4—氨基水杨酸治疗溃疡性结肠炎

４－氨基水杨酸治疗溃疡性结肠炎温忠慧欧阳钦近年来国内溃疡性结肠炎（ＵＣ）发病率逐年上升，探索有效的治疗方法逐渐提上日程。我院试制成４－氨基水杨酸（４－ＡＳＡ）灌肠剂，已作为院内处方应用多年，反应尚好。我们采用随机双盲对照方法，考察该药的疗效与安全性，...     

溶栓及PTCA治疗急性心肌梗塞92例临床分析

本文总结１９９１年８月至１９９６年４月应用溶栓及ＰＴＣＡ治疗ＡＭＩ９２例，男７６例，女１６例，年龄４６～７０岁之间，平均年龄６０．２±１０．５岁。治疗分为：①冠状动脉内输注尿激酶（ＩＣＵＫ）组３２例；②静脉输注尿激酶（ＩＶＵＫ）组４１例；③经皮冠状动脉腔内成形（ＰＴＣＡ）组１９例。全组再通６９例，总再通率为７５．０％，ＩＣＵＫ组、ＩＶＵＫ组、ＰＴＣＡ组再通率分别为７５．０％、６５．７％和９４．７％三组再通率比较有显著差异。三组患者近期预后比较：全组９２例，死亡９例，死亡率９．７８％，８例发生于梗塞血管未通者，１例发生于血管再通者。ＩＣＵＫ组３２例，死亡３例（９．３７％），发生心功能不全８例（２５．０％）；ＩＶＵＫ组４１例，死亡５例（１２．０％），发生心功能不全１１例（２６．８３％）；ＰＴＣＡ组１９例，死亡１例，死亡率为５．２６％，ＰＴＣＡ组无心功能不全者。     

应用5-氨基水杨酸保留灌肠治疗溃疡性结肠炎的临床效果

目的探讨5-氨基水杨酸保留灌肠治疗溃疡性结肠炎的临床效果。方法将118例溃疡性结肠炎患者随机分为两组,每组59例。对照组予以氢化可的松保留灌肠,观察组给予5-氨基水杨酸保留灌肠,对比两组治疗效果、临床症状缓解时间、结肠镜观察、大便常规改善情况。结果观察组治疗总有效率为94.9%,高于对照组的79.7%(P0.05);结肠镜改善率为71.2%、大便常规改善率为86.4%,明显高于对照组的47.5%、67.8%(P0.05);治疗后,观察组临床症状改善时间优于对照组,差异显著(P0.05)。结论溃疡性结肠炎患者采用5-氨基水杨酸保留灌肠治疗能有效缓解患者临床症状,提高治疗效果,安全性高。     

胃舒胶囊治疗消化性溃疡236例

目的观察胃舒胶囊治疗消化性溃疡（ＰＵ）的临床疗效．方法用胃舒胶囊（６粒，ｐｏ，３次／ｄ×２ｗｋ×２）治疗ＰＵ２３６例（男１９２例，女４４例；年龄１８岁～７４岁，平均３２岁±７岁；病程１ａ～１５ａ，平均４９ａ±３５ａ；ＤＵ１０６例，ＧＵ８３例，ＣＵ４７例），用纤维内镜观察不同证型ＰＵ患者的治疗效果．结果用胃舒胶囊两个疗程，对消化道症状改善率达９１２％～１００％，溃疡愈合率达９２８％，对肝胃气滞、寒邪犯胃、脾胃虚寒、胃热炽盛和瘀血阻络各型的治愈率分别为９２８％，９３５％，９４２％，８００％和８５７％．治疗组的疗效明显优于西咪替丁加胃必治组（Ｐ＜００１）．结论胃舒胶囊治疗ＰＵ具有显著疗效，其治疗作用可能与保护胃粘膜，中和胃酸和杀灭Ｈｐ等有关．     

