清热化湿肠宁汤治疗大肠炎症性息肉(湿热蕴脾证)的疗效分析

目的观察清热化湿肠宁汤对大肠炎症性息肉(湿热蕴脾证)的临床疗效。方法将70例为临床研究对象,随机分为两组。对照组患者使用常规的结肠镜治疗,实验组患者使用中医药清热化湿肠宁汤治疗,对比两组治疗的效果。结果实验组患者的总有效率更高,患者中医证候积分改善更优,复发率更低。结论使用清热化湿肠宁汤对大肠炎症性息肉(湿热蕴脾证)患者的治疗效果较好,可以提高疗效,改善临床症状,且降低复发率。

大肠炎症性出血与肠源性感染（附67例分析）

回顾性分析６７例大肠炎症性出血的临床资料。大肠炎症性疾病的诊断应在排除癌肿及痔或肛裂后才能确诊；其手术治疗的原则是在出现并发症或非手术治疗无效的情况下方可考虑；介绍一种控制肠源性感染的方法，认这对于出现肠源性感染者应尽早进行治疗干预。

内镜下诊断40例非炎症性肠病大肠溃疡患者的临床分析

目的探讨40例非炎症性肠病大肠溃疡患者在内镜诊断下的应用效果。方法 40例非炎症性大肠溃疡患者作为研究对象,采用内镜进行诊断并治疗,分析内镜诊断下的评价及临床效果。结果所有患者经内镜诊断,8例患者为肠结核、4例患者为感染性肠炎、13例患者为溃疡型大肠癌、3例患者为吻合口溃疡、3例患者为缺血性肠炎、3例患者为急性阑尾炎、3例患者为放射性肠炎、3例患者为内痔术后,以上为导致非炎症性肠病大肠溃疡的主要病因。结论内镜在非炎症性肠病大肠溃疡患者的诊断中具有一定的特异性,并且在临床应用中具有重要的价值。

大肠炎促进大肠癌发生发展的实验研究

目的通过建立小鼠结肠炎相关大肠癌模型,证实炎症加速大肠癌发生过程。方法联合或单独使用AOM致癌剂腹腔注射与DSS致肠炎药物自由饮用建立小鼠大肠炎症-癌症模型,实验共分为4组:大肠炎-癌症模型组(AOM/DSS组),单纯高剂量致癌剂-癌前病变模型组(AOM组),大肠炎症模型组(DSS组)及对照组。进行大体与病理组织学评估。结果 AOM/DSS组小鼠远端肠黏膜在4周时除表现为急性黏膜炎症外,还出现了肠隐窝病变(ACF),7周为腺瘤中-重度不典型增生改变,100天时80%的小鼠出现典型的腺癌特征。AOM组于4周时尚未见到异常组织学改变,7周时可见到ACF灶,100天时可见腺瘤样突起,灶性中-重度不典型增生。DSS组可见由急性肠黏膜炎症向慢性炎症的转化过程。结论炎症性肠癌发生的过程与散发性大肠癌的成癌过程一致,即ACF-腺瘤-腺癌三个疾病过程;炎症损伤可加速小鼠大肠癌疾病过程。

大肠癌手术病人的护理体会

大肠癌包括结肠癌和直肠癌。大肠癌与长期高脂肪、低纤维素饮食、遗传、大肠腺瘤、大肠慢性炎症、血吸虫病、放射线损害等因素有关。其常见症状有便血、排便习惯改变、腹壁肿块、大便次数增多,里急后重,大便带血或粘液。随着癌肿的增大,逐渐出现大便扁细、排便费力,甚至出现腹痛、腹胀等梗阻表现。手术切除是主要治疗手段。对大肠癌手术病人的护理就显得特别重要。

炎症性大肠疾病的诊治进展

炎症性大肠疾病的诊治进展郭文平徐达华汤永胜（合肥市第二人民医院２３００１１）炎症性大肠疾病缺乏严格的定义和范畴，按一般理解系炎症性肠病的同义语。炎症性肠病（ｉｎｆｌａｍｍａｔｏｒｙｂｏｗｅｌｃｌｉｓｏａｓｅ，ＩＢＤ）是属于一类原因不明的的肠道炎症性...

