糖皮质激素治疗重度溃疡性结肠炎的临床效果观察

目的：观察糖皮质激素在治疗重度溃疡性结肠炎的临床疗效。方法选取2012年11月1日-2014年1月31日医院重度溃疡性结肠炎患者40例,随机分为治疗组和对照组各20例。对照组予基础治疗,口服氨基水杨酸制剂;治疗组在基础治疗的基础上加用糖皮质激素。第12周时观察2组治疗效果。结果治疗组总有效率为90.0%明显高于对照组的60.0%;治疗组临床缓解率为85.0%明显高于对照组的55.0%,差异均有统计学意义（ P<0.05）。治疗组肠黏膜愈合率为65.0%明显高于对照组的45.0%,但2组比较差异无统计学意义（ P﹥0.05）。结论糖皮质激素治疗重度溃疡性结肠炎有较好疗效,值得临床进一步研究。     

糖皮质激素联合康复新灌肠治疗重度溃疡性结肠炎效果分析

目的 观察糖皮质激素（GC）联合康复新液治疗重度溃疡性结肠炎（UC）的临床效果.方法 选取2004年10月-2012年12月我院治疗的重度UC患者83例,将患者随机分为研究组（47例）及对照组（36例）,两组均在联合波尼松1~2mg·kg-1·d-1顿服及常规治疗基础上进行试验.治疗组加用康复新液100ml保留灌肠,2次/d.对照组仅使用0.9%氯化钠溶液100ml保留灌肠.对比分析治疗后2、4、6、8周后两组疾病活动指数（DAI）及UC缓解情况.结果 治疗前及治疗2、4周后两组DAI比较,差异无统计学意义（P＞0.05）;治疗第6、8周后,研究组DAI均低于对照组,差异有统计学意义（P＜0.05）.治疗2、4周后,两组比较差异无统计学意义（P＞0.05）.治疗6、8周后,研究组有效率高于对照组,差异有统计学意义（P＜0.05）.结论 GC联合康复新液治疗重度UC可明显提高UC完全缓解率,但有待更多研究.     

石榴皮水提物治疗溃疡性结肠炎模型大鼠的实验研究

目的：观察石榴皮水提物对慢性溃疡性结肠炎模型大鼠的治疗作用。方法：将80只SD大鼠随机分为正常对照组、模型组、柳氮磺吡啶（SASP）组、石榴皮水提物低、中、高剂量组（200、400、800 mg/kg）。用2,4-二硝基氯苯（DNCB）复合乙酸法建立大鼠溃疡性结肠炎模型。连续给药4周后麻醉处死动物,观察大鼠结肠大体形态的变化并进行结肠黏膜损伤指数（CMDI）评分,并测定大鼠结肠重量、肠重指数、组织髓过氧化物酶（MPO）活力、白介素1β（IL-1β）、肿瘤坏死因子α（TNF-α）及丙二醛（MDA）含量。结果：与模型组比较,石榴皮水提物中、高剂量组及SASP组大鼠腹泻症状明显缓解。IL-1β、TNF-α、MDA含量和MPO活力显著降低（P〈0.05）;病理学检查或尸检可见结肠组织溃疡面积明显缩小,水肿缓解,组织坏死减轻,未见肠壁增厚。石榴皮水提物高、中剂量组治疗效果明显优于SASP组（P〈0.05）。结论：石榴皮水提物能显著缓解DNCB复合乙酸法所致慢性溃疡性结肠炎的症状,治疗作用明显。     

一例溃疡性结肠炎患者糖皮质激素治疗的临床药学分析

目的对1例溃疡性结肠炎患者糖皮质激素治疗方案进行分析,并实施药学监护,保障溃疡性结肠炎患者安全、合理、有效用药。方法对1例溃疡性结肠炎患者,通过临床药师参与糖皮质激素治疗方案的制定,采取相应的药学监护计划,根据治疗效果和病情变化针对性提出用药建议,并对患者进行用药教育。结果临床药师参与患者治疗过程,提高了溃疡性结肠炎患者用药的安全性、有效性、依从性,从而改善了患者生活质量。结论临床药师参与制定药学治疗方案和药学监护,能有效提高临床用药安全性、有效性、合理性,确保用药安全有效。     