急性冠状动脉缺血综合症400例住院患者的临床特点及预后

目的：了解急性冠状动脉缺血综合症（ＡＣＩＳ）住院患者的基本临床特点、干预措施及预后。对象与方法：选择因急性缺血性胸痛而住院的患者（即不稳定性心绞痛或非Ｑ 波心肌梗死）,登记并随访｀半年情况。用多中心前瞻性研究方法。结果：完成ＡＣＩＳ登记４００ 例,其中男性占６５．７％ ; 平均年龄６０．９±９．３岁; 平均心率７９．３±１４．４次／分; 发病到就诊平均时间为１２．７±９．９ 小时; 心电图异常者占７５％ ,其中ＳＴ段明显下降者占４８．０％ ,Ｔ波倒置占２８．４％ ;入院时初诊为非Ｑ波心肌梗死者为６．３％ , 不稳定心绞痛（ＵＡ）者占８７．３％ ; 住院期间死亡５例;出院诊为心肌梗死者占１３．２％ （５３ 例）, ＵＡ为８３．５％ 。登记后半年随访２６６ 例（６６．５％ ）, 平均随访１８６．９±２２．７ 天;半年内有规律的应用β－阻滞剂者占４４．４％ , 钙拮抗剂占５４．２％ , 抗血小板剂６４．７％ , 抗凝剂２９．８％ , 硝酸盐８５．５％ ,血管紧张素转换酶抑制剂３８．５％ 。随访期间因心绞痛需要住院治疗者占１６．２％ ; 心绞痛症状频发或加重者占１２．４％ ,无变化者９．５％ ,减少者４９．８％ , 缓解或消失者２４．７％ ;死亡８例, 其     

根除幽门螺杆菌治疗十二指肠溃疡的随机对照研究

通过根除幽门螺杆菌（Ｈｐ）治疗（不加用任何抗酸或抑酸药物）观察十二指肠溃疡（ＤＵ）的愈合率。方法：１１５例Ｈｐ感染的ＤＵ患者随机分为两组,接受７天铋剂三联治疗。Ａ组口服替硝唑５００ｍｇ、克拉霉素２５０ｍｇ和胶体次构橼酸铋２２０ｍｇ各每日２次,疗程７天,Ｂ组在Ａ组基础上加服奥美拉唑每日２０ｍｇ,疗程４周。服药前和停止抗ＨＰ治疗后４周作胃镜检查及~ （１３）Ｃ－尿素呼气试验。结果：１０７例患者完成治疗和复查,８例失访。Ａ、Ｂ两组的ＤＵ愈合率分别为９２．５％（９５％可信区间为８５．４％～９９．６％）和９６．３％（９５％可信区间为９１．３％～１００％）;两组Ｈｐ根除率分别为９４．３％（９５％可信区间为８８．１％～１００％）和９８．１％（９５％可信区间为９４．５％～１００％）,统计学上均无显著差异（＞０．０５）。服药１周内上腹痛缓解率Ｂ组明显高于Ａ组（Ｐ＜０．００５）。两组方案均未发现有明显不良反应。结论：Ｈｐ感染的ＤＵ患者经根除ＨＰ治疗,溃疡能自行愈合而不需使用抑酸药物;奥美拉唑能迅速减轻或消除ＤＵ患者的上腹痛症状;本治疗方案具有Ｈｐ根除率高、疗程短、依从性好和不良反应少等优点。     

结直肠癌患者血液和组织中鸟氨酸脱羧酶活性和腐胺含量的测定

本文用改良分光光度法测定３１例经结肠镜及活检病理确诊的结直肠癌患者血液和组织中鸟氨酸脱羧酶（ＯＤＣ）活性和腐胺（ＰＵＴ）含量，并与２５例轻度结肠炎患者对照。结果显示结直肠癌患者血液和组织中ＯＤＣ活性，以及血液中ＰＵＴ含量均极显著地高于对照组，分别为４．２３±０．４０对２．４０±０．３０，Ｐ＜０．００１；１１．７５±１．３２对７．３６±０．９０μｇ／ｍｇ蛋白质，Ｐ＜０．００１；和８４．９７±６．１０对６１．３６±６．０１μｇ％，Ｐ＜０．０１。组织中ＰＵＴ含量两组间差异无显著性。这些结果表明结直肠癌患者ＯＤＣ活性增强，多胺合成增多。测定这些指标可能有助于结直肠癌的诊断。     

