肠易激综合征患者肠黏膜肥大细胞与神经纤维的关联

目的　探讨肠黏膜肥大细胞与神经纤维之间的关联及其与肠易激综合征 (IBS)发病的关系。方法　应用电镜和免疫组化双重染色技术 ,对 5 6例符合罗马Ⅱ标准的腹泻型IBS患者和 12例非IBS对照组患者末端回肠和直肠 乙状结肠交界部位肠黏膜内的肥大细胞与神经纤维的关联进行了检测。结果　IBS患者和对照组肠黏膜内多数肥大细胞与神经纤维紧邻。患者末端回肠、直肠 乙状结肠交界处黏膜内神经元特异性烯醇化酶 (NSE)、P物质、5 羟色胺 (5 HT)的表达明显高于对照组 (P <0 .0 5 ) ,肥大细胞周围NSE、P物质、降钙素基因相关肽 (CGRP)、5 HT的表达也明显增强。IBS患者末端回肠黏膜内肥大细胞的数目 (10 .98± 2 .96 )与对照组 (6 .0 5± 0 .5 1)相比明显增多 (P <0 .0 1)。IBS患者与对照组相比 ,末端回肠内NSE(6 .73± 1.0 2比 4 .2 5± 0 .5 0 )、P物质 (6 .84± 0 .85比 4 .2 8± 0 .4 0 )、CGRP(6 .73± 0 .82比 4 .33± 0 .5 4 )、5 HT(6 .72± 0 .81比 4 .0 0± 0 .6 3)阳性神经纤维紧邻的肥大细胞数目亦明显增多 (P <0 .0 1)。结论　IBS患者肠黏膜内肥大细胞数量的增多及其周围神经肽表达的增强表明 :免疫系统与肠神经丛之间通路的活化可能与IBS的发病有关。     

便秘型肠易激综合征与5-HT的相关性研究

目的探讨便秘型肠易激综合征（IBS—C）与5-羟色胺（5-HT）的相关性。方法IBS—C患者30例和对照组30例,均行电子结肠镜检查,在直肠和乙状结肠交界处活检,组织切片行免疫组化5-HT抗体染色。结果IBS—C结肠黏膜中5-HT阳性表达率为23．3％,免疫组化5-HT染色强度与对照组比较明显增强（P〈0．05）。结论IBS—C的发病与5-HT有一定的相关性。     

肠黏膜细胞因子在肠易激综合征患者回肠及升结肠组织中的表达

目的:研究肠易激综合征(IBS)患者回肠末端及升结肠黏膜组织中炎性因子白介素(IL)-6、IL-23及LTGF-β1的表达,探讨IBS的发病机制.方法:选取110例IBS患者,另选40例健康体检者为对照,内镜下取回肠及升结肠肠黏膜组织各1块,用免疫组织化学法测定回肠末端及升结肠肠黏膜中IL-6、IL-23及TGF-β1...     

感染后肠易激综合征患者结肠黏膜P物质与白细胞介素、干扰素表达的相关性研究

目的探讨肠道感染对肠易激综合征（IBS）患者结肠黏膜P物质（SP）、Th1细胞因子表达的影响。方法经结肠镜钳取77例IBS（20例感染后）患者及30例对照者的降结肠和直肠黏膜标本，采用免疫组化染色法检测肠黏膜SP与白细胞介素（IL）-2、干扰素（IFN）-γ的表达情况。结果IBS伴腹泻型患者结肠黏膜SP、IFN-γ和IL-2表达与对照组间差异有统计学意义（P〈0．05），感染后IFN-γ和IL-2阳性的IBS伴腹泻型患者结肠黏膜SP表达与对照组间差异亦有统计学意义（P〈0．05），而非感染后IBS患者结肠黏膜IFN-γ和IL-2阳性SP表达与对照组间差异无统计学意义（P〉0．05），但有增加趋势。结论感染可促进SP表达增加，进而促使Th1细胞因子表达上调。感染可通过黏膜免疫／肠神经系统改变参与IBS发病。     