Colorectal cancer and dysplasia in inflammatory bowel disease

Both ulcerative colitis and Crohn’s disease carry an increased risk of developing colorectal cancer. Established risk factors for cancer among patients with inflammatory bowel disease (IBD) include the younger age at diagnosis, greater extent and duration of disease, increased severity of inflammation, family history of colorectal cancer and coexisting primary sclerosing cholangitis. Recent evidence suggests that current medical therapies and surgical techniques for inflammatory bowel disease may be reducing the incidence of this complication. Nonetheless heightened vigilance and a careful, comprehensive approach to prevent or minimize the complications of invasive cancer are warranted in this unique cohort of patients. Current guidelines for the prevention and early detection of cancer in this high risk population are grounded in the concept of an inflammation-dysplasia- carcinoma sequence. A thorough understanding of the definition and natural history of dysplasia in IBD, as well as the challenges associated with detection and interpretation of dysplasia are fundamental to developing an effective strategy for surveillance and prevention, and understanding the limitations of the current approach to prevention. This article reviews the current consensus guidelines for screening and surveillance of cancer in IBD, as well as presenting the evidence and rationale for chemoprevention of cancer and a discussion of emerging technologies for the detection of dysplasia.

Positions of selective leukocytapheresis in the medical therapy of ulcerative colitis

Ulcerative colitis （UC） and Crohn＇s disease （CD） are the major forms of idiopathic inflammatory bowel disease （IBD）. Both UC and CD are debilitating chronic disorders that afflict millions of individuals throughout the world with symptoms which impair function and quality of life. The etiology of IBD is inadequately understood and therefore, drug therapy has been empirical instead of being based on sound understanding of IBD pathogenesis. This is a major factor for poor drug efficacy and drug related side effects that often add to the disease complexity. The development of biologicals notably infliximab to intercept tumor necrosis factor （TNF）-α reflects some progress, albeit major concern about their side effects and lack of long-term safety and efficacy profiles. However, IBD seems to be perpetuated by inflammatory cytokines like TNF-α, interleukin （IL）-Iβ, IL-6 and IL-8 for which activated peripheral granulocytes and monocytes/macrophages （GH） are major sources. Further, in IBD, peripheral GHs are elevated with activation behavior, increased survival time and are found in vast numbers within the inflamed intestinal mucosa; they are suspected to be major factors in the immunopathogenesis of IBD. Hence, peripheral blood GMs should be appropriate targets of therapy. The Adacolumn is a medical device developed for selective depletion of GH by receptor-mediated adsorption （GHA）. Clinical data show GMA, in patients with steroid dependent or steroid refractory UC, is associated with up to 85% efficacy and tapering or discontinuation of steroids, while in steroid nai＇ve patients （the best responders）, GHA spares patients from exposure to steroids. Likewise, GMA at appropriate intervals in patients at a high risk of clinical relapse suppresses relapse thus sparing the patients from the morbidity associated with IBD relapse. Further, GHA appears to reduce the number of patients being submitted to colectomy or exposure to unsafe immunosupressants. First UC episode, steroid naivety and short disease duration appear good predictors of response to GMA and based on the available data, GMA seems to have an excellent safety profile.

Evaluation of the effect of pyrrolidine dithiocarbamate in suppressing inflammation in mice with dextran sodium sulfate-induced colitis

AIM: To evaluate the effect of pyrrolidine dithio- carbamate (PDTC; an NF-κB inhibitor) administered at low (50 mg/kg) and high (100 mg/kg) doses in suppressing colitis in mice with dextran sodium sulfate (DSS)-induced colitis. METHODS: Mice were divided into a DSS-untreated group (normal group), DSS-treated control group, DSS+PDTC-treated groupⅠ(low-dose group), and DSS+PDTC-treated groupⅡ (high-dose group). In each group, the disease activity index score (DAI score), intestinal length, histological score, and the levels of activated NF-κB and inflammatory cytokines (IL-1β and TNF-α) in tissue were measured. RESULTS: The DSS+PDTC-treated groupⅡ exhibited suppression of shortening of intestinal length and reduction of DAI score. Activated NF-κB level and IL-1β and TNF-α levels were significantly lower in DSS+PDTC- treated groupⅡ. CONCLUSION: These findings suggest that PDTC is useful for the treatment of ulcerative colitis.