PPAR-γ在溃疡性结肠炎粘膜中的表达

目的了解过氧化物酶增生激活受体（ＰＰＡＲ－γ）在溃疡性结肠炎（ＵＣ）患者结肠活检粘膜中的表达及其与疾病严重度的关系。方法　采用免疫组化法测定３１例ＵＣ患者和１２例对照组的结肠活检粘膜中ＰＰＡＲ－γ的表达情况。结果　ＵＣ患者受累及相对正常的结肠上皮ＰＰＡＲ－γ的表达均较正常对照组下降，三组分别为２４．７％±１．４９％、４３．８％±２．０３％、７０．２％±３．７５％（Ｐ＜０．０５），且病变越重，表达越低。结论ＵＣ患者内镜下活检粘膜中ＰＰＡＲ－γ的表达下降，并与疾病严重程度成负相关，提示其可能与ＵＣ的发病有关。     

溃疡性结肠炎486例结肠镜检查的评价和分析

过去２０年中经结肠镜检查，结合活检和临床表现符合溃疡性结肠炎（下称ＵＣ）诊断的共４８６例，占结肠镜检查总数的３．５１％。其中男３０４例、女１８２例，平均年龄为４２．４岁。病程少于１０年者４３２例，占８８．９％。临床表现为粘液脓血便和腹泻。结肠镜以粘膜充血、水肿伴糜烂及浅表溃疡最为多见，占８０．８％。分布范围中，直、乙结肠类型占５５．３％。临床类型以慢性活动期型为多见，占８２．３％。癌变４例，占０．８２％。总结认为，结肠镜对ＵＣ确诊率为９６．４％。本组发病有年龄偏大，病程短，左侧结肠炎多，程度轻，癌变率低等特点。     

门冬氨酸钾镁在急性心肌梗塞溶栓治疗中的作用

我院心内科对３２例ＡＭＩ病人应用门冬氨酸钾镁治疗,并与常规极化液治疗３８例进行对照,旨在探讨门冬氨酸钾镁在ＡＭＩ溶栓治疗中的作用及其原理。资料与方法１．临床资料：选择冠心病监护病房（ＣＣＵ）确诊为ＡＭＩ的患者７０例,随机分为治疗组３２例和对照组３８例。治疗组：男２０例,女１２例,年龄４５～７６岁（平均５６．４±７．３岁）,梗塞部位：前壁１５例,下壁１２例,其他部位５例,入院平均时间５．８小时。对照组：男２５例,女１３例,年龄４０～７５岁（平均５５．６±７．２岁）,其中前壁１８例,下壁１４例,其他…     

Propionyl-L-carnitine hydrochloride for treatment of mild to moderate colonic inflammatory bowel diseases

AIM:To assess clinical and endoscopic response to propionyl-L-carnitine hydrochloride(PLC) in colonic inflammatory bowel disease.METHODS:Patients suffering from mild to moderate ulcerative colitis(UC) or Crohn's disease(CD) colitis,with disease activity index(DAI) between 3 and 10 and under stable therapy with oral aminosalicylates,mercaptopurine or azathioprine,for at least 8 wk prior to baseline assessments,were considered suitable for enrollment.Fourteen patients were enrolled to assume PLC 2 g/d(two active tablets twice daily) orally.Clinical-endoscopic and histological activity were assessed by DAI and histological index(HI),respectively,following a colonoscopy performed immediately before and after 4 wk treatment.Clinical response was defined as a lowering of at least 3 points in DAI and clinical remission as a DAI score ≤ 2.Histological response was defined as an improvement of HI of at least 1 point.We used median values for the analysis.Differences pre-and post-treatment were analyzed by Wilcoxon signed rank test.RESULTS:All patients enrolled completed the study.One patient,despite medical advice,took deflazacort 5 d before follow-up colonoscopy examination.No side effects were reported by patients during the trial.After treatment,71%(SE 12%) of patients achieved clinical response,while 64%(SE 13%) obtained remission.Separating UC from CD patients,we observed a clinical response in 60%(SE 16%) and 100%,respectively.Furthermore 60%(SE 16%) of UC patients and 75%(SE 25%) of CD patients were in clinical remission after therapy.The median DAI was 7 [interquartile range(IQR):4-8] before treatment and decreased to 2(IQR:1-3)(P 0.01) after treatment.Only patients with UC showed a significant reduction of DAI,from a median 6.5(IQR:4-9) before treatment to 2(IQR:1-3) after treatment(P 0.01).Conversely,in CD patients,although displaying a clear reduction of DAI from 7(IQR:5.5-7.5) before therapy to 1.5(IQR:0.5-2.5) after therapy,differences observed were not significant(P = 0.06).Seventy-nine percent(SE 11%) of patients showed improvement of HI of at least 1 point,while only one CD and two UC patients showed HI stability;none showed HI worsening.Median HI decreased from 1(IQR:1-2),to 0.5(IQR:0-1) at the endoscopic control in the whole population(P 0.01),while it changed from 1(IQR:1-2) to 0.5(IQR:0-1) in UC patients(P 0.01) and from 1.5(IQR:1-2) to 0.5(IQR:0-1) in CD patients(P = not significant).The two sample tests of proportions showed no significant differences in clinical and histological response or in clinical remission between UC and CD patients.No side effects were reported during treatment or at 4 wk follow-up visit.CONCLUSION:PLC improves endoscopic and histological activity of mild to moderate UC.Further studies are required to evaluate PLC efficacy in colonic CD patients.     