肠易激综合征患者肠黏膜Th1/Th2漂移的研究

目的探讨肠易激综合征(IBS)患者肠黏膜是否存在Th1／Th2免疫调节功能紊乱。方法经结肠镜钳取58例IBS患者及20例对照者的升结肠、降结肠和直肠黏膜标本，采用免疫组化染色检测其肠黏膜主要Th1和Th2细胞因子的表达情况。结果IBS患者肠黏膜大体及组织学表现与对照相比无明显改变；腹泻型IBS患者升结肠、降结肠、直肠黏膜Th1细胞因子干扰素(IFN)-γ的阳性表达率显著高于对照组，白细胞介素(IL)-12的表达率在直肠较对照组显著增高，升结肠、降结肠有升高趋势，但差异无显著性；Th2细胞因子IL-10的表达率与对照组比较呈降低趋势，但差异无显著性。进一步比较腹泻型患者中感染后IBS(pIBS)和非感染后IBS Th1和Th2细胞因子的表达，pIBS中Th1细胞因子IFN-7的表达在升结肠、降结肠和直肠均显著高于对照组，升结肠、直肠IL-12的表达亦显著增高，降结肠的表达有增高趋势：Th2细胞因子IL-4、IL-10较对照组有下降趋势。非感染后IBS患者Th1和Th2细胞因子的表达较对照组差异无显著性。便秘型IBS患者Th1和Th2细胞因子的表达与对照绢比较差异均无显著性。结论腹泻型IBS患者肠黏膜内存在Th1／Th2漂移，Th1反应增强，感染因素影响了腹泻型Th1／Th2漂移，便秘型患者Th1／Th2仍趋于平衡状态。     

肠易激综合征患者结肠黏膜P物质、血管活性肠肽和肥大细胞的变化

背景：肠易激综合征（IBS）的发病机制尚不明确。目的：探讨IBS患者结肠黏膜P物质（SP）、血管活性肠肽（VIP）、肥大细胞（MC）的变化及其在IBS中的可能作用。方法：20例腹泻型IBS患者、22例便秘型IBS患者和18名正常对照者纳入本研究．取回盲部、乙状结肠黏膜行SP、VIP免疫组化染色和MC计数。结果：IBS患者回盲部、乙状结肠黏膜SP、VIP免疫阳性神经纤维较正常对照组增多、增粗，阳性增强（P〈0．05）。IBS患者乙状结肠黏膜SP、VIP免疫阳性神经纤维与回盲部相比无显著差异。IBS患者回盲部黏膜MC计数较正常对照组显著增高（P〈0．01），乙状结肠黏膜MC计数与正常对照组相比无显著差异。IBS患者乙状结肠黏膜MC计数与正常对照组相比，显著低于回盲部（P〈0．01）。结论：SP、VIP和MC在IBS的发病中起有一定作用。     

