溃疡性结肠炎患者Wnt9b的高表达及临床价值

目的研究溃疡性结肠炎和克罗恩病患者Wnt9b的表达,分析血浆Wnt9b水平与炎症性肠病患者内镜下疾病活动性的相关性以及对溃疡性结肠炎和克罗恩病的鉴别诊断价值。方法应用酶联免疫吸附试验(Enzyme-Linked ImmunoSorbent Assay,ELISA)对克罗恩病患者、溃疡性结肠炎患者和正常对照者血浆中Wnt9b的表达进行测定。分析血浆Wnt9b水平与炎症性肠病患者内镜下疾病活动性的相关性,通过受试者工作特征曲线(receiver-operating characteristic,ROC)分析血浆Wnt9b表达对溃疡性结肠炎和克罗恩病的鉴别诊断价值。结果溃疡性结肠炎患者血浆Wnt9b水平显著高于正常对照者(P=0.0324)和克罗恩病患者(P=0.0217),而克罗恩病患者血浆Wnt9b与正常对照者无显著差异(P=0.5919)。但是,溃疡性结肠炎患者血浆Wnt9b水平与内镜下疾病活动程度无显著相关性(Spearmanr=-0.2360,P=0.1102)。ROC曲线分析表明,血浆Wnt9b表达水平在区分溃疡性结肠炎和克罗恩病中具有显著意义(AUC=0.633,P=0.0228)。结论溃疡性结肠炎患者血浆Wnt9b表达水平增高,对于鉴别溃疡性结肠炎患者和克罗恩病患者具有一定意义。     

炎症性肠病患者血浆TRAF1的表达及其临床意义

目的比较炎症性肠病患者血浆肿瘤坏死因子受体相关因子-1（tumor necrosis factor receptor-assoc iated factor-1,TRAF-1）水平和正常对照者的差异,分析血浆TRAF1水平对炎症性肠病的诊断价值以及与内镜下疾病活动性的相关性。方法共纳入62例克罗恩病患者、64例溃疡性结肠炎患者和56例正常对照者。应用酶联免疫吸附试验（Enzym e-linked immuno-sorbent assay,ELISA）分析炎症性肠病患者和正常对照者血浆中TRAF1蛋白的表达,受试者工作特征曲线（rece iver-operating characteristic,ROC）分析血浆TRAF1水平对克罗恩病和溃疡性结肠炎的诊断价值,应用Pearson相关分析研究血浆TRAF1水平与内镜下疾病活动性的相关性。结果克罗恩病患者（P=0.000）和溃疡性结肠炎患者（P=0.000）血浆TRAF1水平显著高于正常对照者,同时TRAF1对区分克罗恩病患者和正常对照者（P=0.000）以及区分溃疡性结肠炎患者和正常对照者（P=0.000）具有显著的诊断价值。克罗恩病患者血浆TRAF1表达水平和内镜下疾病活动指数呈较低的负相关（r=-0.260,P=0.041）,而溃疡性结肠炎患者血浆TRAF1水平与内镜下疾病活动程度无显著相关性（r=0.029,P=0.821）。结论炎症性肠病患者血浆TRAF1水平增高,血浆TRAF1水平对区分炎症性肠病患者和正常对照者具有诊断价值,但血浆中TRAF1的水平不能反应内镜下疾病活动程度。     

