美沙拉嗪联合益生菌制剂（枯草杆菌二联活菌肠溶胶囊）在溃疡性结肠炎治疗中的应用

目的：研究溃疡性结肠炎实施治疗的过程中应用美沙拉嗪联合益生菌制剂治疗的临床效果。方法我院选择2012年2月~2014年2月诊治的42例溃疡性结肠炎患者,将其随机分为两组,对照组的21例患者单纯应用美沙拉嗪实施治疗,观察组的21例患者在应用美沙拉嗪治疗的基础上联合枯草杆菌二联活菌肠溶胶囊进行治疗,比较两组患者治疗的总有效率、复发率以及治疗前后症状的改善情况。结果通过对两组患者进行比较,观察组患者治疗的有效率明显比对照组高(<0.05),观察组患者复发率明显比对照组低(<0.05),两组患者治疗前症状积分未见明显差异,无统计学意义,经过治疗后两组患者症状基本均有所降低,但是观察组更优,两组患者差异显著,有统计学意义(<0.05)。结论对于溃疡性结肠炎患者运用美沙拉嗪联合枯草杆菌二联活菌肠溶胶囊治疗的临床效果显著,能够有效的改善患者的临床症状,降低复发率,值得在临床上推广使用。     

美沙拉嗪联合灌洗剂治疗溃疡性结肠炎的疗效观察

目的：观察美沙拉嗪联合灌洗剂对溃疡性结肠炎患者的疗效。方法2012年1月至2014年1月收治于中国核工业北京四〇一医院内分泌消化科的90例溃疡性结肠炎患者,信封法随机分为治疗组（n =46）和对照组（n =44）。治疗组美沙拉嗪片口服＋美沙拉嗪灌肠液治疗,对照组柳氮磺胺嘧啶片口服＋柳氮磺吡啶栓治疗,口服药治疗8周,灌肠、纳肛（均为睡前排便后）治疗1周。评价治疗前后患者炎症性肠病问卷（IBDQ）量表得分、肠镜下 UC 活动度分级（改良 Baron 活动分级）、临床疗效。结果两组患者治疗8周后 IBDQ 量表中症状积分与治疗前比较,差异均有统计学意义（P 均〈0.05）;两组患者治疗后8周内镜下黏膜改变与治疗前比较,差异均有统计学意义（ P 均〈0.05）;治疗后8周,治疗组患者症状积分、镜下黏膜改变与对照组比较,差异均有统计学意义（P =0.048、0.036,P 均〈0.05）。经过8周的治疗,治疗组患者临床疗效总有效率（91.3%）与对照组（90.9%）比较,差异有统计学意义（P〈0.05）。结论美沙拉嗪联合灌洗剂治疗溃疡性结肠炎疗效显著且安全。     

美沙拉嗪灌肠联合口服对溃疡性结肠炎患者丙二醛、超氧化物歧化酶水平及炎症因子的影响

目的:探讨美沙拉嗪灌肠联合口服对溃疡性结肠炎(Ulcerative Colitis,UC)患者血清丙二醛(Malondialdehyde,MDA)、超氧化物歧化酶(Superoxide dismutase,SOD)水平及炎症因子的影响.方法:选取2017年6月至2020年6月我科收治的100例UC患者作为研究对象,随机...     

利多卡因联合康复新灌肠辅助美沙拉嗪治疗溃疡性结肠炎的疗效观察

目的:观察利多卡因联合康复新液灌肠辅助美沙拉嗪治疗溃疡性结肠炎(UC)的临床疗效。方法:选择98例中度UC(直乙结肠型)患者,随机分为治疗组(50例)和对照组(48例)。对照组给予美沙拉嗪缓释片(1.0g,4次/日)口服及对症和支持治疗,治疗组在对照组基础上辅以利多卡因(10ml)+康复新(50ml)溶液保留灌肠,每晚1次,疗程均为30天。治疗30天后比较两组临床疗效。结果:对照组痊愈3例,显效32例,无效13例,总有效率72.90%;治疗组痊愈1例,显效47例,无效2例,总有效率96.00%,明显优于对照组(P<0.01)。结论:联合利多卡因、康复新灌肠辅助美沙拉嗪治疗溃疡性结肠炎具有更好的临床疗效。     