溃疡性结肠炎经糖皮质激素治疗后并发感染的护理措施探讨

目的探讨溃疡性结肠炎经糖皮质激素治疗后并发感染的临床护理措施。方法选取2002年3月至2012年3月期间收治的溃疡性结肠炎经糖皮质激素治疗后并发感染患者55例,分成新型护理组(33例)和一般护理组(22例)。观察两组患者感染控制情况、抗生素使用时间、住院时间以及主观幸福感。结果感染控制情况中,新型护理组显效率(39.39%)及总有效率(96.97%)均高于一般护理组(13.64%,68.18%)(P<0.05);新型护理组抗生素使用时间(5.6±1.3)d和住院时间(7.5±1.6)d均少于一般护理组[(7.1±1.7)d,(8.6±1.7)d](P<0.05);MUN-SN评定结果为新型护理组总分(13.66±4.26)分和正性因子(17.44±3.27)均高于一般护理组(6.70±3.03,10.33±4.27)(P<0.05)。结论新型护理措施有助于此类并发感染的恢复,可加强对感染的控制、缩短抗生素的使用时间和住院时间,患者对于护理的态度也较为满意,是一种良好护理措施。     

溃疡性结肠炎的护理治疗

溃疡性结肠炎是一种肠道慢性非特异性炎性病变,近几年其发病率有所增加,有轻有重,快慢不一,治疗效果不够理想,部分病人可经久不愈,反复发作,严重影响了患者的生活质量.本文结合临床经验总结了此病的护理治疗方法.     

大鼠溃疡性结肠炎模型的实验研究

目的对不同剂量的三硝基苯磺酸（ＴＮＢＳ）引起的大鼠溃疡性结肠炎（ＵＣ）模型进行观察和评价。方法采用一次性直肠注入大鼠ＴＮＢＳ（２５～１５０ｍｇ·ｋｇ－１）的３０％乙醇溶液，引起慢性炎症性肠疾病（ＩＢＤ），３ｗｋ后外死动物对各剂量下动物结肠的重量、髓过氧化物酶（ＭＰＯ）活性及组织形态学变化进行观察和评价。结果ＴＮＢＳ在１００～１５０ｍｇ·ｋｇ－１剂量下引起的ＵＣ肠壁明显增厚，炎症和溃疡至少维持７ｗｋ时间，ＭＰＯ活性值显著性升高，组织学检查发现粘膜及粘膜下层有大量中性粒细胞及淋巴细胞、巨噬细胞、纤维细胞浸润，肉芽组织及隐窝脓肿形成，５０ｍｇ·ｋｇ－１剂量时有一较轻度的损伤。２５ｍｇ·ｋｇ－１时对结肠的重量、ＭＰＯ活性及损伤指数都没有显著性改变（Ｐ＞０．０５）。结论用ＴＮＢＳ引起大鼠实验性ＵＣ，其溃疡和炎症维持一较长时间，这一病理特征为炎症性疾病防治药物的研究提供了条件；本模型的最佳剂量为１００ｍｇ·ｋｇ－１左右     