单核样髓源性抑制细胞在炎症性肠病中的表达及其临床意义

背景：近年来炎症性肠病（IBD）发病率呈上升趋势,其病理生理学机制复杂且仍未明确。目的：研究单核样髓源性抑制细胞（MDSCs）在IBD患者外周血单核细胞中的比例,分析单核样MDSCs与IBD活动性的关系,从而初步探讨单核样MDSCs在IBD中的作用机制。方法：纳入IBD患者60例,分为克罗恩病（CD）组（n=33）和溃疡性结肠炎（UC）组（n=27）,选取30名同期健康体检者作为正常对照组,采用流式细胞仪检测CD组、UC组、正常对照组患者外周血单核样MDSCs／单核细胞比例,分析单核样MDSCs与IBD患者WBC、PLT、ESR、CRP的相关性。结果：CD组和UC组外周血单核样MDSCs／单核细胞比例较正常对照组相比显著升高[（43．7±23．0）％、（49．1±27．2）％对（10．7±7．4）％]（P〈0．01）,CD组与UC组相比差异无统计学意义（P〉0．05）。活动期CD和UC组外周血单核样MDSCs／单核细胞比例均较缓解期组显著升高[（60．3±16．8）％、（66．3±17．6）％对（28．1±16．2）％、（19．9±9．0）％]（P〈0．01）。IBD患者外周血单核样MDSCs／单核细胞比例与WBC计数、PLT计数呈正相关（r=0．44,P=0．02;r=0．43,P=0．02）,与ESR、CRP不相关（r=0．33,P=0．08;r=0．30,P=0．12）。结论：IBD患者外周血单核样MDSCs比例明显升高,与IBD活动性密切相关。单核样MDSCs在IBD发病中具有重要作用。     

ST2在炎症性肠病中的表达及其作用探讨

目的探讨血清中人基质裂解素（ST2）水平的变化在炎症性肠病（IBD）活动性评估中的意义。方法ELISA法（酶联免疫吸附测定）检测IBD患者45例，其中UC患者29例，CD患者16例，已排除IBD的其他胃肠疾病（包括主诉不明原因腹痛、腹泻、胃肠炎）的患者24例和15例健康人血清中ST2水平，20例IBD患者检测治疗前后ST2水平的改变。结果IBD活动期血清中ST2水平为（1884．72±338．38）pg／mL，显著高于缓解期（1292．27±347．73）pg／mL和健康对照组（1026．85±382．35）pg／mL，血清ST2水平在治疗前和治疗后（t=4．067，P〈0．01）、UC患者和CD患者（t=2．202，P=0．035）之间差异具有统计学意义。结论血清中ST2水平可作为炎症性肠病活动性评估和临床治疗效果的评价指标。     

活动期炎症性肠病患者血清内脂素水平及其临床意义

背景:近年炎症性肠病(IBD)的发病率呈逐年增长趋势,但其发病机制目前仍不明确。既往研究发现一些脂肪因子在肠道炎症调节中起关键作用。目的:探讨脂肪细胞因子内脂素(visfatin)在IBD中的作用及其临床意义。方法:收集2015年5月—2015年12月苏州大学附属第一医院和苏州市立医院91例活动期IBD患者,包括61例克罗恩病(CD)和30例溃疡性结肠炎(UC),以ELISA法检测血清内脂素水平。48名健康体检者作为对照组。分析血清内脂素水平与IBD患者临床特征的关系,以ROC曲线评估血清内脂素水平对IBD的诊断效能。结果:活动期CD和UC患者的血清内脂素水平显著高于对照组[(385.24±112.64)pg/mL和(378.91±118.57)pg/mL对(321.11±96.27)pg/mL,P均0.05]。血清内脂素水平与UC患者的疾病活动性Mayo评分呈显著正相关(r=0.398,P0.05),与CD患者的疾病活动性以及IBD患者的临床常用炎性指标CRP、ESR和病变部位均无关(P均0.05)。血清内脂素水平诊断CD和UC的ROC曲线下面积(AUC)分别为0.654和0.622,诊断准确性较低。结论:血清内脂素水平可能与IBD炎症活动有一定关联,并可能成为活动期UC的临床指标。     

