经肠系膜动脉脐带血干细胞灌注治疗溃疡性结肠炎的围手术期护理

正炎症性肠病是消化科的常见病、难治病、终身病,病情反复发作,病程迁延不愈,其并发症及癌变率逐渐上升,严重威胁患者的身心健康[1-2]。近年来患病率明显升高,且溃疡性结肠炎治疗缺乏特异性,虽有多种治疗药物和方法,对部分患者疗效仍不理想,脐带血干细胞移植是尚未达成共识的治疗方法之一。溃疡性结肠炎是一种病因不明,以结肠黏膜弥漫性损害为特征的肠道疾病[3-5],修复损伤的结肠黏膜是治愈该病的关键。脐带血干细胞是一种具有自我更新,高度增殖,多向     

类固醇激素依赖型溃疡性结肠炎缓解期IL-23表达的研究

目的 探讨IL-23在缓解期类固醇激素依赖型溃疡性结肠炎患者结肠组织中表达的病理意义.方法 采用Western blot分析及免疫组化SABC法检测15例缓解期激素依赖型溃疡性结肠炎患者炎症修复区结肠组织IL-23的蛋白表达情况,予统计学软件统计分析,并以30例缓解期的一般溃疡性结肠炎患者（15例SASP维持治疗,15例强的松维持治疗）炎症修复区结肠组织及10例正常结肠黏膜组织为对照组.结果 与正常对照组比较,SASP维持治疗及强的松维持治疗缓解期一般溃疡性结肠炎患者炎症修复区结肠组织IL-23的蛋白表达均轻度升高（P〉0.05）,而缓解期激素依赖型溃疡性结肠炎患者炎症修复区结肠组织IL-23的蛋白表达显著高于一般溃疡性结肠炎组（P〈0.01）.结论 IL-23的过度表达可能在溃疡性结肠炎类固醇激素依赖发病机制中起关键作用.     

类固醇激素依赖型溃疡性结肠炎缓解期IL-23表达的研究

目的 探讨IL-23在缓解期类固醇激素依赖型溃疡性结肠炎患者结肠组织中表达的病理意义.方法 采用Western blot分析及免疫组化SABC法检测15例缓解期激素依赖型溃疡性结肠炎患者炎症修复区结肠组织IL-23的蛋白表达情况,予统计学软件统计分析,并以30例缓解期的一般溃疡性结肠炎患者(15例SASP维持治疗,15例强的松维持治疗)炎症修复区结肠组织及10例正常结肠黏膜组织为对照组.结果 与正常对照组比较,SASP维持治疗及强的松维持治疗缓解期一般溃疡性结肠炎患者炎症修复区结肠组织IL-23的蛋白表达均轻度升高(P>0.05),而缓解期激素依赖型溃疡性结肠炎患者炎症修复区结肠组织IL-23的蛋白表达显著高于一般溃疡性结肠炎组(P<0.01).结论 IL-23的过度表达可能在溃疡性结肠炎类固醇激素依赖发病机制中起关键作用.     

类固醇激素依赖型溃疡性结肠炎缓解期IL-23表达的研究

目的 探讨IL-23在缓解期类固醇激素依赖型溃疡性结肠炎患者结肠组织中表达的病理意义.方法 采用Western blot分析及免疫组化SABC法检测15例缓解期激素依赖型溃疡性结肠炎患者炎症修复区结肠组织IL-23的蛋白表达情况,予统计学软件统计分析,并以30例缓解期的一般溃疡性结肠炎患者(15例SASP维持治疗,15例强的松维持治疗)炎症修复区结肠组织及10例正常结肠黏膜组织为对照组.结果 与正常对照组比较,SASP维持治疗及强的松维持治疗缓解期一般溃疡性结肠炎患者炎症修复区结肠组织IL-23的蛋白表达均轻度升高(P>0.05),而缓解期激素依赖型溃疡性结肠炎患者炎症修复区结肠组织IL-23的蛋白表达显著高于一般溃疡性结肠炎组(P<0.01).结论 IL-23的过度表达可能在溃疡性结肠炎类固醇激素依赖发病机制中起关键作用.     

顽固性溃疡性结肠炎治疗的新方法

顽固性溃疡性结肠炎患者,传统治疗效果不理想,本文介绍应用干细胞治疗或者英夫利西作为过渡,加用黏膜修复药物,待病情完全缓解且可停用激素后,继续以免疫抑制剂或者氨基水杨酸类药物维持.采用这种限时加速的序贯治疗,可更快诱导缓解,并维持更长时间缓解及内镜下黏膜愈合,从而减少住院率和手术率,为难治性溃疡性结肠炎患者治疗提供新的治疗手段.     