肠炎冲剂对溃疡性结肠炎模型大鼠的治疗作用

目的：研究肠炎冲剂对三硝基苯磺酸(TNBS)所致慢性溃疡性结肠炎模型大鼠的治疗作用。方法：TNBS的50％乙醇溶液一次性注人大鼠直肠，造成大鼠的慢性溃疡性结肠炎模型后，连续给药，观察腹泻率、死亡率，分别于连续给药3周及4周后麻醉处死动物，测定组织髓过氧化物酶(MPO)活力。地塞米松为阳性对照药。结果：地塞米松组动物症状减轻，但解剖学检查可见胸腺明显萎缩；连续给予不同剂量的肠炎冲剂药液(给药剂量为11．4、5．7、2．9g生药／kg体重)，各剂量组动物腹泻明显缓解，动物死亡率、腹泻率、结肠组织MPO活力明显降低，病理学检查或尸检可见结肠组织溃疡面积明显缩小，水肿缓解，坏死减轻，未见肠壁增厚。肠炎冲剂能显著缓解TNBS所致慢性溃疡性结肠炎症状，且未见地塞米松所致免疫器官萎缩的免疫抑制作用。结论：肠炎冲剂连续给药，对慢性溃疡性结肠炎模型大鼠治疗作用明显，并且未见地塞米松所致严重不良反应，是治疗慢性溃疡性结肠炎的较合适药物。     

肠炎宁浸膏粉对大鼠溃疡性结肠炎模型实验研究

目的研究肠炎宁浸膏粉对三硝基苯磺酸致大鼠溃疡性结肠炎模型的治疗作用。方法采用三硝基苯磺酸建立大鼠溃疡性结肠炎模型,各组分别给予肠炎宁浸膏粉低、中、高(相当于2.52、5.05、10.1 g生药·kg-1)剂量,连续给药2周,采血检测血清TNF-α、IL-1、IL-6、IL-8水平及结肠组织病理学检查。结果肠炎宁浸膏粉高剂量能明显降低三硝基苯磺酸致大鼠溃疡性结肠炎模型血清TNF-α、IL-8含量(P<0.05或P<0.01),能明显减少三硝基苯磺酸致大鼠溃疡性结肠模型结肠病理改变。结论肠炎宁浸膏粉对溃疡性结肠炎模型具有明显的治疗作用。     

溃疡性结肠炎的治疗现状及前景

溃疡性结肠炎是结、直肠慢性非特异性炎症性疾病,多呈反复发作的慢性病程。本病治疗难度大,与结肠癌的发病有关,被WHO列为现代难治病之一。目前溃疡性结肠炎的治疗手段多样,出现了许多新技术如生物靶向治疗、干细胞移植等,现将近年来溃疡性结肠炎现代医学研究进展进行综述。     

地塞米松当归多糖前体药对三硝基苯磺酸诱导的大鼠溃疡性结肠炎的治疗作用

目的:探讨地塞米松当归多糖前体药(dexam-ethasone Angelica sinensis polysaccharide prodrug,DEX-AP)对三硝基苯磺酸(TNBS)诱导的溃疡性结肠炎(ulcerative colitis,UC)的治疗作用及副作用。方法:采用TNBS的45%乙醇溶液(50 mg.ml-1)灌肠诱导实验性UC大鼠模型,分别采用0.25μmol.kg-1.d-1地塞米松(DEX)及0.05、0.25、1.25μmol.kg-1.d-1DEX-AP(以地塞米松含量计)灌胃治疗7 d。检测外周血淋巴细胞数后处死动物,取肾脏、脾脏和结肠称重。计算结肠溃疡面积后,取部分结肠粘膜组织测髓过氧化物酶(myeloperoxidase,MPO)活性,部分结肠组织制作石蜡切片,HE染色后进行光镜观察。结果:TNBS诱导的UC大鼠经0.05、0.25、1.25μmol.kg-1.d-1DEX-AP治疗7 d后,与模型组比较,DEX组结肠重量未见明显变化,而DEX-AP各组结肠重量均明显降低(P<0.05);DEX组与DEX-AP各组的结肠组织MPO酶活性均显著降低,且DEX-AP降低MPO酶活性具有剂量依赖性。0.25μmol.kg-1.d-1DEX使UC大鼠外周血淋巴细胞数、胸腺及脾脏重量均显著降低(P<0.01);0.05、0.25μmol.kg-1.d-1DEX-AP对UC大鼠外周血淋巴细胞数、胸腺及脾脏重量未见明显影响(P>0.05);1.25μmol.kg-1.d-1DEX-AP对脾脏重量未见明显影响,却使胸腺重量及外周血淋巴细胞数降低,但仍显著高于0.25μmol.kg-1.d-1DEX组(P<0.01)。UC大鼠经1.25μmol.kg-1.d-1DEX-AP治疗后,结肠粘膜组织结构基本恢复正常。结论:DEX-AP对TNBS诱导的实验性UC大鼠具有显著的治疗作用,且副作用低,具有良好的应用前景。     