异基因造血干细胞移植后肠道病变的内镜表现

目的探讨结肠镜检查在诊断异基因造血干细胞移植（allo-HSCT）后肠道移植物抗宿主病（GI-GVHD）和巨细胞病毒（CMV）肠炎中的作用。方法回顾性对比分析GI-GVHD、CMV肠炎以及GI-GVHD合并CMV肠炎（GC）的结肠镜检查表现及其相关问题。结果47例患者接受50例次结肠镜检查，其中GI-GVHD32例次，CMV肠炎7例次，GC11例次，他们的一般临床资料具有可比性（P〉0．1）；GI-GVHD、CMV肠炎和GC外周血CMV-DNA阳性率分别为28．1％、42．9％和27．3％，三组间差异没有统计学意义（P〉0．1）；肠镜下GI-GVHD和CMV肠炎都有结肠黏膜病变，病变表现呈多样性，除黏膜龟纹样改变和深在溃疡分别是GI-GVHD和CMV肠炎较为特异的病变外，黏膜水肿、红斑、充血、糜烂及浅表溃疡均不能区分GI-GVHD和CMV肠炎；3例GI-GVHD有伪膜形成，1例CMV肠炎有疱疹样黏膜隆起，GC患者容易发生回肠黏膜活动性渗血和回盲瓣炎症。GI-GVHD、CMV肠炎和GC分别有63．8％、70．0％和43．8％的活检标本取自直乙状结肠。结论allo-HSCT患者外周血CMV—DNA检查难以区分GI—GVHD和CMV肠炎；黏膜龟纹样改变和深在溃疡分别是GI-GVHD和CMV肠炎较为特异的改变；GC患者更容易发生回肠黏膜渗血和回盲瓣炎症。左半结肠检查及组织活检能诊断大部分GVHD和CMV感染，但最好进行全结肠检查并到达回肠末端。     

肠易激综合征患者内脏高敏感机制的实验研究

目的:研究肠易激综合征(IBS)患者肠黏膜肥大细胞 (MC)与神经肽免疫反应阳性纤维有无变化及其在IBS中的可能作用和临床意义。方法:黏膜标本取自19例正常人、22例腹泻型IBS患者和20例便秘型IBS患者的回肠末端、回盲部、升结肠、乙状结肠,应用特殊组化染色法(甲苯胺蓝改良染色法)和免疫组化染色法分别对MC和神经肽免疫反应纤维进行染色,并应用彩色病理图像分析软件及免疫组化分析软件进行分析。在回盲部和乙状结肠各加取2块黏膜标本,     

肠易激综合征患者肠黏膜中褪黑素受体的表达及其临床意义

目的探讨肠易激综合征（irritable bowel syndrome，IBS）患者结肠黏膜中褪黑素受体（melatonin receptor，MR）的表达情况及其与肠易激综合征临床症状的相关性。方法用免疫组化法，检测正常对照20例、腹泻型肠易激综合征（diarrhea-predominant IBS，D-IBS）23例、便秘型肠易激综合征（constipation-predominant IBS，C-IBS）20例结肠黏膜中MR的表达情况。使用JEDA801D形态学图像分析系统，测量阳性表达面积及光密度（opacity density，OD）。结果MR在黏膜层含量较多，黏膜下层含量较少。回盲部和乙状结肠MR阳性面积及OD值表现为：D-IBS明显高于正常对照组（P〈0．05），正常对照组明显高于C-IBS（P〈0．05）。与同组IBS乙状结肠相比，回盲部阳性面积增高（P〈0．05）；OD值无明显差异。结论MR在D-IBS中高表达，在C-IBS中低表达，说明MR对IBS患者胃肠道运动有一定影响。     

结肠黏膜肥大细胞及外周T淋巴细胞亚群变化在肠易激综合征发病中的作用研究

目的探讨结肠黏膜肥大细胞（MC）密度和外周T淋巴细胞亚群变化与肠易激综合征（IBS）发病的关系。方法在内镜下钳取结肠黏膜活组织标本。采用SP免疫组化染色进行肥大细胞定量分析；用流式细胞仪测定外周T淋巴细胞亚群对肠易激综合征不同亚型及正常对照组进行比较分析。结果IBS患者回肠末端、回盲部、升结肠黏膜固有层MC密度较对照组明显增高（P〈0.01），在同一结肠部位MC密度腹泻型IBS较便秘型IBS患者高（P〈0.01）；外周T淋巴细胞亚群CD4／CD8比值与正常组比较。腹泻型IBS下降（P〈0.01），而便秘型增高（P〈0.01）。结论结肠黏膜MC密度和T淋巴细胞亚群改变与IBS及其亚型密切相关，可能在IBS发病中起重要作用。     

Full-thickness biopsy of the jejunum reveals inflammation and enteric neuropathy in irritable bowel syndrome

