伏邪理论在中医药抗溃疡性结肠炎复发中的运用

溃疡性结肠炎（Ulcerative Colitis,UC）是一种病因尚未明确的慢性疾病,以大肠（直肠与结肠）黏膜与黏膜下炎症为病变的主要特征。临床上以腹泻、黏液脓血便和腹痛等为主要症状。该病往往反复发作,迁延日久,并与结肠癌的发病有一定关系,被世界卫生组织列为现代难治病之一。     

P选择素单抗对小鼠溃疡性结肠炎治疗的研究

溃疡性结肠炎是常见病 ,近年我国的发病率逐渐增高。其发病机制迄今尚未明了。研究发现 ,细胞黏附分子通过介导中性粒细胞、单核细胞和淋巴细胞与炎症部位血管内皮的黏附、浸润 ,在肠组织炎症形成中起着重要作用[1,2 ] 。我们在建立大鼠溃疡性结肠炎模型的基础上 ,观察黏附分子Ｐ选择素单克隆抗体的防治作用。材料与方法一、动物健康雌性ＢＡＬＢ/ｃ小鼠 ,7～ 9周龄。体重约 2 0ｇ ,共 3 0只。随机分为试验组 (ｎ =2 0 )与正常对照组 (ｎ =10 )。试验组动物口服 5 %硫酸葡聚糖溶液 (ＤＳＳ ,Ｓｉｇｍａ公司 ) 7ｄ ,并随机分为单抗组与ＰＢＳ…     

溃疡性结肠炎患者血小板功能状态和组织因子途径抑制物变化的临床研究

目的　探讨溃疡性结肠炎 (UC)患者血小板功能状态和组织因子途径抑制物 (TFPI)的变化。方法　使用TYXN 91智能血液聚集仪测定 47例UC患者和 3 0例对照组血小板聚集率(PAg) ,同时采用ELISA法检测血清P 选择素 (Ps) ,采用发色底物法测定血浆TFPI含量 ,并对其进行相关性分析。结果　活动期UC患者PAg明显高于缓解期和对照组 (P <0 .0 1) ,活动期和缓解期UC患者Ps和TFPI含量均高于对照组 (P <0 .0 1和P <0 .0 5 ) ,PAg与TFPI呈正相关 (γ =0 .62 3 ,P <0 .0 1) ,Ps与TFPI无明显相关性 (γ =0 .2 3 5 ,P >0 .0 5 )。结论　活动期UC患者体内存在血小板激活 ,在缓解期血小板活化程度仍增高 ;UC患者血浆TFPI含量升高 ,且PAg与TFPI在UC患者的血栓前状态中可能发挥着协同作用。     

益生菌干预下溃疡性结肠炎结肠组织中防御素的表达及意义

目的 研究益生菌治疗溃疡性结肠炎（UC）前后防御素（HNP1-3）在结肠组织中的表达水平,明确益生菌对UC患者的治疗作用,探讨防御素在UC发病机制中的作用以及益生菌治疗UC的作用机制。方法30例UC患者,随机分成A、B、C三组,A组口服柳氮磺胺吡啶和美常安,B组口服柳氮磺胺吡啶和丽珠肠乐,C组口服柳氮磺吡啶,疗程均为1个月。于治疗前后各取病变肠组织,用免疫组化法检测其中HNP。的表达水平。结果A、B、ci组治疗前病变肠组织中HNP。均为阳性表达,治疗后均为阴性或弱阳性表达,各组治疗前后差异有统计学意义（P〈0．01）。A、B两组肠组织中HNP。的表达在治疗前后下降幅度比C组大,其差异有统计学意义（P〈0．01）,而A、B两组服药前后下降幅度比较,其差异无统计学意义（P≥0．05）。结论HNP。参与UC的发生发展,能反映疾病的炎症程度;益生菌能有效降低UC患者的HNP1-3表达水平;HNP1-3可能与益生菌治疗UC的作用机制有关。     

二丙酸倍氯米松治疗溃疡性结肠炎的疗效及对P-选择素、ICAM-1表达影响研究

目的 探讨二丙酸倍氯米松灌肠治疗溃疡性结肠炎(UC)的临床疗效及对P-选择素、ICAM-1表达的影响,探讨其治疗UC的价值.方法 将58例活动期UC患者随机分为2组:治疗组和对照组,均口服美沙拉嗪作为基础治疗.治疗组(n=32)采用二丙酸倍氯米松保留灌肠;对照组(n=26)应用氢化可的松保留灌肠.结果 治疗组总有效率高于对照组(93.75% vs 80.77%),但差异无显著性(P>0.05).P-选择素、ICAM-1表达强度与炎症程度有关(P均<0.01),二丙酸倍氯米松组治疗后其表达程度明显减弱(P<0.01),而氢化可的松组无明显下降(P>0.05).结论 二丙酸倍氯米松保留灌肠治疗溃疡性结肠炎有较好疗效,下调组织中黏附分子的表达是其作用机制之一.     