Regulatory T cells in inflammatory bowel diseases and colorectal cancer

Regulatory T cells(T regs) are key elements in immunological self-tolerance.The number of T regs may alter in both peripheral blood and in colonic mucosa during pathological circumstances.The local cellular,microbiological and cytokine milieu affect immunophenotype and function of T regs.Forkhead box P3+ T regs function shows altered properties in inflammatory bowel diseases(IBDs).This alteration of T regs function can furthermore be observed between Crohn's disease and ulcerative colitis,which may have both clinical and therapeutical consequences.Chronic mucosal inflammation may also influence T regs function,which together with the intestinal bacterial flora seem to have a supporting role in colitis-associated colorectal carcinogenesis.T regs have a crucial role in the immunoevasion of cancer cells in sporadic colorectal cancer.Furthermore,their number and phenotype correlate closely with the clinical outcome of the disease,even if their contribution to carcinogenesis has previously been controversial.Despite knowledge of the clinical relationship between IBD and colitis-associated colon cancer,and the growing number of immunological aspects encompassing sporadic colorectal carcinogenesis,the molecular and cellular links amongst T regs,regulation of the inflammation,and cancer development are still not well understood.In this paper,we aimed to review the current data surrounding the role of T regs in the pathogenesis of IBD,colitis-associated colon cancer and sporadic colorectal cancer.

Relationship and significance between anti-b2-glycoproteinⅠantibodies and platelet activation state in patients with ulcerative colitis

AIM： To study the relationship between anti-β2- glycoprotein Ⅰ （aβ2GPⅠ） antibodies and platelet activation state in patients with ulcerative colitis （UC） and its significance. METHODS： Peripheral blood samples were collected from 56 UC patients （34 males and 22 females, aged 43.5 years, range 21-66 years）, including 36 at active stage and 20 at remission stage, and 25 sex-and age-matched controls. The level of aβ2GP Ⅰ was measured by ELISA. The platelet activation markers, platelet activation complex- Ⅰ （PAC- Ⅰ ） and P-selectin （CD62P） were detected by flow cytometry. RESULTS： The A value for IgG aβ2GP Ⅰ in the active UC group was 0.61 ± 0.13, significantly higher than that in the remittent UC and control groups （0.50 ± 0.13 and 0.22 ± 0.14, P 〈 0.01）. There was a significant difference between the two groups （P 〈 0.01）. The A value for IgM aβ2GP Ⅰ in the active and remittent UC groups was 0.43 ± 0.13 and 0.38 ± 0.12, significantly higher than that in the control group （0.20 ± 0.12, P 〈 0.01）. However, there was no significant difference between the two groups （P 〉 0.05）. The PAC- Ⅰ positive rate for the active and remittent UC groups was 30.6% ± 7.6% and 19.6% ± 7.8% respectively, significantly higher than that for the control group （6.3% ± 1.7%,P 〈 0.01）. There was a significant difference between the two groups （P 〈 0.01）. The CD62P positive rate for the active and remittent UC groups was 45.0% ± 8.8% and 31.9% ± 7.8% respectively, significantly higher than that for the control group （9.2% ± 2.7%, P 〈 0.01）. There was a significant difference between the two groups （P 〈 0.01）. In the active UC group, the more severe the state of illness was, the higher the A value for IgG aβ2GP Ⅰ was, and the positive rate for PAC-Ⅰ and CD62P was positively correlated with the state of illness （Faβ2GP Ⅰ = 3.679, P 〈 0.05; FPAC-Ⅰ （%） = 5.346, P 〈 0.01; and FCD62P （%） = 5. 418, P 〈 0.01）. Meanwhile, in the same state of illness, the A value for IgG aβ2GP Ⅰ was positively correlated to the positive rates for PAC-Ⅰ and CD62P. CONCLUSION： aβ2GP Ⅰ level, platelet activation state and their relationship of them are closely correlated with the pathogenesis and development of UC.