BACKGROUND & AIMS: Irritable bowel syndrome (IBS) is regarded as a functional bowel disorder. Few studies have looked for histopathologic changes in the gut and only then in biopsy specimens from intestinal mucosa. Because bowel function is governed mainly by nerve plexuses in the bowel wall, we have investigated full-thickness bowel biopsy specimens in patients with severe IBS. METHODS: We used a laparoscopy-assisted technique to obtain full-thickness biopsy specimens from the proximal jejunum. Tissue specimens were investigated with light microscopy using routine stainings and immunohistochemical techniques. Horizontal sectioning was done to visualize large areas of the myenteric plexus. Fifteen autopsy specimens were used as controls regarding the myenteric plexus. Colorectal adenoma controls with terminal ileum biopsy specimens and full-thickness jejunal biopsy specimens from patients with degenerative enteric neuropathy were used as control groups for intraepithelial lymphocyte counts. RESULTS: Ten patients (2 males, 8 females) were studied. In 9 patients, we found low-grade infiltration of lymphocytes in the myenteric plexus. Lymphocytes had peri- and intraganglionic location. The mean number of lymphocytes per ganglion ranged from 1.9 to 7.1 per patient, with an overall mean of 3.4. No intraganglionic lymphocytes were found in the control group and only a few periganglionic lymphocytes (mean, 0.2). Four patients had concomitant intraepithelial lymphocytosis. Neuron degeneration was evident in 6 of 9 patients with and 1 patient without ganglionic lymphocyte infiltration. CONCLUSIONS: Our findings indicate that inflammation and neuronal degeneration in the myenteric plexus are involved in the pathogenesis of IBS.     

Impact of elemental diet on mucosal inflammation in patients with active Crohn's disease: cytokine production and endoscopic and histological findings

BACKGROUND: The aim of this study was to examine the impact of elemental diet on mucosal inflammation in Crohn's disease (CD), mainly by cytokine measurements. METHODS: Twenty-eight consecutive patients with active CD were treated with an elemental diet (Elental) for 4 weeks. The mucosal biopsies were obtained from the terminal ileum and large bowel before and after treatment. As a control group, mucosal biopsies were obtained from 20 patients without inflammation. Mucosal cytokine concentrations were measured by enzyme-linked immunosorbent assay. RESULTS: After treatment, clinical remission was achieved in 20 patients (71%). Endoscopic healing and improvement rates were 44% and 76% in the terminal ileum and 39% and 78% in the large bowel, respectively. Histologic healing and improvement rates were 19% and 54% in the terminal ileum and 20% and 55% in the large bowel, respectively. Before treatment, the mucosal concentrations of interleukin (IL)-1beta, IL-1 receptor antagonist (IL-1ra), IL-6, IL-8, and tumor necrosis factor-alpha in the ileum and large bowel were significantly higher than in controls. These cytokine concentrations decreased to the levels of control after treatment. IL-1ra/IL-1beta ratio in the ileum and large bowel was significantly lower than in controls before treatment. The ratio increased to the level of controls after treatment. The endoscopic and histologic healing of the mucosal inflammation was associated with a decline of the mucosal cytokines and an increase of the IL-1ra/IL-1beta ratio. CONCLUSIONS: The elemental diet (Elental) reduced mucosal cytokine production and corrected an imbalance between proinflammatory and anti-inflammatory cytokines in CD.     