益气活血解毒法对溃疡性结肠炎复发患者血浆血栓烷B2和6-酮-前列腺素F1α水平及比值的影响

[目的]探讨益气活血解毒法对溃疡性结肠炎(UC)复发患者血浆血栓烷B2(TXB2)和6-酮-前列腺素F1α(6-Keto-PGF1α)水平及TXB2/6-Keto-PGF1α比值的影响.[方法]90例UC复发患者随机分为2组,各45例,治疗组给予益气活血解毒立法的中药汤剂,对照组给予柳氮磺吡啶(SASP)治疗,治疗前后分别检测血浆TXB2、6-Keto-PGF1α水平.[结果]治疗前UC患者血浆TXB2、6-Keto-PGF1α水平及TXB2/6一Keto-PGF1α比值均高于正常人(P<0.01);复发者血浆TXB2、6-Keto-PGF1α水平及TXB2/6-Keto-PGF1α比值均高于未复发者(P<0.01,<0.05).治疗组治疗后、随访时血浆TXB2、6-Keto-PGF1α水平及TXB2/6一Keto-PGF1α比值均低于对照组(P<0.01,<0.05).[结论]以益气活血解毒立法的中药对UC复发治疗,与SASP比较,可有效降低血浆TXB2、6-Keto-4-PGF1α水平及TXB2/6-Keto-PGF1α比值,从而阻抑血小板活化,可能是抗UC复发作用机制之一.     

溃疡性结肠炎患者P-选择素和血小板参数分析

背景：研究发现凝血机制活化在炎症性肠病（IBD）的进展过程中起重要作用。P-选择素（CD62P）参与介导凝血和炎症反应时中性粒细胞和单核细胞与活化的血小板或内皮细胞的黏附。目的：探讨血小板活化标记物P．选择素以及血小板计数（PLT）、平均血小板体积（MPV）用于溃疡性结肠炎（UC）疾病活动度评估的价值。方法：纳入65例活动期UC患者、31例缓解期UC患者和60例健康对照者。流式细胞术测定外周血P-选择素阳性率,血细胞分析仪测定PLT、MPV,分析三者与UC活动度的相关性。结果：UC患者外周血CD62P阳性率、PLT显著高于对照组（P〈0．01）,MPV显著低于对照组（P〈0．01）;活动期UC患者三项指标的变化均较缓解期UC患者更为显著,组间差异有统计学意义（P〈0．05）。外周血CD62P、PLT与UC活动度呈正相关（P〈0．05）,MPV与UC活动度呈负相关（P〈0．05）。结论：UC患者的机体处于高凝状态。P-选择素、PLT、MPV能反映UC疾病活动度,对病情评估和治疗方案的制定有一定参考价值。     

防御素在溃疡性结肠炎结肠组织中的表达及意义

目的研究防御素（HNP13）、白细胞介素-8（IL-8）在溃疡性结肠炎（UC）结肠组织中的表达分布以及与UC病变范围和病变程度的关系，探讨其在UC发病机制中的作用；明确IL-8与HNP1-3的相关性。方法用免疫组化法检测36例活动期UC及30例正常对照石蜡包埋组织中HNP1-3及IL-8的表达情况。结果UC组HNP1-3及IL-8均为阳性表达。对照组均为阴性或弱阳性表达。两者在UC组的表达与对照组相比，差异均有统计学意义（P〈0．01）。UC病变范围越广、程度越重，HNP13及IL-8表达的阳性率越高。UC患者受累黏膜的HNP1-3和IL-8水平明显高于未受累黏膜。且HNP1-3和IL-8表达具有明显的相关性（rs=0．957，P〈0．01）。结论HNP1-3的表达与IL-8呈正相关且均参与了UC的发生和发展；HNP1-3可能在UC局部结肠组织破坏和病理变化中起了更重要的作用；HNP1-3、IL-8反映了疾病的炎症程度，并且可作为病情严重程度评定的指标。     