Effect of smoking on inflammatory bowel disease: Is it disease or organ specific?

Smoking is an important environmental factor in inflammatory bowel disease （IBD） with differing effects in ulcerative colitis （UC） and Crohn＇s disease （CD）. Never smoking and formerly smoking increase the risk of UC, whereas smoking exacerbates the course of CD. The potential mechanisms involved in this dual relationship are yet unknown. A reasonable assumption is that smoking has different effects on the small and large intestine. This assumption is based on animal and human studies that show that the effects of smoking/nicotine on CD and UC depend on the site of inflammation and not on the type of disease.

Myo-inositol reduces β-catenin activation in colitis

To assess dietary myo-inositol in reducing stem cell activation in colitis, and validate pβ-cateninS552 as a biomarker of recurrent dysplasia.METHODSWe examined the effects of dietary myo-inositol treatment on inflammation, pβ-cateninS552 and pAkt levels by histology and western blot in IL-10-/- and dextran sodium sulfate-treated colitic mice. Additionally, we assessed nuclear pβ-cateninS552 in patients treated with myo-inositol in a clinical trial, and in patients with and without a history of colitis-induced dysplasia.RESULTSIn mice, pβ-cateninS552 staining faithfully reported the effects of myo-inositol in reducing inflammation and intestinal stem cell activation. In a pilot clinical trial of myo-inositol administration in patients with a history of low grade dysplasia (LGD), two patients had reduced numbers of intestinal stem cell activation compared to the placebo control patient. In humans, pβ-cateninS552 staining discriminated ulcerative colitis patients with a history of LGD from those with benign disease.CONCLUSIONEnumerating crypts with increased numbers of pβ-cateninS552 - positive cells can be utilized as a biomarker in colitis-associated cancer chemoprevention trials.

The role of granulocyte macrophage-colony-stimulating factor in acute intestinal inflammation

An imbalance of mucosal proand anti-inflammatory cytokincs is crucial in the pathogenesis of inflammatory bowel disease （IBD）. GM-CSF influences the development of hemopoietic cells. The precise role of GM-CSF in IBD remains to be elucidated. GM-CSF gene knockout （GM-CSF^-/-） and wild-type （Wt） mice were challenged with 2.5% dextran sulfate sodium （DSS） for 7 days. The ensued clinical and pathological changes, macrophage infiltration, colonic cytokine production, and bacterial counts were examined. DSS-treated GM-CSF^-/- mice developed more severe acute colitis than DSS-treated Wt mice, reflected by a greater body weight loss, more rectal bleeding, and aggravated histopathological changes. More infiltrating macrophages were observed in GM-CSF^-/-, compared with Wt mice following DSS challenge, correlating with monocyte chemoattractant protein-1 （MCP-1） production. The levels of colonic IL-17 and TNF-α were increased significantly in GM-CSF^-/- mice, but not in Wt mice, following DSS administration. The level of IL-6 was increased by 1.5- and 2-fold in the colon of GM-CSF^-/- and Wt mice, respectively, following DSS challenge. No significant changes in IL-4 and IFN-γ were detected in Wt and GM-CSF^-/- mice following DSS treatment. The bacteria recovery from colon was increased about 15- and 5-fold, respectively, in Wt mice and GM-CSF^-/- mice following DSS challenge. These results suggest that GM-CSF^-/- mice are more susceptible to acute DSS-induced colitis, possibly because of an impaired gut innate immune response as a result of diminished GM-CSF.

Common carotid arterial thrombosis associated with ulcerative colitis

A 26-year-old woman with ulcerative colitis was transferred to our hospital with left hemiparesis due to cerebral infarction. Cervical ultrasonography and magnetic resonance imaging angiography revealed thrombosis at the right common carotid artery and the right internal carotid artery. Antithrombotic and anticoagulant therapies were commenced. After about 2 wk of the treatment, the frequency of her diarrhea increased. She underwent emergency subtotal colectomy, but 10 d later an abundant hemorrhage from the remnant rectum occurred, so the remnant rectum was resected and an ileal pouch anal anastomosis was performed. Antithrombotic and anticoagulant therapies were continued, but neither her neurological status nor magnetic resonance imaging angiography findings showed subsequent changes. She was discharged 3 mon after operation. This is a rare case of common carotid arterial thrombosis occurring as a complication of ulcerative colitis, in which antithrombotic and anticoagulant therapies are considered to provoke a deterioration of the patient’s bowel disease.