美沙拉嗪对高龄溃疡性结肠炎患者C反应蛋白及TNF-α的影响

目的 探讨美沙拉嗪对高龄溃疡性结肠炎患者的C反应蛋白、TNF-α的影响及其疗效.方法 选取于成都医学院第一附属医院就诊的高龄溃疡性结肠炎患者150例,并随机分成两组;对照组和观察组,各75例.对照组:接受高龄溃疡性结肠炎的常规治疗.观察组:在接受高龄溃疡性结肠炎的常规治疗的基础上加上美沙拉嗪辅助治疗.结果 治疗后,观察组患者总有效率(90.67％)明显高于对照组总有效率(77.33％),差异具有统计学意义(P＜0.05).观察组患者的血清炎症因子hs-CRP、IL-8以及TNF-α水平明显低于对照组患者,差异具有统计学意义(P＜0.01).观察组患者的MDA水平明显低于对照组患者、而观察组SOD水平则明显高于对照组患者,差异具有统计学意义(P＜0.01).观察组患者的Mayo评分、内镜分级评分明显低于对照组患者,差异具有统计学意义(P＜0.01).结论 美沙拉嗪治疗高龄溃疡性结肠炎疗效佳,因其具有显著的抗氧化的作用,同时能够有效清除自由基、抑制炎性介质的释放.     

美沙拉嗪对DSS诱导小鼠溃疡性结肠炎模型Th1、Th17及Treg细胞亚群的影响

 目的:观察葡聚糖硫酸钠（DSS）诱导小鼠溃疡性结肠炎（UC）模型中辅助性T细胞（Th1、Th17亚群）及调节性T细胞（Treg）细胞亚群的变化,探讨美沙拉嗪（MSLZ）治疗UC的免疫学机制。方法: 采用流式细胞分析术检测DSS诱导的小鼠UC模型结肠组织及外周血单个核细胞中白细胞介素17（IL-17）、γ-干扰素（IFN-γ）及核转录因子Foxp3的表达,并检测MSLZ预治疗对小鼠UC 模型Th1、Th17和Treg亚群的影响。结果: 在DSS诱导的小鼠UC模型中,其外周血单个核细胞（PBMC）中CD3+T细胞高表达IL-17、IFN-γ及Foxp3,肠黏膜单个核细胞（LPMC）中CD3+T细胞高表达IFN-γ和Foxp3,但IL-17的表达与对照组无差异。进一步发现UC模型小鼠LPMC中Th17、Th1和Treg均显著高于对照组,但PBMC中只有Treg高于对照组。MSLZ预治疗能显著下调UC 模型小鼠PBMC和LPMC中Th17、Th1和Treg细胞亚群。结论: DSS诱导的小鼠 UC模型中CD4+T细胞亚群Th1、Th17及Treg细胞显著升高,提示CD4+T细胞亚群在UC发病中起重要作用,美沙拉嗪可能通过调节Th1、Th17及Treg细胞亚群发挥抗炎及治疗UC作用。     

穴位埋线疗法联合口服美沙拉嗪治疗溃疡性结肠炎的 护理分析

目的 分析探讨护理干预对穴位埋线疗法联合口服美沙拉嗪治疗溃疡性结肠炎患者的作用。 方法 选取我院2010年8月～2013年3月诊治的位于UC缓解期1周的患者62例,随机分为美沙拉嗪组32例与美沙拉嗪联合穴位埋线治疗组(30例)联合治疗组(30例)采用穴位埋线疗法并予美沙拉嗪口服,同时给予实施综合护理干预。观察美沙拉嗪组及联合治疗组12个月后的缓解时长、复发率以及不良反应情况。结果 美沙拉嗪组、联合治疗组复发率分别为13（40.6％）、5（16.7％）,两组相比较P<0．05;联合治疗组的缓解时间(260±67) d比美沙拉嗪组的缓解时间(219±77) d相对较长,差异有统计学意义（P<0．05）。结论 护理干预对穴位埋线疗法同时使用美沙拉嗪来治疗溃疡性结肠炎有积极意义,有利于减少病情复发,提高患者的生活质量。     

疏肝健脾法联合美沙拉嗪栓治疗对溃疡性直肠炎患者治疗效果的影响

目的:分析疏肝健脾法联合美沙拉嗪栓治疗对溃疡性直肠炎患者临床疗效.方法:收集2018年8月至2019年12月本院收治的溃疡性直肠炎患者99例,根据患者治疗方式不同分为对照组(美沙拉嗪栓)48例,观察组(疏肝健脾法联合美沙拉嗪栓)51例.对比两组患者治疗后临床疗效、炎性因子水平、不良反应以及复发率.结果:观察组临床总有效...     