5-脂氧合酶在溃疡性结肠炎黏膜中的表达

目的 检测溃疡性结肠炎（UC）患者结肠黏膜5-脂氧合酶（5-LOX）蛋白及5-LOXmRNA的表达及其与UC内镜分级、组织学分级的关系.方法 取32例UC患者结肠黏膜标本根据内镜及组织学进行分级,同时收集正常对照者结肠黏膜标本26例.采用实时荧光定量反转录聚合酶链反应和免疫组化法检测UC患者结肠黏膜5-LOX mRNA及蛋白的表达.结果 32例UC患者内镜分级Ⅰ级10例,Ⅱ级19例,Ⅲ级3例 组织学分级1级19例,2级9例,3级4例.UC患者结肠黏膜5-LOX mRNA和蛋白表达显著高于正常对照组（P＜0.05）,5-LOX蛋白的阳性表达率随内镜分级、组织学分级增加而增加 5-LOX蛋白表达与内镜分级之间存在相关（P＜0.05）,但与组织学分级之间不相关（P＞0.05）.结论 UC患者结肠黏膜中5-LOX mRNA和蛋白的表达增加,5-LOX蛋白的阳性表达率在一定程度上可以反映疾病的活动度,可作为UC治疗的靶位,在UC治疗中具有重要意义.     

Butyrate inhibits NF-kappaB activation in lamina propria macrophages of patients with ulcerative colitis

BACKGROUND: In ulcerative colitis (UC) the activation (i.e. nuclear translocation) of nuclear factor kappa B (NF-kappaB) is an important step in the regulation of cytokines secreted by lamina propria macrophages. Clinical trials suggest anti-inflammatory effects of locally administered butyrate in UC. The potential effects of butyrate on NF-kappaB activation in lamina propria macrophages of UC patients were investigated. METHODS: Eleven patients with distal UC were treated for up to 8 weeks with butyrate at 100 mM (n = 6) or placebo (n = 5) enemas. At entry and after 4 and 8 weeks, clinical status was noted and intestinal inflammation was graded endoscopically and histologically. Double-staining with antibodies against NF-kappaB (p65) and CD68 was employed to detect NF-kappaB and macrophages, respectively. RESULTS: In untreated patients, nuclear translocation of NF-kappaB was detectable in virtually all macrophages. Butyrate treatment for 4 and 8 weeks resulted in a significant reduction in the number of macrophages being positive for nuclear translocated NF-kappaB. In addition, butyrate significantly reduced both the number of neutrophils in crypt and surface epithelia and of the lamina propria lymphocytes/plasma cells. These findings correlated with a significant decrease in the Disease Activity Index (DAI). CONCLUSIONS: The decrease in DAI and mucosal inflammation in butyrate-treated patients is associated with a reduction of NF-kappaB translocation in lamina propria macrophages. Since the inflammatory process in UC is mainly sustained by macrophage-derived cytokines, the known anti-inflammatory effects of butyrate may in part be mediated by an inhibition of NF-kappaB activation in these macrophages.     