溃疡性结肠炎复发因素的研究现状

溃疡性结肠炎(UC)是一种以局部结肠黏膜炎症反应为主的,以腹痛、腹泻、黏液脓血便、里急后重为主要特征的慢性非特异性炎症性肠病,其病因尚未完全阐明。近20年的研究表明,该病主要与免疫异常、基因变异相关,而感染、饮食、职业、慢性阑尾炎、口服避孕药、围生期和儿童等因素以及是否维持治疗、心理因素等则是导致UC的复发因素;中医学认为饮食因素、外邪侵袭、七情内伤则是造成UC复发的主要原因。1现代医学对UC复发因素的研究1.1感染与UC复发的关系1.1.1感染引起肠道菌群失调有人[1]总结到,大肠埃希菌、分枝秆菌、拟杆菌、温和气单孢菌、…     

溃疡性结肠炎患者外周血中性粒细胞凋亡与粘附分子水平的关系及意义

目的　探讨溃疡性结肠炎 (U C)患者外周血中性粒细胞 (PMN)凋亡机制。方法　采用流式细胞术检测 32例 UC患者外周血 PMN凋亡 ,EL ISA法检测 P-选择素 (P- sel)和细胞间粘附分子 - 1(ICAM- 1)的水平。结果　活动期 UC患者 PMN凋亡率明显低于对照组和缓解期 UC患者 (P<0 .0 1)。不同病情活动期 U C患者 PMN凋亡有显著性差异 (P<0 .0 1)。活动期 UC患者外周血中 P- sel和 ICAM- 1水平均高于对照组和缓解期 U C患者(P<0 .0 1或 (P<0 .0 5 ) ,且与 PMN凋亡呈负相关 (r值分别为 - 0 .72 38和 - 0 .5 2 13,P均 <0 .0 1) ,与病情呈正相关。结论　各种免疫细胞粘附分子表达上调可能是导致 UC患者 PMN凋亡延迟的重要机制     

活血健脾补肾法治疗溃疡性结肠炎

[目的]探讨活血健脾补肾法方药治疗小鼠溃疡性结肠炎(UC)疗效机制.[方法]雌性BALB/C小鼠随机分为正常、模型、柳氮磺胺吡啶(SASP)、活血法、健脾法及补肾法组;除正常组外,以葡聚糖硫酸钠(DSS)诱导小鼠产生UC模型后,药物组分别灌胃给药,疗程结束后取小鼠结肠组织,采用免疫组化、原位杂交方法观察核因子-κBP65(NF-κBP65)、转化生长因子-β1(TGF-β1)、环氧合酶-2(COX-2)及其mRNA的表达.[结果]活血、健脾及补肾组结肠COX-2、NF-κBP65及其mRNA的表达和活血、补肾组结肠TGF-β1及其mRNA的表达均低于模型组(均P<0.05).[结论]活血、健脾、补肾方药通过降低NF-κBP65、COX-2及TGF-β1的表达分别发挥作用.     

Carcinoma of the colon and rectum complicating chronic ulcerative colitis

Patients with pancolonic chronic ulcerative colitis are at increased risk to develop carcinoma of the colon. Controversy continues, however, as to whether this carcinoma is more “virulent” than “type ordinaire” carcinoma of the colon and as to the best way to manage these patients. This study reviews the characteristics and survival of 70 patients with cancer of the colon superimposed on chronic ulcerative colitis. Patients with carcinoma identified incidentally during prophylactic colectomy for chronic ulcerative colitis fared well (5-year survival of 72 per cent), while those with clinical symptoms or radiographic suggestion of cancer had a poor survival rate (5-year survival of 35 per cent). Patients with panproctocolitis, 10 years of disease, and early onset of disease are most likely to have cancer superimposed on chronic ulcerative colitis. This cancer is likely to have a poorer prognosis than type ordinaire cancer of the colon. Prophylactic proctocolectomy should be considered before evidence suggesting carcinoma develops. Read at the meeting of the American Society of Colon and Rectal Surgeons, Atlanta, June 10 to 14, 1979. This paper received the Harry E. Bacon Foundation Award.     

