老年溃疡性结肠炎的临床特点

目的探讨老年溃疡性结肠炎(UC)患者的临床特点。方法对2000年1月～2012年3月在本院门诊和住院的213例UC患者临床特点进行回顾性分析。60或60岁以上发病的患者为老年组,60岁以下发病的患者为中青年组,对两组患者的临床特点进行比较分析。结果 213例UC患者中,老年组51例,中青年组162例,两组患者在性别比例上无明显不同。老年UC患者中便血明显较中青年组少见(P<0.05)。与中青年组相比,老年组疾病的严重程度及内镜分级相对较轻(P<0.05)。老年UC患者的病变部位以直肠、直乙结肠和左半结肠受累最常见,明显高于中青年组(P<0.05)。结论老年UC患者临床表现相对较轻,病变部位以直肠、直乙结肠和左半结肠受累多见,内镜下病变较局限,表现较轻。     

溃疡性结肠炎患者结肠黏膜中胸腺基质淋巴细胞生成素的表达水平

目的研究溃疡性结肠炎(UC)患者结肠黏膜中胸腺基质淋巴细胞生成素的表达水平及其与病变范围、病变程度间的关系,初步探讨UC的发病机制。方法 34例UC住院患者作为研究组,29例结肠息肉患者作为对照组,采用实时定量PCR法测定两组结肠黏膜组织中TSLP mRNA表达水平,比较血清CRP及血沉的变化。结果研究组与对照组结肠黏膜TSLP mRNA表达水平及CRP、血沉存在显著差异(P0.01);UC患者中结肠黏膜TSLP mRNA表达水平、CRP以及血沉在不同病变程度及不同病变部位间存在显著性差异(P0.01);UC患者TSLP mRNA表达水平与CRP、血沉之间存在显著正相关(P0.01),TSLP mRNA表达水平与病变程度间存在显著正相关(P0.01)。结论与正常人比较,UC患者结肠黏膜中TSLP表达水平明显升高,结肠黏膜TSLP表达水平与UC病变程度和范围存在显著相关性。     

恶唑酮结肠炎小鼠模型的建立

建立合适的动物模型有助于炎症性肠病(IBD)的研究，然而目前尚缺乏类似人类溃疡性结肠炎(UC)的动物模型。目的：建立恶唑酮诱导的小鼠结肠炎模型，并评估其在IBD研究中的价值。方法：予BALB／c小鼠皮肤涂搽0．2ml3％恶唑酮(溶解于100％乙醇中)2次致敏，5天后予0.15ml1％恶唑酮(溶解于50％乙醇中)灌肠。观察小鼠的疾病活动指数(DAI)和病变结肠的组织学改变，并测定髓过氧化物酶(MPO)活性以及肿瘤坏死因子(TNF)-α干扰素(IFN)-γ和白细胞介素(IL)-4的含量。结果：结肠炎模型小鼠的DAI、组织学损伤评分和MPO活性均较对照组有明显改变，病变结肠组织的IL-4含量显著增高，TNF-α和IFN-γ含量则基本正常；结肠炎症可持续2周左右。结论：恶唑酮诱导的结肠炎是一种IL-4介导的2型辅助性T细胞(Th2)型炎症，其组织学特征和炎症分布均类似人类UC。恶唑酮小鼠结肠炎模型可作为研究UC发病机制和评估药物疗效的有益工具。     

溃疡性结肠炎相关肿瘤3例诊疗报道并文献复习

目的探讨溃疡性结肠炎(ulcerative colitis, UC)相关肿瘤的临床特点、诊治、预后。方法对3例UC相关肿瘤患者的临床资料进行回顾性分析并复习相关文献。结果 3例UC相关肿瘤患者病程均超过10年;肠镜提示肿瘤性病变均为息肉样病变;2例为广泛结肠型结肠炎,1例为左半结肠型结肠炎;病理1例提示癌,2例活检组织提示中-度和重度异型增生;异型增生患者内镜下切除后经规范5-氨基水杨酸(5-aminosailcylic acid, 5-ASA)治疗及内镜下监测,病变处于黏膜愈合;1例癌变患者因未及时治疗,后期出现肿瘤多处转移。结论 UC相关肿瘤患者病程长,多见于广泛结肠受累的患者,以息肉样病变为主的肿瘤性病变可以内镜下切除,辅以规范治疗及监测,预后较好。     

溃疡性结肠炎的中西药物治疗概况

近年来,溃疡性结肠炎(ulcerative colitis,UC)的发病率无论在国外还是国内均有逐年增高的趋势.其病变累及范围包括直肠、乙状结肠、左半结肠(脾曲以远)、广泛结肠(脾曲以近)、全结肠.对于不同的病变范围患者,需要给予不同的药物剂型.本文对治疗UC的药物剂型的发展进行了总结和回顾,讨论了药物剂型的选择对提高疗效和改善患者的生存质量的意义.     