Biomarkers for colitis-associated colorectal cancer

Patients with extensive ulcerative colitis(UC) of more than eight years duration have an increased risk of colorectal cancer. Molecular biomarkers for dysplasia and cancer could have a great clinical value in managing cancer risk in these UC patients. Using a wide range of molecular techniques- including cutting-edge OMICS technologies- recent studies have identified clinically relevant biomarker candidates from a variety of biosamples, including colonic biopsies, blood, stool, and urine. While the challenge remains to validate these candidate biomarkers in multi-center studies and with larger patient cohorts, it is certain that accurate biomarkers of colitis-associated neoplasia would improve clinical management of neoplastic risk in UC patients. This review highlights the ongoing avenues of research in biomarker development for colitis-associated colorectal cancer.

Isolated lymphoid follicles in colon: Switch points between inflammation and colorectal cancer?

Gut-associated lymphoid tissue is supposed to play a central role in both the organization of colonic repair mechanisms and colorectal carcinogenesis. In inflammatory conditions, the number, diameter and density of isolated lymphoid follicles (ILFs) increases. They are not only involved in immune surveillance, but their presence is also indispensable in normal mucosal regeneration of the colon. In carcinogenesis, ILFs may play a dual role. On the one hand they may support tumor growth and the metastatic process by vascular endothelial growth factor receptor signaling and producing a specific cytokine and cellular milieu, but on the other hand their presence is sometimes associated with a better prognosis. The relation of ILFs to bone marrow derived stem cells, follicular dendritic cells, subepithelial myofibroblasts or crypt formation, which are all involved in mucosal repair and carcinogenesis, has not been directly studied. Data about the putative organizer role of ILFs is scattered in scientific literature.

Is there an association of microscopic colitis and irritable bowel syndrome-A subgroup analysis of placebo-controlled trials

With great interest we read the recent retrospectice study by Barta et al （1） dealing with the clinical presentation of patients with microscopic colitis. They investigated in a cohort of 53 patients with microscopic colitis （46 with collagenous colitis, 7 with lymphocytic colitis） the relationship between microscopic colitis and both constipation and diarrhea. One of their mean finding was that abdominal pain, diarrhea and constipation was a common symptom complex of patients with microscopic colitis, thus the face of microcopic colitis resembles the subgroups of irritable bowel syndrome （IBS）.

Benign retroperitoneal schwannoma presenting as colitis:A case report

We report a case of a patient presenting with clinical,radiological and endoscopic features of colitis due to a compressive left para-aortic mass. Total open surgical excision was performed,which resulted in complete resolution of colitis. Histopathology and immunohistochemistry revealed benign retroperitoneal schwannoma. These neural sheath tumors rarely occur in the retroperitoneum. They are usually asymptomatic but as they enlarge they may compress adjacent structures,which leads to a wide spectrum of non-specific symptoms,including lumbar pain,headache,secondary hypertension,abdominal pain and renal colicky pain. CT and MR findings show characteristic features,but none are specific. Schwannoma can be isolated sporadic lesions,or associated with schwannomatosis or neurofibromatosis type Ⅱ (NF2). Although they vary in biological and clinical behavior,their presence is,in nearly every case,due to alterations or absence of the NF2 gene,which is involved in the growth regulation of Schwann cells. Both conditions were excluded by thorough mutation analysis. Diagnosis is based on histopathological examination and immunohistochemistry. Total excision is therapeutic and has a good prognosis. Schwannomatosis and NF2 should be excluded through clinical diagnostic criteria. Genetic testing of NF2 is probably not justified in the presence of a solitary retroperitoneal schwannoma.