炎症性肠病患者CD27-CD70共刺激途径的激活研究

目的 探讨CD27-CD70共刺激途径在炎症性肠病患者外周循环和肠黏膜中的表达,比较炎症性肠病患者CD27-CD70表达与正常对照者间的差异.方法 共纳入62例克罗恩病(CD)、64例溃疡性结肠炎(UC)患者和56名正常对照者.应用酶联免疫吸附试验分析炎症性肠病患者和正常对照者血浆中CD27-CD70蛋白的表达;SYBR-green实时PCR法分析炎症性肠病患者和正常对照者外周血单个核细胞中CD27-CD70 mRNA的表达;免疫组化法分析炎症性肠病患者和正常对照者肠黏膜组织CD27-CD70蛋白的表达.结果 CD和UC患者血浆中CD27-CD70的表达均显著高于正常对照者(P值均<0.05).ROC曲线的分析表明,CD27-CD70对区分CD患者和正常对照者以及区分UC患者和正常对照者具有显著的诊断价值(P值均<0.05).CD患者血浆中CD27和CD70水平与内镜下疾病活动性(EDAI)无关(r值分别=0.055和0.024,P值分别为0.673和0.852),且UC患者血浆中CD27和CD70水平与EDAI无关(r值分别=0.077和0.021,P值分别为0.547和0.869).CD患者和UC患者外周血单个核细胞CD27和CD70 mRNA表达均显著高于正常对照者外周血单个核细胞中mRNA的表达(P值均=0.000).免疫组化实验表明CD患者和UC患者肠黏膜组织CD27和CD70的表达均显著高于正常对照者(P值均=0.000).结论 炎症性肠病患者血浆、外周血单个核细胞和肠黏膜中均存在CD27-CD70途径的激活,但血浆中CD27-CD70的水平不能反映内镜下疾病活动程度.选择性干预CD27-CD70共刺激通路可能成为缓解或减轻炎症性肠病进程的有益尝试.     

半胱氨酸天冬氨酸蛋白酶-3在炎症性肠病中的差异表达

目的 研究血浆半胱氨酸天冬氨酸蛋白酶-3(cysteine-aspartic acid protease-3,caspase-3)与炎症性肠病患者临床疾病活动性的相关性及对疾病的诊断价值.方法 对克罗恩病患者、溃疡性结肠炎患者和正常对照者血浆中caspase-3的表达情况应用酶联免疫吸附试验(ELISA)进行分析.进一步分析血浆caspase-3浓度与内镜下疾病活动性的相关性.通过受试者工作特征曲线(receiver-operating characteristic,ROC)观察炎症性肠病患者中血浆caspase-3水平的潜在临床及科研价值.数据处理使用GraphPad Prism 5.结果 克罗恩病患者血浆caspase-3水平显著高于正常对照组(P=0.0022),但溃疡性结肠炎患者血浆caspase-3水平与对照组无显著差异(P=0.6377).easpase-3表达水平在区分克罗恩病患者和溃疡性结肠炎患者中诊断价值较低(AUC=0.6339,P=0.0039).克罗恩病患者血浆caspase-3水平与内镜下疾病活动性无显著相关性(r=-0.089,P=0.5172).结论 克罗恩病患者血浆caspase-3表达水平增高,与溃疡性结肠炎及正常对照者存在差异.     

HO-1在炎症性肠病中的表达及其与疾病活动度的关系

目的 探讨血红素氧化酶-1(HO-1)在炎症性肠病（IBD）中的表达及其与疾病活动度的关系。方法 选择2020年1月至2022年3月四川绵阳四〇四医院收治的76例IBD患者纳入研究组,其中溃疡性结肠炎（UC）有40例（设为UC组）,克罗恩病（CD）有36例（设为CD组）;另选择同期在该院体检的50名健康志愿者纳入对照组。收集所有受试者的外周血样本和肠黏膜组织,采用ELISA法测定外周血HO-1的表达水平,采用免疫组织化学染色SABC法测定肠黏膜组织中HO-1的表达水平。采用ROC曲线分析IBD患者外周血和肠黏膜组织中HO-1的表达水平对疾病的诊断效能。根据改良Mayo内镜评分（IMES）评估UC患者疾病活动度,根据克罗恩病活动指数（CDAI）评估CD患者疾病活动度。采用Pearson相关系数法分析IBD患者外周血和肠黏膜组织中HO-1的表达水平与疾病活动度的相关性。结果 UC组和CD组外周血和肠黏膜组织中HO-1的表达水平均显著高于对照组,差异均有统计学意义（P均<0.01）。联合外周血和肠黏膜组织中HO-1的表达水平诊断IBD的敏感度、特异度、准确度和曲线下面积（AUC）分别为...     