Activated platelets as a possible early marker to predict clinical efficacy of leukocytapheresis in severe ulcerative colitis patients

Background Leukocytapheresis (LCAP) is an effective adjunct for patients with active ulcerative colitis (UC). Because LCAP may have the potential to remove and modulate not only leukocytes but also platelets, we evaluated the correlation between activated platelets and the therapeutic response to LCAP. Methods Fourteen patients with severe UC received weekly LCAP for 5 consecutive weeks. Their average clinical activity index (CAI) and endoscopic index (EI) were 9.6 ± 3.4 and 10.9 ± 1.0, respectively. Their peripheral blood was sampled before and after every LCAP and stained with fluorescent antibodies to the activation-dependent surface antigens of platelets (CD63, CD62-P) prior to flow cytometry. Endoscopic evaluations were performed after the last LCAP. Results Clinical remission (CAI < 4) was induced in 50% of the patients (7/14) after 5 weeks, and there were no significant differences observed in clinical background between the responder group (RG) and the nonresponder group (NG). In the RG, the populations of CD63⁺ (P < 0.03) and CD62-P⁺ (P < 0.05) platelets were significantly decreased after the first LCAP, and their reduction ratio decreased gradually with repeated LCAP. A significant improvement of the EI score, especially mucosal damage, was achieved in RG (P < 0.04) but not in NG. Conclusions These results indicate that the therapeutic responses to LCAP were reflected in modulations of population and/or platelet functions, especially after the first session. The decrease of such activated platelets immediately after the first LCAP may be an early marker for predicting the response in patients with severe UC.     

Two-color immunofluorescence and flow cytometric analysis of lamina propria lymphocyte subsets in ulcerative colitis and Crohn's Disease

By using two-color immunofluorescence with fluorescein isothiocyanate (FITC) and phycoerythrin (PE)-labelled monoclonal antibodies and multiparameter flow cytometry, we investigated lamina propria lymphocyte subsets of patients with ulcerative colitis (UC) and Crohn's disease (CD). Leu-3/Leu-2 (CD4/CD8) ratio of lamina propria lymphocytes (LPL) of CD (mean±sd: 1.9±0.8,P<0.01) was significantly decreased compared with controls (3.3±1.1), because of an increased number of CD8+lymphocytes. The majority of lamina propria CD4+cells were CD4+, Leu-8-and CD4+, CD45R-both in controls and IBD tissue. Many lamina propria T lymphocytes were activated, expressing HLA-DR antigen not only in IBD but also in controls. NK cells defined by CD16 and CD 56 (3.0±1.4%,P<0.01) were significantly decreased in patients with UC compared with controls (6.5±3.0%). A low proportion of B cells in the intestinal mucosa expressed Leu-8 antigen and CD23 antigen. The proportion of activated B cells of LPL was high in IBD mucosa as well as normal mucosa. These findings suggest that local activation of B cells leads to the loss of the expression of Leu-8 antigen and CD23.     

11beta-hydroxysteroid dehydrogenase 1 and 2 expression in colon from patients with ulcerative colitis

BACKGROUND AND AIM: 11beta-hydroxysteroid dehydrogenase (11betaHSD) is an enzyme responsible for the interconversion of active 11beta-hydroxysteroids (cortisol) into biologically inactive 11-oxosteroids (cortisone). The isoform 11betaHSD1 operates predominantly as a reductase converting cortisone to cortisol, whereas 11betaHSD2 catalyzes oxidation of cortisol to cortisone. This mechanism of peripheral metabolism of glucocorticoids has been suggested to be involved in increasing the availability of anti- inflammatory glucocorticoids as a response to inflammatory stimuli. The aim of this study therefore was to investigate the impact of inflammatory bowel disease on the expression of colonic 11betaHSD1 and 11betaHSD2. METHODS: Quantitative real-time RT-PCR was used to assess messenger RNA for 11betaHSD1 and 11betaHSD2 in bioptic samples taken from patients with ulcerative colitis and in healthy controls, and in colon of rats with colitis induced by dextran sulfate sodium (DSS). Rat colonic fragments were used for assessment of local metabolism of glucocorticoids. RESULTS: In both human and rat specimens colitis up-regulated the expression of colonic 11betaHSD1 mRNA and down-regulated 11betaHSD2 mRNA. A similar pattern was observed at the level of local metabolism of corticosterone. Oxidation of corticosterone to 11-dehydrocorticosterone was decreased and reduction of 11-dehydrocorticosterone to corticosterone was increased in colonic tissue of rats with DSS-colitis. CONCLUSIONS: Colonic inflammation induces local glucocorticoid activation via 11betaHSD1 and impairs glucocorticoid inactivation via 11betaHSD2. The observed changes indicate a role for local metabolism of glucocorticoids in the control of colonic inflammation.     