美沙拉嗪通过抑制经典炎性信号通路激活治疗噁唑酮诱导的小鼠结肠炎中炎症反应

目的：探究美沙拉嗪在噁唑酮诱导的小鼠溃疡性结肠炎模型中的治疗作用与机制。方法：60只小鼠随机分为对照组、模型组、低剂量给药组和高剂量给药组,所有小鼠按照相同方式先后进行2次致敏。致敏5 d后麻醉小鼠,对照组小鼠按0.15 ml/g体重灌肠50%乙醇水溶液,灌注后倒置小鼠30 s,其余各组小鼠按相等剂量灌肠1%噁唑酮乙醇（50%）溶液。给药组按体重不同分别给予不同剂量的美沙拉嗪灌胃,对照组和模型组给予相同体积的溶剂灌胃。结果：噁唑酮造模后小鼠体重明显下降,给药组较模型组体重有所恢复;模型组小鼠肠道结构损伤严重,给药后炎症和损伤程度有所缓解;模型组小鼠血清中Th2型细胞因子含量显著增多（P<0.05）,美沙拉嗪能够缓解炎症因子的大量释放,同时模型小鼠结肠组织NF-κB信号通路关键蛋白p-p65、p-IκB蛋白的表达显著增加,同时p65、IκB蛋白的降低,给药后蛋白水平恢复。结论：美沙拉嗪能够有效地恢复噁唑酮引起的小鼠体重下降和结肠组织炎性细胞浸润,同时能够保护噁唑酮引起的结肠组织损伤,美沙拉嗪同时对于噁唑酮诱导的Th2型细胞因子释放具有显著的抑制作用,可以通过抑制NF-κB通路的激活,从而经经典炎症通路发挥抗炎作用。     

美沙拉秦、蒙脱石散和酪酸梭菌对溃疡性结肠炎大鼠血细胞因子的影响

目的:研究美沙拉秦、蒙脱石散、酪酸梭菌对2,4,6三硝基苯磺酸(TNBS)/乙醇法诱导的溃疡性结肠炎大鼠IL-17、IL-23、TGF-β1、IFN-γ的影响。方法:将85只大鼠随机分为模型组、美沙拉秦组、蒙脱石散组、酪酸梭菌组、美沙拉秦联合蒙脱石散组5组,每组15只;正常大鼠为空白对照组10只,一共6组。通过TNBS/乙醇法建立溃疡性结肠炎的大鼠模型。按大鼠体表面积折算药量,分别给予相应剂量生理盐水、美沙拉秦、蒙脱石散、酪酸梭菌、美沙拉秦联合蒙脱石散治疗。12 d后处死全部大鼠,收集大鼠的血标本及结肠标本。采用ELISA法测定血清中IL-17、IL-23、TGF-β1、IFN-γ的含量,分别对比6组细胞因子的水平。结果:(1)通过TNBS/乙醇法建立大鼠模型,HE染色病理切片发现大鼠结肠远端炎症明显。(2)模型组、美沙拉秦组、蒙脱石散组、酪酸梭菌组、美沙拉秦联合蒙脱石散组较空白对照组的血清IL-17、IL-23和IFN-γ含量均升高,血清TGF-β1含量均降低,差异有统计学意义(P0.05)。(3)与模型组比较,蒙脱石散组、酪酸梭菌组、美沙拉秦组的血清IL-17、IL-23和IFN-γ含量均降低,血清TGF-β1含量均升高,差异有统计学意义(P0.05)。(4)美沙拉秦、蒙脱石散、酪酸梭菌和美沙拉秦联合蒙脱石散的治疗效果比较,美沙拉秦和美沙拉秦联合蒙脱石散疗效较好,差异有统计学意义(P0.05),酪酸梭菌与蒙脱石散疗效差异不明显。结论:(1)从症状体征及病理学检查表明:TNBS/乙醇法成功建立了大鼠溃疡性结肠炎模型。(2)在TNBS/乙醇法诱导的实验性溃疡性结肠炎大鼠血清中IL-17、IL-23、IFN-γ表达增高,与炎症呈正相关;结肠炎大鼠血清中TGF-β1表达降低,与炎症呈负相关。(3)美沙拉秦、蒙脱石散、酪酸梭菌、美沙拉秦联合蒙脱石散可能通过下调模型大鼠促炎因子IL-17、IL-23和调节因子IFN-γ的分泌,上调抗炎因子TGF-β1的分泌,缓解大鼠炎症症状,利于大鼠溃疡性结肠炎的修复。     

258例溃疡性结肠炎临床特征分析

目的探讨溃疡性结肠炎（uc）的临床特征,为UC的诊治提供依据。方法回顾性分析258例UC患者的临床症状、内镜下表现及病变分布、临床分期、实验室检查及治疗和预后等情况。结果UC的临床表现以腹泻伴黏液或脓血便为主;肠镜下表现主要为粘膜血管纹理模糊、紊乱、充血、水肿、易脆、伴脓性分泌物附着;病变分布以全结肠和直肠和乙状结肠及左半结肠为主;UC的治疗以综合性内科保守治疗为主。结论UC临床特征明确,诊治不困难,治疗上以保守治疗为主。     