中西医结合治疗溃疡性结肠炎32例临床观察

溃疡性结肠炎是一种原因不明、主要发生在结肠黏膜的慢性炎症性病变,治疗棘手。2003年8月-2005年5月,笔者采用中西医结合的方法治疗溃疡性结肠炎32例,疗效满意,报告如下。     

中医药调节肠道菌群防治溃疡性结肠炎的研究进展

溃疡性结肠炎是一种慢性非特异性炎症,其病变主要累及结肠、直肠黏膜和黏膜下层,病因及发病机制尚不明确。中医药在治疗溃疡性结肠炎上有明显的优势与鲜明的特点。近年来有研究表明溃疡性结肠炎的发病可能与肠道菌群有密切关系。本文通过综述肠道菌群与溃疡性结肠炎的相互关系以及中医药通过调节肠道菌群防治溃疡性结肠炎的研究进展,以期为临床治疗溃疡性结肠炎提供新的治疗策略和思路。     

苦豆子总碱治疗大鼠溃疡性结肠炎的实验研究

[目的]研究苦豆子总碱(TASA)治疗溃疡性结肠炎的作用机制。[方法]选取雄性Wistar大鼠96只,随机分为正常对照组、模型组、TASA组和柳氮磺胺吡啶组,每组24只,除正常对照组外,其余3组用2,4二硝基氯苯建立大鼠创伤性溃疡性结肠炎模型,比较4组大鼠结肠黏膜组织病理学、结肠损伤分数、红细胞超氧化物歧化酶(SOD)活性、结肠黏膜过氧化脂质(LPO)含量及肠黏膜周边组织核因子(NF)-κB和白细胞介素(IL)-1β因子的表达。[结果]TASA组大鼠经治疗后,结肠黏膜光镜下组织学有明显改变,结肠损伤分数、大便乳酸含量降低,SOD活性升高,LPO含量降低,NF-κB和IL-1β因子表达进一步下调,与模型组比较差异有统计学意义(P0.01)。[结论]TASA发挥抗溃疡性结肠炎的机制之一可能与其下调NF-κB和IL-1β的表达,降低结肠黏膜LPO含量,增强红细胞SOD活性,进而增加机体对氧自由基的清除,从而达到促进大便乳酸排泄,减少结肠炎症损伤有关。     

溃疡性结肠炎并脑出血、脑梗塞、血小板减少症1例

溃疡性结肠炎(ulcerative colitis,UC)又称非特异性UC,是一种病因尚不十分清楚的结肠和直肠慢性非特异性炎症性疾病,病变局限于大肠黏膜及黏膜下层.通过本病例的学习希望临床医生对该病引起足够的重视.     

溃疡性结肠炎的药物治疗

溃疡性结肠炎（ulcerative colitis,UC）是一种局限于结肠和直肠黏膜或黏膜下层的、边界清楚的炎性反应,属于炎症性肠病（inilaramatory bowel disease,IBD）的一种。由于该病的病因和发病机制尚未完全阐明,治疗缺乏特异性,导致病情迁延反复,甚至癌变,严重影响患者的身心健康,被世界卫生组织（WHO）列为疑难病。经过多年的摸索和总结,UC的治疗药物不断增加,治疗方法不断提高,治疗方案也初步成形。现将治疗该病的药物及研究现状综述如下。     

Corticotropin releasing hormone in colonic mucosa in patients with ulcerative colitis.

Corticotropin releasing hormone (CRH) is a key hormone in integrated response to stress, acting as the major regulator of the hypothalamic-pituitary-adrenal axis. Recently, local production of CRH has been detected in normal human colonic enterochromaffin cells. CRH is locally secreted in granulomatous and arthritic tissues in rats and humans, where it seems to act as a local proinflammatory agent. To find out if CRH is present in colonic tissues of patients with ulcerative colitis, this study examined the expression of this peptide in the large bowel of patients with ulcerative colitis. Colonic tissues of patients with ulcerative colitis obtained by endoscopic biopsy were immunostained with anti-CRH antibody. CRH messenger (m) RNA was also examined in biopsy specimens of ulcerative colitis by the reverse transcribed polymerase chain reaction method and by in situ hybridisation. Considerably enhanced expression of immunoreactive CRH was found in mucosal inflammatory cells. Intense staining with anti-CRH antibody was also shown in mucosal macrophages. CRH mRNA was expressed in mucosal epithelial cells. The expression of immunoreactive CRH in colonic mucosal epithelial cells of ulcerative colitis slightly increased, but not significantly, compared with normal colonic mucosal epithelial cells. These results suggest that CRH may play a part in the modulation of intestinal immune and inflammatory system, and as a modulator in the pathogenesis of ulcerative colitis.     

Mucosal and plasma prostaglandin E2 in ulcerative colitis.