Cyclosporine Enemas for Treatment-Resistant, Mildly to Moderately Active, Left-Sided Ulcerative Colitis

Ten patients with treatment-resistant left-sided ulcerative colitis were treated in an open protocol with 350 mg cyclosporine enemas nightly for 4 wk. A 12-point clinical disease activity index (DAI) score was calculated at baseline and after 4 wk. Whole blood and colonic tissue cyclosporine concentrations were determined by HPLC at the end of the study. Five of 10 patients responded to treatment, defined as a decrease in the clinical DAI score ≥3 points. Responders retained the enemas longer than nonresponders (7.5 ± 1.3 vs. 3.3 ± 2.2 h, p = 0.01), and there was a positive correlation between decrease in the clinical DAI score and enema retention time ( r = 0.64, p = 0.05). The mean colonic tissue cyclosporine concentration was not significantly higher in responders than in nonresponders (2884 ± 1635 vs. 2359 ± 576 ng/g, p = 0.52), and the correlation between decrease in the clinical DAI score index and colonic tissue cyclosporine was weak ( r = 0.39, p = 0.26). Cyclosporine was undetectable in whole blood samples from all patients, and there were no apparent side effects with treatment. In conclusion, 50% of patients with treatment-resistant left-sided ulcerative colitis significantly improved during therapy with cyclosporine enemas for 4 wk. Patients with longer enema retention times were more likely to respond. A controlled trial is underway to investigate these findings further.     

Treatment of left-sided ulcerative colitis with 4-aminosalicylic acid enemas. A double-blind, placebo-controlled trial

Twenty-five patients with active left-sided ulcerative colitis were randomly assigned to receive either 2 g of 4-aminosalicylic acid (para-aminosalicylic acid) or placebo in a 60-mL volume as a nightly retention enema. The duration of treatment was 8 weeks. Disease activity was assessed by grading clinical symptoms of blood, mucus, urgency, sigmoidoscopic findings, and degree of histologic inflammation in rectal biopsies. At 8 weeks, 10 of 12 patients (83%; 95% confidence interval [CI], 55% to 97%) who received 4-aminosalicylic acid showed improvement in clinical, sigmoidoscopic, and histologic variables. In contrast, only 2 of 13 patients (15%, 95% CI, 4% to 38%) who had received placebo showed clinical improvement (P less than 0.005). The 11 patients in the placebo group who showed no improvement were treated subsequently with open-label 4-aminosalicylic acid enemas. Of the 11, 9 showed clinical, sigmoidoscopic, and histologic improvement. No adverse effects were seen. 4-Aminosalicylic acid enemas are a safe and effective means of treating left-sided ulcerative colitis.     

Butyrate Inhibits NF-κB Activation in Lamina Propria Macrophages of Patients with Ulcerative Colitis

Background: In ulcerative colitis (UC) the activation (i.e. nuclear translocation) of nuclear factor kappa B (NF- &#115 B) is an important step in the regulation of cytokines secreted by lamina propria macrophages. Clinical trials suggest anti-inflammatory effects of locally administered butyrate in UC. The potential effects of butyrate on NF- &#115 B activation in lamina propria macrophages of UC patients were investigated. Methods: Eleven patients with distal UC were treated for up to 8 weeks with butyrate at 100 mM ( n = 6) or placebo ( n = 5) enemas. At entry and after 4 and 8 weeks, clinical status was noted and intestinal inflammation was graded endoscopically and histologically. Double-staining with antibodies against NF &#115 B (p65) and CD68 was employed to detect NF- &#115 B and macrophages, respectively. Results: In untreated patients, nuclear translocation of NF- &#115 B was detectable in virtually all macrophages. Butyrate treatment for 4 and 8 weeks resulted in a significant reduction in the number of macrophages being positive for nuclear translocated NF- &#115 B. In addition, butyrate significantly reduced both the number of neutrophils in crypt and surface epithelia and of the lamina propria lymphocytes/plasma cells. These findings correlated with a significant decrease in the Disease Activity Index (DAI). Conclusions: The decrease in DAI and mucosal inflammation in butyrate-treated patients is associated with a reduction of NF- &#115 B translocation in lamina propria macrophages. Since the inflammatory process in UC is mainly sustained by macrophage-derived cytokines, the known anti-inflammatory effects of butyrate may in part be mediated by an inhibition of NF- &#115 B activation in these macrophages.     