重视黏膜低度炎症在肠易激综合征发病机制中的作用

研究发现一些肠易激综合征（IBS）患者结肠和回肠黏膜中存在低度炎症，急性肠道感染、遗传因素、食物过敏、肠道菌群改变、社会心理因素等可能触发肠道低度炎症的发生，并使之持续存在。这种低度炎症可导致胃肠运动功能紊乱．激活内脏感觉系统，可能在IBS的发病机制中起一定作用，应予重视；     

肠易激综合征患者小肠黏膜5-HT信号系统的研究

目的探讨肠易激综合征（IBS）患者不同部位小肠黏膜5-羟色胺（5-HT）水平及肠嗜铬细胞（EC细胞）数量是否改变。方法选取24例便秘型IBS（IBS-C）、26例腹泻型IBS（IBS-D）患者和26名健康人,行小肠镜及结肠镜检查并取十二指肠降段、近端空肠和回肠末段黏膜,用高压液相色谱-电化学法和免疫组织化学检测5-HT含量和EC细胞。结果IBSC患者近端空肠黏膜的5-HT含量与健康人相比有统计学意义（122±54ng／mg蛋白比188±91ng／mg蛋白,P〈0．05）,而十二指肠降段和回肠末段黏膜5-HT含量（182±90ng／mg蛋白、61±35ng／mg蛋白）与健康人相比（256±84ng／mg蛋白、93±45ng／mg蛋白）无统计学意义（P〉0．05）。IBS-D患者不同部位小肠黏膜5-HT含量与健康人相比均无统计学意义（P〉0．05）。IBS-C和IBSD患者不同部位小肠黏膜EC细胞数量与健康人相比均无统计学意义（P〉0．05）。结论上述结果提示1BS患者小肠黏膜5HT信号系统异常是其发病机制之-,但是在IBS-C和IBS-D之间有差异。     

Abnormal electroencephalogram in irritable bowel syndrome.

BACKGROUND: Irritable bowel syndrome (IBS) is a functional bowel disorder characterized by abdominal pain and abnormal bowel habits. IBS patients sometimes complain of sleep disturbance, depression, and various autonomic symptoms. Our hypothesis is that the central nervous system (CNS) might play a role in the pathogenesis of IBS. METHODS: We conducted two experiments using an electroencephalogram (EEG) to evaluate brain activity while at rest and during mental arithmetic stress with pharmacologic neostigmine administered to IBS patients. The first experiment was conducted on 48 conscious and relaxed patients (24 IBS patients and 24 normal controls). EEG recordings were evaluated for visual and power spectrum data. In the second experiment colonic manometric studies combined with EEG recordings were performed in 21 of 24 IBS patients and 8 of 24 normal controls under mental arithmetic stress and the administration of neostigmine. RESULTS: Inspection of the EEG showed significantly greater EEG abnormality in the IBS patients (29.2%) than in the controls (4.2%) (P < 0.02). In the power spectrum analysis of the EEG the IBS patients showed significantly greater beta power percentage than did the normal subjects (P < 0.02). A significant positive correlation was observed between the colonic motility index and beta power percentage after the administration of neostigmine, 10 microg/kg, only in the IBS patients (P < 0.05). CONCLUSION: A brain dysfunction as indexed by the EEG suggests an electrophysiologic brain-gut interaction in IBS.     

肠黏膜雌孕激素受体表达在肠易激综合征发病机制中的作用研究

目的 探讨雌、孕激素受体在肠易激综合征（IBS）患者肠道内分布、变化及其临床意义，并对在消化道的作用靶点和可能的细胞学机制做出合理解释和推断。方法 经结肠镜钳取24名正常人和59例肠易激综合征患者的回肠末端、盲肠和降结肠黏膜，分别采用抗人雌、孕激素受体抗体标识肠黏膜上雌、孕激素受体，并应用免疫组化方法检测了雌、孕激素受体阳性细胞数目改变。结果 1、IBS患者回肠末端和盲肠黏膜雌激素受体阳性细胞数目增多（P＜0.01)，降结肠黏膜与正常组无显著差别；2、肠道黏膜未见孕激素受体表达 结论 IBS患者肠黏膜雌激素受体高表达在IBS病理过程中发挥一定作用，并认为肥大细胞为雌激素在消化道的重要靶点，其对于揭示IBS在女性中的高发病率和月经期加重的临床现象有重要意义；同时提示雌激素受体拮抗剂可能对部分患者有效。     