BACKGROUND/AIMS: Despite extensive studies, the role of prostaglandins in the course of inflammatory bowel diseases and their possible usefulness as predictive indicators of inflammation, remain largely speculative. The aim of this study was to determine whether mucosal and plasma concentrations of prostaglandin E2 (PGE2) are affected by the clinical course and degree of colonic injury in patients with ulcerative colitis. METHODOLOGY: PGE2 concentration was measured with an enzyme immunoassay (EIA) in biopsies of rectal mucosa and in the plasma of 38 patients with ulcerative colitis and 12 controls. Patients were divided into groups according to mild or severe clinical course of the disease, and with respect to scored endoscopical picture. RESULTS: Ulcerative colitis resulted in an increase of mucosal and plasma concentrations of PGE2, that was significantly elevated in patients with a severe clinical course of the disease. These concentrations increased depending on degree of mucosal injury. A significant, positive correlation with endoscopical score regarding plasma and mucosal PGE2 concentration, as well as between them, was found. CONCLUSIONS: Plasma and mucosal PGE2 rise simultaneously with degree of colonic injury. Because of a good correlation with mucosal injury and PGE2 content, measurement of plasma PGE2 could be considered as a possible surrogate marker of bowel inflammation.     

Intraluminal excretion of PAF,lysoPAF, and acetylhydrolase in patients with ulcerative colitis

PAF-acether (PAF) is a phospholipid synthesized by numerous inflammatory cells. PAF can produce several pathological changes in various organs, especially in the colon. In animals PAF causes colonic ulceration and inflammation, which are similar to the anatomic lesions seen in human ulcerative colitis. The aim of this study was to measurein vivo colonic production of PAF in active ulcerative colitis using a modified colonic perfusion method. Ten patients with active ulcerative colitis and six control patients were investigated. A colonic segment was continuously perfused with a buffer and the liquid was recovered 20 cm distally, after a 45-min period of equilibration, at 20-min intervals. PAF, lysoPAF, and acetylhydrolase were measured in the colonic samples. PAF and lysoPAF outputs were significantly higher in patients with active ulcerative colitis compared to controls patients. There was a significant correlation between colonic PAF output and, respectively, macroscopic mucosal lesions and myeloperoxidase colonic output. We thus conclude: (1) the colonic perfusion method allowsin vivo study of the metabolism of PAF during ulcerative colitis and could also be used to study the efficiency of PAF antagonists in UC; and (2) colonic production of PAF is increased during ulcerative colitis and correlated to local injury and inflammation. Whether or not PAF plays a role in the pathogenesis of ulcerative colitis remains open for further investigations.     

Increased group II phospholipase A2 in colonic mucosa of patients with Crohn's disease and ulcerative colitis.

The immunochemical protein content of group II phospholipase A2 (PLA2) and PLA2 enzymatic activity were measured for colonic mucosal biopsy samples obtained from patients with either Crohn's disease of the colon or ulcerative colitis, and control patients without inflammatory bowel disease. Immunoreactive group II PLA2 (IR-PLA2 II) content and PLA2 activity in actively inflamed colonic mucosa of Crohn's disease patients were significantly higher than those in inactively inflamed mucosa of Crohn's disease patients and the colonic mucosa of controls. IR-PLA2 II content and PLA2 activity in severely inflamed mucosa of ulcerative colitis patients were significantly higher than those in the colonic mucosa of the controls. Mucosal PLA2 enzymatic activity was closely correlated with mucosal IR-PLA2 II content in patients with Crohn's disease and ulcerative colitis. These results suggest that an increase in PLA2 enzymatic activity in inflamed colonic mucosa of Crohn's disease and ulcerative colitis was mainly attributed to increased protein content of group II PLA2, and that an increase in mucosal group II PLA2 may be involved in the pathogenesis of intestinal inflammation of Crohn's disease and ulcerative colitis.     

Colonic production of nitric oxide gas in ulcerative colitis, collagenous colitis and uninflamed bowel

BACKGROUND: Nitric oxide (NO) produced in excess by the inflamed human colon is generally considered a pathway of mucosal damage. In an attempt to quantify colonic mucosal production of NO in various forms of colitis we performed 'steady-state' gas perfusion of whole colon in 11 patients with ulcerative colitis, 10 patients with collagenous colitis and 20 controls with uninflamed mucosa. METHODS: The tip of a Teflon tube was placed in the caecum during colonoscopy. Subsequently, argon was infused at a constant rate for 70-180 min. Argon and NO in gas sampled from the rectum were measured by neutron activation analysis and the chemiluminescence technique, respectively. RESULTS: The use of argon as a marker of colonic NO output was justified by complete recovery (96%+/-2; mean +/- s(x); n = 5) of argon in gas collected from the rectum and a constant output of NO at varying perfusion rates (25, 50 and 75 ml/min coefficient of variation 21%; n = 6). In patients with ulcerative colitis, colonic output of NO was 10-fold higher (P < 0.001) than in controls and positively correlated (P < 0.01) to indices of disease activity. In patients with collagenous colitis, colonic output of NO was 50-fold higher (P < 0.01) than in controls during periods with watery diarrhoea (n = 6), but within the range observed in ulcerative colitis in the absence of diarrhoea (n = 4). CONCLUSIONS: Argon gas perfusion of whole colon using chemiluminescence technique for measurement of NO is a reliable method for quantification of colonic mucosal NO production. Increased colonic production of NO in collagenous colitis, which exceeds the output observed even in extensive ulcerative colitis, militates against the theory that NO per se is a cause of mucosal injury.     

