慢性结肠炎患者保留灌肠方法的临床研究

目的 :探讨用改进的保留灌肠方法治疗护理慢性结肠炎的效果 :方法 :随机将 6 0例慢性结肠炎患者分为对照组和观察组 ,对照组用传统保留灌肠方法 ,观察组的用注射式接尿管 (代肛管 )方法。结果 :与对照组比较 ,观察组药液在肠道内保留的时间延长 (P <0 0 1) ,灌肠药液外溢减少 (P <0 0 1) ,总有效率明显增高 (P <0 0 5 )。结论 :改进保留灌肠方法可减少药物外溢 ,延长药物在肠内保留的时间 ,提高治疗护理效果。现报告如下     

Indikation für eine immunsuppressive Therapie bei chronisch entzündlichen Darmerkrankungen

Zusammenfassung Der immunsuppressiven Therapie kommt bei chronischen Darmerkrankungen gro?e Bedeutung zu, insbesondere dort, wo die Standardtherapie nicht den gewünschten Erfolg zeigt. Als Therapie der ersten Wahl gelten bei Colitis ulcerosa 5-Aminosalizyls?ure-freisetzende Medikamente, bei Morbus Crohn Kortikosteroide. Innerhalb der Gruppe immunsuppressiver Pr?parate gibt es erhebliche Wirkungsunterschiede. Darüber hinaus ist die Immunsuppression auch mit ernstzunehmenden Nebenwirkungen belastet. über den Stellenwert der Immunsuppression als Erg?nzung, m?gliche oder bei Unvertr?glichkeit notwendige Substitution der Standardtherapien von Colitis ulcerosa und Morbus Crohn wird hier eingehend referiert. Auch die Behandlung dieser Erkrankungen in der Schwangerschaft wird dabei erl?utert.     

慢性非特异性溃疡性结肠炎中医研究述评

本文通过对古典医籍及近１０年文献有关慢性非特异性溃疡性结肠炎的资料分析，认为本病的证候特点与中医病名“休息痢”相符，病机归纳为脾虚为发病之本，湿热为致病之标，血瘀为局部病理变化，治疗方面得出了健脾益气化湿、活血化瘀解毒、托疮祛腐生肌等方法是治疗本病之关键的结论，提出分期治疗本病的思想，认为提高近期治愈率、降低复发率及做好癌前监测是今后研究的努力方向。     

Imaging biomarkers of inflammation <Emphasis Type="Italic">in situ</Emphasis> with fun ctionalized quantum dots in the dextran sodium sulfate (DSS) model of mouse colitis

Objective and design: Myeloperoxidase (MPO) and proinflammatory cytokines play an important role in the development of inflammation. These markers are generally measured using tedious ELISA procedures. In this study, a novel technique utilizing antibody conjugated quantum dot nanoparticles was developed to detect Myeloperoxidase, Interleukin-1α (IL-1α) and Tumor Necrosis Factor-α (TNF-α) in vivo in the dextran sodium sulfate (DSS) model of experimental colitis. Materials and methods: Colitis was induced in animals (n = 8 animals/group) by feeding 4% DSS solution ad libitum for seven to eight days. Quantum Dots (QDs) exhibiting fluorescence at various wavelengths were conjugated to MPO, IL-1α and TNF-α polyclonal antibodies and tested in vivo at various stages of colitis. Tissue sections obtained were imaged with confocal microscope. The image intensity obtained from the tissue specimen was correlated with clinical activity measured as Disease Activity Index (DAI). Results: Myeloperoxidase, IL-1α and TNF-α were visualized with quantum dots on various days of disease. The intensity of quantum dots increased with the increase in inflammation. The increase in intensity showed an excellent correlation with the DAI based on the clinical parameters. Conclusion: The study demonstrated that multiple biomarkers can be detected simultaneously and their quantitative expression correlated well with clinical disease severity. This novel technology should facilitate design of a novel optical platform for imaging various biomarkers of inflammation, early detection of acute and chronic disease markers and inflammation-mediated cancer markers. This detection may also facilitate determination of therapeutic success. Received 14 March 2007; returned for revision 8 May 2007; accepted by M. Parnham 27 June 2007     

Long-term treatment with anti-alpha 4 integrin antibodies aggravates colitis in G alpha i2-deficient mice

Targeted deletion of the heterotrimeric G protein, Galphai2, in mice induces lethal colitis closely resembling ulcerative colitis. In chronic colitis, migration of circulating leukocytes into the intestinal mucosa is partially dependent on alpha4 integrins. In previous studies, short-term administration of anti-alpha4 integrin antibodies has been shown to attenuate intestinal inflammation, and here we elucidate the effect of long-term administration of anti-alpha4 integrin antibodies on colitis in Galphai2(-/- )mice. Long-term blockade of alpha4 integrin significantly increased the severity of colitis in Galphai2(-/-) mice. The inflammation was confined to the colon, associated with increased cancer in situ, destruction of crypt architecture, and increased production of IL-1beta, TNF-alpha and IFN-gamma. Blockade of alpha4 integrin reduced the recruitment of activated T cells to the small intestine. In strong contrast, there were significantly higher numbers of activated T cells in the colonic lamina propria and epithelium, most probably due to in situ proliferation. Furthermore, treatment with alpha4 integrin antibodies induced decreased levels of total IgA and IgG in sera, whereas total IgM levels were unchanged. These new findings may have implications in the understanding of the progression of chronic intestinal inflammation.     