Budesonide for the treatment of ulcerative colitis

Introduction: Budesonide is a synthetic corticosteroid characterized by enhanced topical potency and limited systemic bioavailability. Its use in ulcerative colitis (UC) was limited to rectal preparations until recently when the new oral budesonide formulation incorporating the multi-matrix system technology was introduced. The purpose of this review is to evaluate the current role of oral and rectal budesonide in managing UC patients

Areas covered: In this paper, we described the chemical structure and pharmacologic characteristics of the different oral and rectal budesonide preparations, provided a summary of the published trials that evaluated the efficacy and safety of budesonide in UC, and discussed the current status of its use in this population

Expert opinion: Budesonide is effective in inducing remission in a subset of patients with mild-moderate UC. Nevertheless, the current evidence suggests inferiority of oral budesonide to 5-aminosalisylates (5-ASA) and systemic steroids, whereas rectal applications are comparable to other rectal steroid preparations, but still inferior to rectal 5-ASA. In clinical practice, several issues need clarification including, its exact position in the line of induction agents; the role of combining budesonide and 5-ASAs; the role of combining oral and rectal budesonide; and the role of budesonide in maintenance therapy.     

Novel therapies in the treatment of ulcerative colitis

Ulcerative colitis is a chronic inflammatory disease of unknown cause. Its course is one of relapse and remission and requires therapy for both the induction and maintenance of remission. The progress in the fields of genetics and immunology has afforded important advances in our understanding of the inflammatory process. Traditional therapy with non-specific anti-inflammatories for ulcerative colitis remains our gold standard as newer targeted therapies have failed to provide any improved efficacy. This review examines the most recent compounds in development for the treatment of ulcerative colitis, including data from early clinical trials and the potential clinical impact of future entities.     

Novel therapies in the treatment of ulcerative colitis

Ulcerative colitis is a chronic inflammatory disease of the colon of unknown cause. Its course is one of relapse and remission and requires therapy for both the induction and maintenance of remission. Progress in the fields of genetics and immunology affords important advances in our understanding of the inflammatory process. Traditional therapy for ulcerative colitis with nonspecific anti-inflammatories remains our gold standard. This review examines the most recent compounds in development for the treatment of ulcerative colitis, including data from early clinical trials and the potential clinical impact of future entities.     

Infliximab: the evidence for its place in therapy in ulcerative colitis

Introduction:

Refractory ulcerative colitis has a high, unmet medical need for avoiding steroid dependency and avoiding colectomy. Controlled trials with biologic agents have recently been reported.

Aims:

We aimed to review the current evidence supporting the use of the monoclonal antitumor necrosis factor antibody, infliximab, in active ulcerative colitis and determine its current place in therapy.

Evidence review:

Although faced with initial conflicting data particularly in steroid-refractory patients, two large, placebo-controlled trials have shown that intravenous infliximab induces and maintains clinical improvement in a clinically significant proportion of patients when used with scheduled re-treatment. Infliximab also spares steroids and induces endoscopic remission in moderately ill patients. In fulminant colitis unresponsive to intravenous steroids, one placebo-controlled trial indicates that infliximab is able to prevent colectomy in this patient population. Evidence for cost effectiveness and avoidance of colectomy long term are still lacking.

Place in therapy:

Infliximab 5 mg/kg induction at 0, 2, and 6 weeks, and every 8 weeks thereafter should be considered in patients with moderately to severely active ulcerative colitis failing medical therapy. Steroid-dependent and steroid-refractory patients also qualify for infliximab therapy.