中国炎症性肠病的诊断

炎症性肠病(IBD)是一种病因及发病机制尚不十分清楚的慢性肠道炎症性疾病,包括溃疡性结肠炎(UC)和克罗恩病(CD).UC是一种慢性非特异性结肠炎症,病变主要累及结肠黏膜层和黏膜下层;CD是一种胃肠道的慢性肉芽肿性炎性疾病,病变可累及消化道各部位,以末端回肠及邻近结肠最为常见,病变为穿壁性炎症,呈节段性、非对称性分布.     

缺血性结肠炎与溃疡性结肠炎的临床鉴别诊断

背景:缺血性结肠炎(IC)与溃疡性结肠炎(UC,左半结肠型)在临床和内镜表现上有一定相似之处,对于临床表现不典型者,初步诊断颇具难度。目的:分析IC与UC的临i床鉴别诊断要点。方法:收集武汉大学中南医院2008年1月～2009年12月确诊为IC或UC左半结肠炎的住院患者,对其病史资料进行回顾性分析。结果:21例IC和25例UC患者纳入研究。IC患者以老年女性居多,病程相对较短,常伴有高血压和糖尿病,最突出的临床表现为突发腹痛后24 h内出现便血,贫血少见;UC患者的主要临床表现为黏液血便伴腹痛,贫血常见。IC病变多仅累及单一肠段,直肠受累少见,溃疡小而表浅,病理学表现为慢性炎,隐窝炎罕见;UC病变多起源于直肠,呈连续性,溃疡弥漫,病理学表现为慢性炎伴多种炎性细胞浸润,隐窝炎、隐窝脓肿常见。结论:根据性别、年龄、病程以及临床、实验室、内镜和病理检查结果进行综合分析,有助于IC与U C的鉴别诊断。     

溃疡性结肠炎患者内镜分析

目的 回顾性探讨昆明市近10年来溃疡性结肠炎(UC)住院患者内镜表现.方法 选取昆明市1998年1月～2009年3月期间7家大型综合医院379例住院的炎症性肠病患者作为调查对象,诊断均符合2007年中华医学会消化病学分会的UC诊治标准,分析UC患者内镜下表现.结果 有98.2％的病例接受结肠镜检查,其诊断符合率为88.4％.100％为活动期,其中轻度38.3％,中度42.2％,重度19.5％.分型如下:直肠型者13.2％,直肠和乙状结肠型26.9％,左半结肠型34.9％,右半结肠型3.2％,全结肠型21.7％.内镜下表现病变呈弥漫性分布90.50％,充血水肿86.20％,糜烂或溃疡76.90％,活动性出血60％,脓性分泌物25％,假性息肉18％.结论 昆明市UC患者的病期以中度为主,病变范围以左半结肠型和直肠和乙状结肠型为主,以弥漫性分布、充血水肿、糜烂或溃疡为主要表现.     

TLR3与TLR9在溃疡性结肠炎中表达状态及临床意义的研究

目的观察TLR3和TLR9在溃疡性结肠炎(UC)患者病变组织和正常大肠组织中的表达情况,探讨其在UC发病机制中的作用。方法收集UC病例及正常对照结肠镜活检标本各30例。采用免疫组化和实时荧光定量PCR技术,检测UC患者及正常对照组肠黏膜中TLR3、TLR9的表达情况。结果 UC病变组织、正常结肠组织中均有TLR3 mRNA及TLR9 mRNA的表达,但UC组织中TLR9 mRNA表达显著高于正常结肠组织,而TLR3 mRNA与正常结肠组织相比差异无统计学意义。在免疫组化染色图片上,发现TLR3、TLR9主要在细胞的胞浆中表达,在UC病变组织中TLR9阳性表达率明显高于正常结肠组织(P0.05)。结论TLR9在UC患者中表达高度上调,推测它可能参与了UC的发病过程。     