老年炎症性肠病患者的骨代谢和骨密度分析

目的 探讨老年炎症性肠病（inflammatory bowel disease,IBD）患者的骨代谢和骨密度情况与健康对照者的差异,为临床防治IBD引起的骨质疏松提供依据.方法 纳入复旦大学附属华东医院IBD患者20例为IBD组,同期健康体检者20例为对照组.记录并比较两组的年龄、病程、病变部位、糖皮质激素（Glucocorticoids,GCs）应用、骨代谢相关血清学指标检查结果以及髋关节和股骨颈骨密度T值.结果 溃疡性结肠炎组髋关节骨量减少的发生率高于对照组,差异有统计学意义（64.3％ vs 30.0％,P=0.048）.UC组的血清25-羟维生素D[25-hydroxyvitamin D,25-（OH） D]浓度低于对照组（t=0.036,P=-2.100）,IBD组的血清β-CTX浓度高于对照组（UC：=0.003,P=2.975; CD：t=0.024,P=2.253）.结论 老年UC患者髋关节骨量减少的发生率增加,25-（OH）D浓度降低;IBD患者血清β-CTX浓度升高.     

血浆TRAF-3表达在炎症性肠病中的意义

目的分析血浆肿瘤坏死因子受体相关因子-3(tumor necrosis factor receptor-associated fac-tor-3,TRAF3)水平对于炎症性肠病的诊断价值以及与内镜下疾病活动性的相关性。方法应用酶联免疫吸附试验(Enzyme-Linked ImmunoSorbent Assay,ELISA)分析炎症性肠病患者和正常对照者血浆中TRAF3蛋白的表达,受试者工作特征曲线(receiver-operating characteristic,ROC)分析血浆TRAF3水平对于克罗恩病和溃疡性结肠炎的诊断价值,应用Pearson相关分析研究血浆TRAF3水平与内镜下疾病活动性的相关性。数据处理使用GraphPad Prism 5。结果克罗恩病患者(P=0.000)和溃疡性结肠炎患者(P=0.000)血浆TRAF3水平显著高于正常对照者,同时TRAF3对区分克罗恩病患者和正常对照者(P=0.000)以及区分溃疡性结肠炎患者和正常对照者(P=0.000)具有显著的诊断价值,克罗恩病患者(r=-0.093,P=0.473)以及溃疡性结肠炎患者(r=0.043,P=0.733)血浆TRAF3表达水平和内镜下疾病活动指数均无显著的相关性。结论炎症性肠病患者血浆TRAF3水平增高,对区分炎症性肠病患者和正常对照者具有诊断价值,但血浆中TRAF3的水平不能反应内镜下疾病活动程度。     

NLRP3炎性小体在炎症性肠病中的研究进展

炎症性肠病（IBD）是一类因免疫反应失调所致的反复发作的肠道慢性炎症性疾病,包括克罗恩病（CD）和溃疡性结肠炎（UC）。白细胞介素（IL）-1β和IL-18是IBD发病中的重要致炎因子,近年研究发现NLRP3炎性小体可调节IL-lβ和IL-18的分泌,因此有望成为IBD治疗的新靶点。本文就NLRP3炎性小体在IBD中的研究进展作一综述．并提出未来的可能研究方向。     

Studies of Isolated Parietal and Enterochromaffin-Like Cells from the Rat

Background: The mechanisms for the observed low prevalence of Helicobacter pylori infection in inflammatory bowel disease (IBD) are unknown, but might be important for the pathogenesis of IBD. We have studied the seroprevalence of H. pylori in different categories of IBD and evaluated the role of medical therapy, smoking and social status. We also analysed the effect of seropositivity on the age of onset of IBD in order to find possible evidence for the protective effect of the infection. Methods: We studied 296 (mean age 43 years, range 18-79; women 144) unselected patients with IBD, including 185 with ulcerative colitis (UC), 94 with Crohn disease (CD), and 17 with indeterminate colitis (IC). Seventy healthy age- and sex-matched subjects served as controls. Serum samples were studied for H. pylori antibodies. Detailed clinical history was obtained from patient records and by face-to-face interview. Results: The prevalence of H. pylori infection was lower in IBD patients (24%) than in controls (37%; P = 0.029), and in CD lower (13%) than in UC (30%; P = 0.002). Seropositivity was not related to sulphasalazine treatment or smoking. Age of onset of IBD was higher in seropositive (mean 40 years) than in seronegative patients (30 years; P < 0.001). The age of onset of IBD showed unimodal distribution in H. pylori seronegative patients, with a peak between 30 and 40 years, although there was some evidence of bimodality in CD. In contrast, H. pylori seropositive patients had clear bimodal pattern with peaks at 20-40 and 50-60 years of age. Conclusions: Our results confirm the low prevalence of H. pylori infection in IBD, and in particular in CD. The significantly higher age of onset and bimodal pattern of age-specific incidence in seropositive IBD patients suggest that H. pylori infection significantly modifies the development of IBD and may have a protective effect.     