Effect of gender on the manifestations of celiac disease: Evidence for greater malabsorption in men

Background: Nitric oxide (NO) produced in excess by the inflamed human colon is generally considered a pathway of mucosal damage. In an attempt to quantify colonic mucosal production of NO in various forms of colitis we performed 'steady-state' gas perfusion of whole colon in 11 patients with ulcerative colitis, 10 patients with collagenous colitis and 20 controls with uninflamed mucosa. Methods: The tip of a Teflon tube was placed in the caecum during colonoscopy. Subsequently, argon was infused at a constant rate for 70-180 min. Argon and NO in gas sampled from the rectum were measured by neutron activation analysis and the chemiluminescence technique, respectively. Results: The use of argon as a marker of colonic NO output was justified by complete recovery (96% ± 2; mean ± s- x ; n = 5) of argon in gas collected from the rectum and a constant output of NO at varying perfusion rates (25, 50 and 75 ml/min; coefficient of variation 21%; n = 6). In patients with ulcerative colitis, colonic output of NO was 10-fold higher ( P < 0.001) than in controls and positively correlated ( P < 0.01) to indices of disease activity. In patients with collagenous colitis, colonic output of NO was 50-fold higher ( P < 0.01) than in controls during periods with watery diarrhoea ( n = 6), but within the range observed in ulcerative colitis in the absence of diarrhoea ( n = 4). Conclusions: Argon gas perfusion of whole colon using chemiluminescence technique for measurement of NO is a reliable method for quantification of colonic mucosal NO production. Increased colonic production of NO in collagenous colitis, which exceeds the output observed even in extensive ulcerative colitis, militates against the theory that NO per se is a cause of mucosal injury.     

Enhanced colonic nitric oxide generation and nitric oxide synthase activity in ulcerative colitis and Crohn's disease.

Recent studies have suggested that nitric oxide (NO.), the product of nitric oxide synthase in inflammatory cells, may play a part in tissue injury and inflammation through its oxidative metabolism. In this study the colonic generation of oxides of nitrogen (NOx) and nitric oxide synthase activity was determined in ulcerative colitis and Crohn's disease. Colonic biopsy specimens were obtained from inflammatory bowel disease patients and from normal controls. Mucosal explants were cultured in vitro for 24 hours and NOx generation was determined. Nitric oxide synthase activity was monitored by the conversion of [3H]-L-arginine to citrulline. Median NOx generation by inflamed colonic mucosa of patients with active ulcerative colitis and Crohn's colitis was 4.2- and 8.1-fold respectively higher than that by normal human colonic mucosa. In ulcerative colitis and Crohn's colitis nitric oxide synthase activity was 10.0- and 3.8-fold respectively higher than in normal subjects. Colonic NOx generation is significantly decreased by methylprednisolone and ketotifen. The decrease in NOx generation by cultured colonic mucosa induced by methylprednisolone suggests that NO synthase activity is induced during the culture and the steroid effect may contribute to its therapeutic effect. Enhanced colonic NOx generation by stimulated nitric oxide synthase activity in ulcerative colitis and Crohn's disease may contribute to tissue injury.     

Mucosal blood flow and generation of superoxide in rat experimental colitis induced by succinic acid

As we consider succinic acid to be an exacerbating factor in ulcerative colitis, we investigated its influence on rat colonic mucosa in terms of mucosal blood flow and superoxide generation. We measured mucosal blood flow by the hydrogen gas clearance method and superoxide generation by the chemiluminescence method, and observed histopathological findings to determine the effects of succinic acid. After the instillation of succinic acid of any concentration tested to the colon, mucosal blood flow decreased. Histopathologically, the higher the concentration of succinic acid, the greater was the erosion formation in the colonic mucosa, while significant polymorpho-nuclear cell infiltration and superoxide generation from colon tissue were observed with 0.01% succinic acid compared with higher or lower concentrations. Succinic acid, at fecal concentrations found in active stage ulcerative colitis, appears to be implicated in mucosal injury, mediated by a decrease in colonic mucosal blood flow and infiltration of superoxide-generating polymorpho-nuclear cells into the mucosa.