通因通用法治疗溃疡性结肠炎的临床及实验研究

[目的]观察调肠通络饮(TTD)对溃疡性结肠炎(UC)患者的疗效及对实验性UC大鼠血小板功能的影响.[方法]103例UC患者随机分为两组,分别予TTD、柳氮磺胺砒啶(SASP)治疗后,观察临床综合疗效与结肠黏膜病变疗效;以2,4,6三硝基苯磺酸(TNBS)诱导实验性大鼠结肠炎,分别予TTD、SASP治疗后腹主动脉采血,测血小板黏附率、血小板聚集性,血浆与结肠组织中血栓烷B2(TXB2)、6-酮-前列腺素F1α(125 I-6-Keto-PGF1α),并取结肠组织,作病理观察.[结果]TTD组综合疗效明显优于SASP组;TTD能显著改善UC大鼠结肠病理状态,降低血浆及结肠组织中TXB2,升高血浆6-Keto-PGF1α.[结论]TTD为治疗UC的有效方药,能改善UC大鼠病损状况,有抑制血小板功能亢进的作用.     

Correlation between Saccharomyces cerevisiae DNA in intestinal mucosal samples and anti-Saccharomyces cerevisiae antibodies in serum of patients with IBD

AIM: To investigate the correlation between ASCA and presence of mucosal S. cerevisiae DNA in a population of CD, ulcerative colitis (UC) patients and controls. METHODS: S. cerevisiae-specific primers and a fluorescent probe were designed for a 5' exonuclease real time PCR (TaqManTM) assay, which is a homogenous system using a fluorescent-labelled probe for the detection of PCR product in real time. We analyzed the relation of the PCR results with the ASCA findings in a group of 76 inflammatory bowel disease (IBD) patients (31 CD, 45 UC) and 22 healthy controls (HC). RESULTS: ASCA (IgA or IgG) were positive in 19 (61%) patients with CD, 12 (27%) with UC and none of the HC. PCR amplification was inhibited and excluded from the final results in 10 (22%) UC patients, 7 (22%) CD patients, and 6 (30%) HC. In only 15 of the mucosal samples, S. cerevisiae DNA was detected by real time PCR, including 7 (29%) in CD, 7 (19%) in UC, 1 (6%) in HC. In 4 CD and in 4 UC patients, ASCA and mucosal S. cerevisiae were positive. Mucosal S. cerevisiae was present in combination with negative ASCA IgA and IgG in 3 UC, and 3 CD patients. CONCLUSION: We conclude that since the presence of S. cerevisiae in colonic mucosal biopsy specimens is very rare, ASCA is unlikely to be explained by continuous exposure to S. cerevisiae in the mucosa. Therefore, ASCA formation must occur earlier in life and levels remain relatively stable thereafter in immunological susceptible persons.     

Rectal Substance P Concentrations Are Increased in Ulcerative Colitis But Not in Crohn's Disease

Substance P, a neurotransmitter found in colonic mucosa, can alter gut immunologic, vascular, and motor phenomena. Thus, it may have an important role in the pathogenesis of ulcerative colitis (UC) and Crohn's disease (CD). By radioimmunoassay of the extracts of endoscopically obtained rectal mucosal biopsies in affected patients, we evaluated mucosal substance P levels. Non-inflammatory bowel disease patients undergoing lower endoscopies and biopsies served as controls. There were significantly increased concentrations of substance P in patients with UC, compared with controls ( p < 0.05) and compared with patients with CD ( p < 0.005). The mucosal levels in CD patients were significantly lower than in controls ( p < 0.05). Patients with active rectal CD had lower levels than patients with no evidence of active rectal disease. For the CD and UC patients, there was a strongly positive correlation between rectal mucosal substance P concentrations and total histologic inflammation scores ( r = 0.7, p = 0.001). A strong correlation existed for rectal mucosal substance P concentrations and mucosal mononuclear cell scores ( r = 0.7, p = 0.001) and for rectal mucosal substance P concentrations and the combined scores of mucosal neutrophils and eosinophils ( r = 0.7, p = 0.002).
In conclusion, the rectal mucosal substance P concentrations in patients with UC and CD are significantly different. Thus, substance P may have a different role in the pathogenesis of each of these entities. It is possible that the elevated concentrations in patients with UC are contributing to the increased inflammation seen in these patients. Alternatively, measured mucosal substance P levels may simply reflect the end result of the different inflammatory processes in UC and CD, rather than the cause. It is possible that the inflammatory cells are contributing to the measured concentrations.     