Oxazolone‐induced murine model of ulcerative colitis

OBJECTIVE: Animal models are useful for studying disease, but there is a shortage of suitable models of ulcerative colitis. The aim of the present study was to set up an oxazolone‐induced murine colitis model and use it to research the pathogenesis of inflammatory bowel disease. METHODS: BALB/c mice were presensitized by painting the skin with 0.2 mL 3% oxazolone in 100% ethanol on days 0 and 1 followed by intrarectal administration of 0.15 mL 1% oxazolone in 50% ethanol on day 7. The disease activity index (DAI), histological changes of the colon, myeloperoxidase (MPO) activity and production of cytokines (TNF‐α, IL‐4, IFN‐γ) by the mucosa were evaluated. RESULTS: There were obvious changes in the DAI, histology and MPO activity, and the production of interleukin‐4 was markedly increased compared with the concentrations of TNF‐α and IFN‐γ, which remained normal, in the lesions. CONCLUSION: Oxazolone colitis is Th2‐mediated and has similar histologic features and distribution of inflammation to ulcerative colitis (UC), which has important implications for the use of this model in the study of the pathogenesis and treatment of UC.     

Vanilloid receptor-1 containing primary sensory neurones mediate dextran sulphate sodium induced colitis in rats

BACKGROUND AND AIMS: The role of sensory neurones in colitis was studied by chemical denervation of primary sensory neurones as well as antagonism of the vanilloid receptor-1 (VR-1) in rats prior to administration of dextran sulphate sodium (DSS) to induce colitis. METHODS: Neonatal rats were chemically denervated by subcutaneous administration of capsaicin; controls received capsaicin vehicle only. When animals reached maturity, colitis was induced by administration of 5% DSS in drinking water for seven days. Additionally, normal adult rats were treated with a VR-1 antagonist capsazepine (CPZ) or vehicle twice daily via an enema from day 0 to day 6 of the DSS regimen. Control rats were treated with an enema infusion of vehicle and 5% DSS, or without either an enema infusion or DSS in drinking water. For both groups of rats, severity of inflammation was quantitated by disease activity index (DAI), myeloperoxidase (MPO) activity, and histological examination. RESULTS: DSS induced active colitis in all control rats with resultant epithelial ulceration, crypt shortening, and neutrophil infiltration. Both neonatal capsaicinised rats and normal adult rats treated with CPZ enemas exhibited significantly lower levels of DAI, MPO, and histological damage compared with vehicle treated rats (p< 0.05). CONCLUSIONS: Neonatal capsaicinisation and local administration of CPZ prevents intestinal inflammation in a well established model of colitis indicating that primary sensory neurones possessing VR-1 receptors are required in the propagation of colonic inflammation.     

A randomized trial of nicotine enemas for active ulcerative colitis.

BACKGROUND & AIMS: Ulcerative colitis (UC) is largely a disease of nonsmokers in which transdermal nicotine improves the symptoms but often causes adverse events (AEs). Nicotine enemas cause fewer AEs and were used as supplemental treatment for active UC. METHODS: We treated 104 patients with active UC with either 6-mg nicotine enemas or placebo enemas for 6 weeks in a randomized double-blind study. Patients continued their oral therapy, if any, for UC: 68 patients were taking mesalamine, 15 patients were taking prednisolone, and 12 patients were taking thiopurines during the study. Clinical, sigmoidoscopic, and histologic assessments were made at baseline and at the end of the study and symptoms were recorded daily on a diary card. The primary end point was induction of clinical remission and clinical improvement also was measured by the UC disease activity index. After the study, patients then used nicotine enemas daily for 4 weeks and sigmoidoscopy with a biopsy examination was repeated. AEs and salivary cotinine levels were monitored throughout the study. RESULTS: Clinical remission was achieved in 14 of 52 (27%) patients on active treatment and 14 of 43 (33%) patients on placebo (P = .55). The UC disease activity index improved by 1.45 points in the active group and by 1.65 points for those on placebo (P = .88). Only 1 patient discontinued treatment because of an AE (abdominal pain). In the 47 patients taking mesalamine only, active treatment conferred benefit that was not statistically significant; disease remission occurred in 9 of 25 patients on active therapy and 4 of 21 patients on placebo (P = .20). CONCLUSIONS: Six-milligram nicotine enemas were well tolerated but were not found to be efficacious for active UC.