Role of non-adrenergic non-cholinergic inhibitory nerves in the colon of patients with ulcerative colitis

The cause of impaired colonic motility in patients with ulcerative colitis (UC) is unknown. The non-adrenergic non-cholinergic (NANC) inhibitory nervous system is one of the most important factors in the enteric nervous system of human gut. To assess the physiological significance of NANC inhibitory nerves in the colon of patients with UC, we investigated the enteric nerve responses of colonic tissues from patients with this disease. Colonic tissues were obtained from the lesional sigmoid colons of six patients with UC. Normal sigmoid colonic tissues obtained from ten patients with colonic cancer were used as controls. A mechanographic technique was used to evaluate in-vitro muscle responses to the electrical field stimulation (EFS) of adrenergic and cholinergic nerves before and after treatment with various autonomic nerve blockers. NANC inhibitory nerves were found to act on both normal colon and the lesional colon of patients with UC, but colon with UC was more strongly innervated by NANC inhibitory nerves than was the normal colon. These findings suggest that NANC inhibitory nerves play an important role in the impaired motility observed in the colon of patients with UC. Received Feb. 3, 1997; accepted May 23, 1997     

Survival and causes of death in Italian patients with ulcerative colitis A GISC nation-wide study

BACKGROUND: Death rate for patients with ulcerative colitis has changed over last few decades. Recent studies indicate that cumulative long-term mortality is comparable to that in general population, and that deaths may depend on causes not strictly related to colonic disease. AIM: To evaluate overall and cause-specific mortality rate in a large group of Italian patients with ulcerative colitis. METHODS: A total of 2,066 ulcerative colitis patients aged >18 years consecutively diagnosed in twenty Italian Gastroenterology Units between 1964 and 1995 were followed-up from diagnosis until 1997. Standardised Mortality Ratios and Relative Survival Ratios were calculated. RESULTS: Overall mortality of patients with ulcerative colitis was comparable to that in general population with 93 deaths observed versus 92.1 expected (standardises mortality ratio, 1.0; 95% confidence interval, 0.8-1.2). Significantly higher mortality was observed in patients under 30 years of age at diagnosis (standardised mortality ratio, 2.7; 95% confidence interval, 1.3-4.9), and in those diagnosed before 1974 (standardised mortality ratio, 2.7; 95% confidence interval, 1.1-5.7). Proctocolitis and complications from surgery were mentioned in 11 and 5 certificates, respectively. A significant excess of deaths was observed for colorectal cancer (colon: standardised mortality ratio, 3.0; 95% confidence interval, 1.0-6.9; rectum: standardised mortality ratio, 4.4; 95% confidence interval, 1.2-11.3), and haemolymphopoietic neoplasms (standardised mortality ratio, 2.8; 95% confidence interval, 1.0-6.1), in particular multiple myeloma and non-Hodgkin lymphoma. A significant deficit of deaths was observed for cancer of the respiratory system (standardised mortality ratio, 0.3; 95% confidence interval, 0.1-1.0). CONCLUSIONS: This study confirms that, also in Italy, mortality of patients with ulcerative colitis is comparable to that in general population. Only 12% of deaths were due to ulcerative colitis itself, whereas 10% of deaths were attributed to colorectal cancer. Deaths from colorectal cancer occurred, on average, 9 years after diagnosis of ulcerative colitis, suggesting that the risk of cancer is not limited to patients with long-standing colitis. As to mortality for causes unrelated to colitis, there was an excess of deaths due to malignancies of the haemolymphopoietic system.     

Localized giant pseudopolyposis of the colon in ulcerative colitis

Recently a patient with ulcerative colitis developed abdominal pain and a left upper quadrant mass. A⁶⁷Ga-citrate scintiscan showed increased activity over the mass. A barium enema demonstrated retrograde obstruction at the splenic flexure and intraluminal multilobulated tissue masses. The total abdominal colectomy specimen showed localized giant pseudopolyposis at the splenic flexure. This condition is a rare local complication of both ulcerative and granulomatous colitis. It resembles a villous adenoma on barium enema and, although inflammatory, may simulate a colonic carcinoma. When symptomatic, local resection may be sufficient treatment.