Mucosal inflammation in the terminal ileum of ulcerative colitis patients: Endoscopic findings and cytokine profiles

BACKGROUND: Currently, published reports of mucosal inflammation in the terminal ileum of ulcerative colitis (UC) before colectomy are scarce. AIM: To investigate inflammation in the terminal ileum of UC patients by endoscopic examinations and measurement of mucosal cytokine profiles. METHODS: Fifty consecutive patients with active UC were studied. At ileocolonoscopy, mucosal biopsies were taken from the terminal ileum. As control, mucosal biopsies from 20 patients without inflammation were examined. RESULTS: Thirty-eight patients showed endoscopically normal terminal ileum, four showed backwash ileitis, and eight showed non-backwash ileitis (ileitis with normal caecum). Pancolitis was observed in all of four patients with backwash ileitis, in 4 of 8 (50%) with non-backwash ileitis, and in 4 of 38 (11%) without ileal inflammation (P=0.0002). Extraintestinal manifestations were observed in none of 4 patients with backwash ileitis, in 6 of 8 (75%) with non-backwash ileitis, and in 3 of 38 (8%) without ileal inflammation (P<0.0001). In patients with backwash ileitis and non-backwash ileitis, ileal interleukin [IL]-1beta, IL-6, IL-8 and tumour necrosis factor-alpha levels were significantly elevated compared with the control group. Only extraintestinal manifestation was associated with higher ileal cytokine levels, whereas age, sex, and duration, extent and severity of UC did not show any apparent association. CONCLUSIONS: In patients with backwash ileitis, elevated ileal cytokines might reflect a reaction to regurgitation of colonic content into the ileum, but in patients without backwash ileitis, alternative factors are expected to contribute to the aetiology of ileal inflammation. Patients with extraintestinal manifestations had elevated ileal cytokine levels.     

Antibodies to colonic epithelial cells from the serum and colonic mucosal washings in ulcerative colitis.

It has been suggested that antibodies to a colonocyte protein of 40 kD (an intestinal isoform of tropomyosin) are specifically found in the serum and mucosa of patients with ulcerative colitis, which has important pathogenic implications. This study isolated and purified tropomyosin from the colonic mucosa, but no specific binding to this protein has been detected in serum samples or immunoglobulins isolated from mucosal washings of 20 ulcerative colitis (UC) patients by enzyme linked immunosorbent assay (ELISA) compared with 21 controls or 17 Crohn's disease (CD) patients. Samples from a further 12 patients with UC and primary sclerosing cholangitis (it is proposed that cross reactivity against the intestinal tropomyosin isoform accounts for the extraintestinal disease) also did not show binding to tropomyosin, whereas monoclonal antitropomyosin antisera bound both ELISAs and western blots. This study also examined the proteins in the normal colonic biopsy specimens on western blots that are bound by both serum samples and mucosal immunoglobulin preparations from these patients groups; there was no specific IgG or IgA binding to patients with UC or UC/primary sclerosing cholangitis, whereas binding to mitochondrial proteins of 70,000 and 45,000 was seen in samples from 12 primary biliary cirrhosis positive controls. This work does not support the hypothesis that autoimmune activity against the intestinal isoform or tropomyosin is important in the pathogenesis of ulcerative colitis.     

溃疡性结肠炎360例临床特征分析

近年溃疡性结肠炎（UC）的发病率明显升高,明确临床特征有助于其诊断。目的：探讨UC的临床特征。方法：收集2008年7月-2011年7月西京医院收治并确诊的活动期UC患者的临床资料,回顾性分析其临床特征。结果：共收治活动期UC患者360例,男女之比1．25：1;平均就诊年龄40．5岁。疾病严重程度以轻中度UC多见（84．4％）。病变累及以左半结肠和直肠、乙状结肠多见;18例病变呈节段性分布,其余均为连续分布。本组患者以腹泻、黏液脓血便、腹痛为主要临床表现,内镜下黏膜弥漫性充血、水肿、糜烂和溃疡,44例伴有肠外表现。多数患者的白细胞、ESR和CRP水平增高。52例患者合并并发症。349例患者接受内科治疗,病情明显缓解。结论：UC患者以中青年男性多见,内镜下病变以左半结肠和直肠、乙状结肠多见,常见并发症为结肠假性息肉。UC确诊主要根据临床表现、结肠镜检查、病理学检查,其中结肠镜检查可明确病变部位、范围、程度以及肠腔有无狭窄或癌变,有助于临床病情分期,对指导临床治疗方案的选择具有重要意义。     

Frequency and prognostic role of mucosal healing in patients with Crohn’s disease and ulcerative colitis after one-year of biological therapy

