative colitis: what are the clinical implications?

Substantial progress has been made in the last years in characterizing the susceptibility genes involved in IBD pathogenesis, especially for Crohn's disease. Although some genetic factors associated with Crohn's disease also predispose individuals to ulcerative colitis, markers specific only for ulcerative colitis have been found. Recent genome-wide association studies in ulcerative colitis have identified several new loci, and suggested many new potential pathways. The identified susceptibility genes and their variants could be useful to predict disease course and to improve stratification of patients, when correlated with other subphenotypes. Moreover, understanding the biological pathways involved in the disease could lead to the development of new treatments and molecules that specifically target such pathways, discover different therapeutic approaches and eventually progress to personalized treatment.     

Review article: potential therapeutic applications and mechanisms of action of heparin in inflammatory bowel disease

Unfractioned heparin was recently reported to be beneficial in the treatment of inflammatory bowel disease. The available uncontrolled data show that it may be effective in steroid-resistant ulcerative colitis with a percentage of complete clinical remission of over 70% after an average of 4-6 weeks of therapy. The administration of unfractioned heparin is not currently justified by the very limited available data. The worsening of rectal bleeding is infrequent in treated ulcerative colitis patients and only rarely does it require blood transfusion or a colectomy. Low molecular weight heparin was used in a single trial in patients with steroid-refractory ulcerative colitis, with results similar to those observed with unfractioned heparin. Since a prothrombotic state has been described in inflammatory bowel disease, and microvascular intestinal occlusion seems to play a role in the pathogenesis of inflammatory bowel disease, it is reasonable that part of the beneficial effects of unfractioned heparin in inflammatory bowel disease may result from its anticoagulant properties. However, beyond its well-known anticoagulant activity, unfractioned heparin also exhibits a broad spectrum of immunomodulating and anti-inflammatory properties, by inhibiting the recruitment of neutrophils and reducing pro-inflammatory cytokines. Moreover, it can restore the high-affinity receptor binding of basic fibroblast growth factor and this would aid healing of the ulcerated mucosa. In conclusion, unfractioned heparin may represent a safe therapeutic option for severe, steroid-resistant ulcerative colitis, although randomized, controlled trials are needed to confirm these data.     

Efficacy of Lactobacillus GG in maintaining remission of ulcerative colitis

BACKGROUND: Aminosalicylates are the mainstay of therapy to prevent relapse of quiescent ulcerative colitis. The rationale for using probiotics is based on the evidence implicating intestinal bacteria in the pathogenesis of this disorder. AIM: To evaluate the efficacy of Lactobacillus GG alone or in combination with mesalazine vs. mesalazine as maintenance treatment in ulcerative colitis. PATIENTS AND METHODS: 187 ulcerative colitis patients with quiescent disease were randomized to receive Lactobacillus GG 18 x 10(9) viable bacteria/day (65 patients), mesalazine 2400 mg/day (60 patients) or Lactobacillus GG + mesalazine (62 patients). Disease activity index, endoscopic and histological scores were determined at 0, 6 and 12 months and in case of relapse. The primary end point was to evaluate sustained remission. RESULTS: Overall analysis showed no difference in relapse rate at 6 (P = 0.44) and 12 months (P = 0.77) among the three treatment groups. However, the treatment with Lactobacillus GG seems to be more effective than standard treatment with mesalazine in prolonging the relapse-free time (P < 0.05). CONCLUSIONS: Lactobacillus GG seems to be effective and safe for maintaining remission in patients with ulcerative colitis, and it could represent a good therapeutic option for preventing relapse in this group of patients.     

Delineation of the protective action of zinc sulfate on ulcerative colitis in rats

The protective action of zinc compounds in Crohn's disease-like inflammatory bowel disease in animals has been shown. A similar action of zinc sulfate on ulcerative colitis has not been defined. The present study aimed to delineate the protective action of zinc sulfate and the pathogenic mechanisms of 2,4-dinitrobenzene sulfonic acid (DNBS)-induced ulcerative colitis in rats. Zinc sulfate at different concentrations was given either orally (p.o.) or rectally (p.r.) to rats at 42, 48, 66 and 72 h following the induction of colonic inflammation by DNBS. Rats were killed 96 h after instillation of DNBS rectally to assess the severity of colonic damage, myeloperoxidase and xanthine oxidase activities. The involvement of mast cell degranulation and histamine release in the pathogenesis of DNBS-induced colitis was determined by using a mast cell stabilizer (ketotifen) and histamine receptor blockers (terfenadine and ranitidine). DNBS given rectally produced inflammation and ulceration in rats with a pathology resembling ulcerative colitis. Myeloperoxidase activity but not xanthine oxidase activity was sharply increased by this agent. Intrarectal administration of zinc solution and parenteral injection of histamine blockers significantly reduced tissue damage and myeloperoxidase but not xanthine oxidase activity. Ketotifen, a mast cell stabilizer, also significantly decreased mucosal injury and myeloperoxidase activity in the colon. In conclusion, mast cell degranulation followed by histamine release plays an important role in the pathogenesis of DNBS-induced ulcerative colitis. Zinc given rectally has a therapeutic effect against this colitis model, perhaps through the reduction of inflammation and inhibition of the above pathogenic mechanisms.     

Bcl一2／Bax在溃疡性结肠炎肠黏膜中的表达及与细胞凋亡的关系

目的研究溃疡性结肠炎患者肠黏膜中的凋亡调控蛋白Bcl-2／Bax表达状态及其与细胞凋亡的关系,探讨溃疡性结肠炎的发病机制。方法应用脱氧核糖核酸转移酶介导的缺口末端标记技术和免疫组化方法分析36例溃疡性结肠炎患者和25例正常对照肠黏膜细胞凋亡、凋亡调控蛋白Bcl-2／Bax的表达。结果溃疡性结肠炎组凋亡调控蛋白Bcl-2／Bax：的表达指数显著高于正常对照组（P〈0．05）,凋亡调控蛋白Bcl-2／Bax的表达与凋亡指数呈正相关（r=0．709,P=0．000;r=0．589,P=0．000）。结论溃疡性结肠炎患者肠黏膜凋亡调控蛋白Bel-2／Bax表达增加,诱导肠黏膜细胞凋亡。