microRNA在炎症性肠病中的研究进展

炎症性肠病（IBD）是一种病冈尚未完全阐明的肠道慢性炎症性疾病,近年研究发现IBD患者肠黏膜组织和血清的诸多microRNA（miRNA）表达异常,且其表达异常与疾病活动度、病变部位等相关,可能在IBD的诊断、发病机制探索和靶向治疗中发挥一定作用。本文就IBD患者特异性miRNA表达异常的研究现状作一综述,以期阐明miRNA在IBD发生、发展中的作用,为其临床应用提供依据。     

巨细胞病毒在炎症性肠病中的研究进展

炎症性肠病（IBD）是一种病因尚不十分清楚的慢性非特异性炎症性疾病，在国内的发病率逐年增高。巨细胞病毒（CMV）属疱疹病毒科B属双链DNA病毒，近年随着IBD与CMV研究的深入，发现CMV在IBD的发生和疾病进展中起一定作用，且对IBD的临床诊治亦有一定指导价值。本文就CMV的检测方法学、其在IBD患者中的流行病学情况和相关研究进展作一综述。     

Increased Serum Levels of Eotaxin in Patients with Inflammatory Bowel Disease

Background: The CC-chemokines eotaxin and eotaxin-2, produced by epithelial and phagocytic cells, are potent and selective chemoattractants for eosinophils and basophils. The eosinophil is a potent inflammatory cell thought to play an important role in the pathogenesis of inflammatory bowel disease (IBD). In this study we investigated the serum concentrations of eotaxin and eotaxin-2 in patients with Crohn disease and ulcerative colitis. Methods: Thirty-one patients with Crohn disease, 35 patients with ulcerative colitis and 41 control patients were studied. Eotaxin and eotaxin-2 serum levels were measured with solid phase sandwich enzyme-linked immunosorbent assays. Results:     

Mucosal and Invading Bacteria in Patients with Inflammatory Bowel Disease Compared with Controls

Background: Endogenous intestinal bacteria and/or specific bacterial pathogens are suspected of being involved in the pathogenesis of inflammatory bowel diseases (IBD). The aim of this study was to investigate IBD tissues for different bacterial population groups harbouring the mucosal surface and/or invading the mucosa. Methods: Tissue sections from surgical resections from the terminal ileum and/or the colon from 24 IBD patients (12 active ulcerative colitis (UC), 12 active Crohn disease (CD)) and 14 non-IBD controls were studied by fluorescent in situ hybridization on a quantifiable basis. Results: More bacteria were detected on the mucosal surface of IBD patients than on those of non-IBD controls ( P < 0.05). Bacterial invasion of the mucosa was evident in 83.3% of colonic specimens from the UC patients, in 55.6% of the ileal and in 25% of the colonic specimens from the CD patients, but no bacteria were detected in the tissues of the controls. Colonic UC specimens were colonized by a variety of organisms, such as bacteria belonging to the gamma subdivision of Proteobacteria , the Enterobacteriaceae , the Bacteroides/Prevotella cluster, the Clostridium histolyticum/Clostridium lituseburense group, the Clostridium coccoides/Eubacterium rectale group, high G + C Gram-positive bacteria, or sulphate-reducing bacteria, while CD samples harboured mainly bacteria belonging to the former three groups. Conclusion: Pathogenic events in CD and UC may be associated with different alterations in the mucosal flora of the ileum and colon.     