AIM:To assess the endoscopic activity before and after a one-year period of biological therapy and to evaluate the frequency of relapses and need for retreatment after stopping the biologicals in patients with Crohn’s disease(CD)and ulcerative colitis(UC).METHODS:The data from 41 patients with CD and 22 patients with UC were assessed.Twenty-four CD patients received infliximab,and 17 received adalimumab.The endoscopic severity of CD was quantified with the simplified endoscopic activity score for Crohn’s disease in CD and with the Mayo endoscopic subscore in UC.RESULTS:Mucosal healing was achieved in 23 CD and7 UC patients.Biological therapy had to be restarted in78%of patients achieving complete mucosal healing with CD and in 100%of patients with UC.Neither clinical remission nor mucosal healing was associated with the time to restarting the biological therapy in either CD or UC.CONCLUSION:Mucosal healing did not predict sustained clinical remission in patients in whom the biological therapies had been stopped.     

Histological healing after infliximab induction therapy in children with ulcerative colitis

AIM: To verify the impact of induction therapy with infliximab(IFX) on mucosal healing in children with ulcerative colitis(UC).METHODS: The study included all UC pediatric patients treated with IFX at our center over the last10 years. The data were collected from patients' medical charts and analyzed retrospectively. A total of 16 patients with UC underwent colonoscopy with sample collection before and after three IFX injections.Pediatric Ulcerative Colitis Activity Index(PUCAI)was used to assess the clinical condition; endoscopic features were classified according to the Baron scale;and histological changes were evaluated according to the protocol of The British Society of Gastroenterology and Geboes Index. Clinical response was defined as a ≥ 20-point reduction in PUCAI index, and clinical remission as PUCAI index 10 points. Endoscopic mucosal remission was defined as completely normal(score 0) on the Baron scale. Histological remission was defined as grade 0 in the Geboes Index. To assess correlation between variables, Spearman's rank correlation coefficient was used.RESULTS: Clinical remission(PUCAI 10) at week 8 was achieved in 68.75% of investigated subjects. Endoscopic mucosal remission at week 8(Baron 0) was observed in 12.5% of patients. Histological remission(Geboes 0)after induction therapy with IFX was noticed in 18.75%cases. A general histological improvement, expressedby normal surface and crypt architecture, number of crypts, and lamina propria cellularity, was observed in six(37.5%) patients; there was no improvement in nine(56.25%) individuals, and worsening was observed in one(3.75%) case. Changes were not related to UC location. A reduction of inflammatory process was observed in 10(62.5%) patients; there were no changes in four(25%) individuals, and the inflammation became more severe in two(12.5 %) cases. Simultaneous clinical, endoscopic and histological improvement of parameters assessing disease activity at week 8 was noticed in six(37.5%) patients. 55.5% of investigated patients with normal mucosa seen on endoscopy showed no inflammation on histology. A Baron score of 2 and 3showed a good correlation with histology results(78.2%of patients with a Geboes Index ≥ 3).CONCLUSION: IFX has a positive histological effect in more than one-third of UC patients. IFX reduces intestinal inflammation and improves clinical condition.     

Increased leukotriene B4 release from ileal pouch mucosa in ulcerative colitis compared with familial adenomatous polyposis.

Pouchitis may complicate the construction of an ileal pouch after colectomy for ulcerative colitis (UC) but not familial adenomatous polyposis (FAP). To examine whether differences in eicosanoid metabolism might explain why pouchitis is largely confined to UC patients, this study compared arachidonic acid stimulated release of immunoreactive leukotriene B4 (LTB4) and prostaglandin E2 (PGE2) from macroscopically uninflamed pouch mucosal biopsy specimens incubated in vitro from patients with UC and FAP. The study also compared eicosanoid release from inflamed and uninflamed pouches in patients with UC. In uninflamed pouches, median LTB4 release was nearly twice as high in UC as in FAP (p = 0.001), but there was no significant difference in PGE2 production. In UC, stimulated eicosanoid release from uninflamed functioning pouch mucosa was not significantly different from that from either ileostomy or defunctioned pouch mucosa. LTB4 and PGE2 release were significantly greater from inflamed than uninflamed pouch mucosa in UC (p = 0.001 and 0.01, respectively). Leukotriene synthesis inhibition or receptor antagonism, or both merit therapeutic evaluation in pouchitis. Increased release of LTB4 from endoscopically normal pouch mucosa suggests increased 5-lipoxygenase activity in patients with UC and could contribute to their predisposition to pouchitis.