Persistent and selective effects of inflammation on smooth muscle cell contractility in rat colitis

Intestinal inflammation affects smooth muscle contractility contributing to altered motility, but changes to the individual smooth muscle cells are not well described. We used video microscopy to study the contractility of circular smooth muscle cells (CSMC) isolated from the rat mid-descending colon throughout the course of TNBS-induced colitis, measuring their shortening response to carbachol (CCh), 5-HT, histamine or high K⁺. In control CSMC, CCh caused a maximal shortening response of 28 (2%), similar to that for 5-HT of 27 (1%), but by day 4 of colitis, these responses were decreased by 35% and 37%, respectively. By day 36, all aspects of cholinergic contraction returned to control levels, while 5-HT-induced contraction remained significantly attenuated. In contrast, the contractile responses to histamine remained similar at all time points. K⁺-induced contraction was impaired only on day 4, and the maximal response remained substantially greater than CCh or 5-HT. Colitis caused a 121% increase in CSMC length by day 2 that persisted through day 36, independent evidence for phenotypic change. We conclude that impaired CSMC contractility at both the receptor and non-receptor levels contribute to altered smooth muscle function during colitis. Persistent changes in contractile response remained detectable after resolution of inflammation, and similar events may occur in post-enteritis syndromes seen in humans.     

柳氮磺胺吡啶对溃疡性结肠炎患者血清IFN-γ、IL-4及黏膜炎症的影响

目的： 探讨柳氮磺胺吡啶（SASP）对溃疡性结肠炎（UC）患者血清干扰素（IFN）-γ、白细胞介素（IL-4)和黏膜炎症的影响。方法： 活动期中度UC患者50例，口服SASP 1 g，每日3次，共6周，应用ELISA法检测血清IFN-γ、IL-4，组织学检测黏膜炎症。结果： 患者治疗前血清IFN-γ为（31.6±4.3) ng/L，显著高于治疗后的(22.3±5.6) ng/L（P<0.05），治疗前IFN-γ明显高于对照组的(17.5±5.9) ng/L（P<0.01）；治疗前IL-4为(4.6±1.8) ng/L，显著低于治疗后的(8.9±2.0) ng/L（P<0.05），治疗前IL-4明显低于对照组的(10.9±2.7) ng/L（P<0.01）。治疗前后嗜酸性粒细胞浸润率分别为100.0%和90.0%（P<0.05），隐窝脓肿分别为48.0%和13.3%（P<0.01），黏膜组织学分级分别为（2.49±0.84）级和（1.31±0.75）级（P<0.01）。结论： SASP能明显逆转中度活动期UC患者的Th1和Th2细胞的失衡状态和UC炎症黏膜的隐窝脓肿，减少中性白细胞和嗜酸性粒细胞的浸润，从而促进炎症黏膜的愈合。     

70. Ileorectostomie versus ileo-anale Anastomose mit Reservoir bei Colitis ulcerosa und Adenomatosis coli

Zusammenfassung Ca. 2000 Proktomucosektomien sind in den letzten Jahren durchgeführt worden als Alternative zur Proktocolektomie, aber auch zur Ileorectostomie bei AC und CU. Bei minimaler Operationsletalität ist die Rate der Frühkomplikationen (Ileus, Anastomoseninsuffizienz, Anastomosenstenose) nicht unbeträchtlich (> 10%). Die funktionellen Ergebnisse dagegen sind nach einer Phase der Adaptation vorwiegend gut. Die nicht unerheblichen Risiken der Ileorectostomie bei AC (Entartungsrate bis 20%) und bei CU (Entzündungsrezidiv 20–30%, sekundäre Entartung um 5%) haben die Proktomucosektomie an gröeren Zentren zu einem etablierten Verfahren werden lassen.     

生长抑素对溃疡性结肠炎患者炎症反应及氧化应激的调节作用

目的探讨生长抑素对溃疡性结肠炎(UC)患者炎症因子和氧化应激的改善作用。方法收集2019年1-12月法库县卫生健康服务中心收治的活动期UC患者40例,随机分为对照组和观察组各20例。对照组采用常规治疗方案,观察组在其基础上加用生长抑素,0.1mg/次,1次/8h,两组均治疗14d。比较两组治疗后炎症水平和氧化应激状态改善情况。结果两组治疗后各炎症和氧化应激指标差异均有统计学意义(P<0.05)。结论生长抑素能够进一.步改善活动期UC患者的炎症和氧化应激水平,值得推荐使用。     

超氧化物歧化酶对大鼠乙酸性结肠炎粘膜的保护作用

本文观察了超氧化物歧化酶（ＳＯＤ）对大鼠乙酸性结肠炎的粘膜保护作用。与生理盐水组对照，预防性静脉给予１万Ｕ ＳＯＤ能显著降低粘膜损伤指数以及肠粘连和狭窄的发生率。但是，腹腔注射与灌肠相同剂量的ＳＯＤ与各自生理盐水对照组比较，并无显著差别。ＳＯＤ的粘膜保护作用呈剂量效应。测定结肠粘膜ＳＯＤ、谷胱甘肽过氧化物酶、髓化氧化物酶活性以及过氧化脂质含量，提示ＳＯＤ的保护作用机理是减少炎症过程中的氧自由基。