炎症性肠病血栓栓塞机制的研究进展

静脉血栓栓塞(VTE)是炎症性肠病(IBD)公认的肠外表现,发病率和死亡率均较高。IBD血栓栓塞的机制尚不完全清楚,涉及多种获得性和遗传性因素。目前主要指南推荐给予IBD患者机械或药物治疗以预防血栓栓塞,但临床上尚未广泛应用。本文就IBD血栓栓塞的机制作一综述。     

西方国家与我国炎症性肠病的过去、现在和将来

20世纪以来,炎症性肠病(IBD)的发病率呈持续上升趋势,其病因尚未完全阐明,目前普遍的观点认为,肠道菌群在遗传易感者肠道启动了持续的免疫和炎症反应。本文就过去对IBD的描述、现在对IBD发病机制的重要发现和治疗以及将来对IBD研究的设想作一概述。     

STAT蛋白在炎症性肠病发病机制中的作用

炎症性肠病主要包括溃疡性结肠炎和克罗恩病,是肠道慢性非特异性炎症性疾病,病因尚不十分明确,近年来认为STAT蛋白,尤其是STAT3和STAT1通过细胞因子和JAK途径在炎症性肠病的发病机制中发挥重要作用,而SOCS家族参与STAT信号通路的负向调控.     

Hyperhomocysteinaemia,Coagulation Pathway Activation and Thrombophilia in Patients with Inflammatory Bowel Disease

Background : The 5,10-methylenetetrahydrofolate reductase (MTHFR) 677C → T polymorphism encoding the thermolabile variant is, when present as homozygote type (TT variant), a known genetic cause of mild hyperhomocysteinaemia (HHCY). This polymorphism has been observed in increased numbers in patients with inflammatory bowel disease (IBD). Coagulation and fibrinolysis are activated in patients with active IBD, but it is not known whether raised plasma homocysteine (HCY) found in patients with IBD significantly contributes to this activation. The aim of this study was to investigate if HHCY or presence of the TT variant significantly induces a hypercoagulable state in IBD patients receiving anti-inflammatory therapy during active disease, and to study if genetic determinants for thromboembolic disease are more frequent in these patients. Methods : The study was designed as a cross-sectional study in an outpatient clinic comprising 106 IBD patients receiving anti-inflammatory therapy. Markers of coagulation were measured in order to elucidate whether patients with HHCY or the MTHFR TT variant were hypercoagulant compared with patients with no impairment of HCY metabolism. In addition, markers of inflammation and acute-phase reactants were measured in order to compare activity during active disease and during remission. Genetic determinants of thromboembolic disease in patients with IBD and in relevant controls were investigated in the expectation of a more frequent occurrence of these markers of thrombophilia if hypercoagulability could be a primary or contributory factor in IBD. Results : No significant difference could be found in coagulation activity, acute-phase reactants or inflammatory markers in IBD patients with the TT variant of the 677C → T polymorphism or high (>15 μmol/L) plasma HCY levels, compared with IBD patients with no impairment of HCY metabolism. In patients with IBD, the coagulation activity was significantly increased during active disease compared with a state of remission. As expected, a significant difference regarding interleukin 6, C-reactive protein and erythrocyte sedimentation rate was present in IBD, comparing active disease with a state of remission. No significant complement activation was present in either of the groups or during active disease. Neither of the allele frequencies of genetic determinants for thrombophilia (coagulation factor V 1691G → A (factor V Leiden) and factor II 20210G → A polymorphisms) in the background population differed significantly from that in IBD patients. Conclusions : This study found no correlation between the MTHFR TT variant or HHCY and a hypercoagulable state in IBD patients receiving anti-inflammatory treatment. This coagulation activity is high during exacerbations of disease, but a considerable reduction is seen in patients on anti-inflammatory therapy compared with non-treated patients. Coagulation activation in IBD is probably a consequence of the inflammatory nature of the disease. That thrombophilia could be a contributory or primary factor in the development of IBD is not supported by the present study, as the frequencies for the genetic determinants for thrombophilia are similar in IBD patients and controls.