The development of irritable bowel syndrome after Shigella infection: 3 year follow-up study]

BACKGROUND/AIMS: Bacterial gastroenteritis seems to be a risk factor of irritable bowel syndrome (IBS). The incidence of post-infectious IBS (PI-IBS) was reported to be in the range of 7-31%, but few studies have reported long term follow-up results. So, we investigated the clinical course and prognosis of PI-IBS three years after shigella infection. METHODS: The subjects were recruited from our previous study, in which we investigated the incidence and risk factors of PI-IBS. We had a questionnaire based on interview with 120 controls and 124 patients who had shigella infection three years ago. Both groups were evaluated for the presence of IBS, functional bowel disorders (FBD) except IBS before, one and three years after the infection, respectively. RESULTS: Ninety-five patients (76.6%) and 105 controls (87.5%) completed the questionnaire. In patients group, 7 cases had IBS prior to infection (previous IBS), 12 cases (13.8%) had IBS after 1 year (PI-IBS). Four cases developed IBS newly after 3 years (new IBS). Thirteen cases (14.9%) in patients and 4 cases (4.5%) in controls had IBS over 3 years (OR 3.93: 1.20-12.86). The recovery rate over 3 years were 50.0% (2/4) in previous IBS and 25% (3/12) in PI-IBS. The incidence of PI-IBS after 3 years in previous FBD subjects was 28.6% and was 10.6% in normals (p<0.05). The female gender was a risk factor for FBD. CONCLUSIONS: Bacterial gastroenteritis is a trigger factor of IBS. About a quarter of PI-IBS patients are recovered over 3 years. Previous FBD except IBS is a risk factor after 3 years.     

Decreased expression of serotonin in the jejunum and increased numbers of mast cells in the terminal ileum in patients with irritable bowel syndrome

AIM： To investigate if there are changes in serotonin （5-HT） levels, enterochromaffin （EC） cells and mast cells in small intestinal mucosa of patients with irritable bowel syndrome （IBS）. METHODS： Diarrhea-predominant （IBS-D, n = 20）, or constipation-predominant （IBS-C, n = 18） IBS patients and healthy controls （n = 20） underwent colonoscopy and peroral small intestinal endoscopy, and mucosal samples were obtained at the descending part of the duodenum, proximal end of jejunum and terminal ileum. High-performance liquid chromatographyelectrochemistry and immunohistochemical methods were used to detect 5-HT content, EC cells and mast cells. RESULTS： （1） There were no differences in the number and distribution of EC cells between IBS patients and the normal group. （2） The mucosal 5-HT contents at the duodenum, jejunum and ileum in IBS-C patients were 182 ± 90, 122 ± 54, 61 ± 35 ng/mg protein, respectively, which were all lower than those in the normal group （256 ± 84, 188 ± 91, and 93 ± 45 ng/ mg protein, respectively）, with a significant difference at the jejunum （P 〈 0.05）. There were no differences in the small intestinal mucosal 5-HT contents between IBS-D patients and the normal group. The mucosal 5-HT contents at the duodenum were significantly higher than those at the ileum in the three groups （P 〈 0.001）. （3） The numbers of mast cells in patients with IBS-C and IBS-D at the ileum were 38.7 ± 9.4 and 35.8 ± 5.5/highpower field （hpf）, respectively, which were significantly more than that in the normal group （29.8 ± 4.4/hpf） （P 〈 0.001）. There was no significant difference in the numbers of mast cells at the other two parts between IBS patients and the normal group. The numbers of mast cells in IBS-C, IBS-D, and normal groups were all significantly higher at the ileum （38.7 ± 9.4, 35.8 ± 5.5, 29.8 ±4.4/hpf, respectively） than at the duodenum （19.6± 4.7, 18.5 ± 6.3, 19.2 ±3.3/hpf, respectively, P 〈 0.001）. CONCLUSIO