Architectural morphometry in ulcerative colitis with dysplasia

Semi-automatic image analysis was used to assess the architectural features of normal colorectal mucosa and ulcerative colitis with and without dysplasia. Eight measured and derived morphometric variables were compared with the histological grading. The main data-set variation was due to: (1) the area of mucosa and epithelium per unit length of muscularis mucosae; (2) mean mucosal and epithelial height; and (3) the percentage epithelium and number of crypts per unit length of muscularis mucosae. Discriminant analysis using the variables mean epithelial height and mean lamina propria area per unit length of muscularis mucosae separated normals (n = 10) from high-grade dysplasia (8). The classification rule allocated low-grade dysplasia (8) to the high-grade category and 60% of regeneration cases (10) to the normal mucosa group. Scatter plots of the two discriminating variables separated normal and regenerative mucosa from dysplasia. Histological review of overlapping cases allowed redesignation of a high-grade dysplasia lesion as low grade. Architectural morphometry may be of use in assessing premalignant mucosal changes in ulcerative colitis as a guide to patient surveillance and therapy.     

Collagenous colitis: an electron microscopic study including comparison with the chronic fibrotic stage of ulcerative colitis

Light and electron microscopic studies of 14 cases of collagenous colitis are reported. Comparative electron microscopic examinations were carried out on 13 cases of ulcerative colitis in the chronic fibrotic stage of the disease. Separation of pericryptal fibroblasts which showed enhanced fibre-forming activity, proliferation of myofibroblasts, accumulation of mast cells and a pericapillary collagen accumulation were noted in both groups. Based on these results, collagenous colitis was considered to result from scar formation secondary to previous superficial inflammation.     

Mucin profiles in ulcerative colitis with dysplasia and carcinoma

Mucin secretion was assessed in Crohn's colitis, in ulcerative colitis with regeneration, dysplasia and carcinoma and in non-colitic adenocarcinoma. The high iron diaminealcian blue (HID–AB) and periodate borohydride–saponification periodic acid Schiff (PB–KOH–PAS) techniques were used to demonstrate sulphomucins and sialomucins, and O-acylated sialomucins respectively. There was mucosal hyperplasia and increased sialomucin secretion in Crohn's disease, quiescent and active ulcerative colitis. In colitis with carcinoma inflamed mucosa away from the tumour had increased sialomucins as had colitis with dysplasia. They did not differ statistically from each other or from colitic controls without cancer. Dysplastic crypts frequently secreted sulphomucins and the increased sialomucins were in transitional-like glands in the surface fronds or adjacent to the dysplasia. A comparative study of the HID–AB technique gave total correct qualitative allocation of individual quantitatively assessed crypts. Routine HID–AB staining did not aid the recognition of dysplasia in ulcerative colitis. With the PB–KOH–PAS technique colorectal adenocarcinoma showed a significant diminution in O-acylated sialomucins compared with its adjacent mucosa. Mucosal dysplasia in ulcerative colitis displayed a similar trend in O-acylated sialic acid variants, differing with respect to age- and sex-matched colitic controls. The PB–KOH–PAS technique may be of help in assessing mucin secretion in ulcerative colitis as a guide to the evolution of malignancy.     

Morphometrical analysis in ulcerative colitis with dysplasia and carcinoma

Semi-automatic image analysis was used to assess the epithelium in ulcerative colitis with dysplasia and carcinoma. There were three main sources of variation within the dataset: (1) nuclear size, nuclear cytoplasmic ratio and nuclear stratification; (2) the variation of nuclear size; and (3) nuclear shape and polarity. Discriminant analysis chose the mean nuclear cytoplasmic ratio % and the coefficient of variation of nucleus to cell apex distance to derive a scoring system which completely separated normal mucosa (n = 20) and carcinoma (n = 30). The classification rule allocated all high grade dysplasia to the tumour category. Scores for regeneration and low grade dysplasia overlapped with each other and the normal and tumour groups. Scatter plots of the two discriminating variables showed good separation of regeneration and high grade dysplasia, and a degree of overlap with low grade dysplasia. The scatter plots allowed identification of overlapping and misallocated cases, requiring review of their histology and redesignation of the diagnosis in five cases. This study confirms quantitatively the visual criteria used in grading mucosal changes and their trend from regeneration through dysplasia to carcinoma. It underlines the necessity of assessing not only cytological but also architectural and inflammatory components when diagnosing regeneration and low grade dysplasia. Mucosal morphometry may be of use in confirming high grade dysplasia which is an indication for colectomy.     

溃疡性结肠炎的心理社会因素研究

采用病例配对方法研究了４３例溃疡性结肠炎的心理社会因素，结果显示，病例组内外倾分，神经质分显著高于对照组；病例组生活事件紧张总值，ＳＣＬ－９０的躯体化，强迫，抑郁，焦虑，恐怖，精神病性和总痛苦水平显著高于对照组，提示溃疡性结肠炎病人存在个性缺陷，心理障碍和生活事件应激过大的趋势。     

Expression of CA2 and CA9 carbonic anhydrases in ulcerative colitis and ulcerative colitis‐associated colorectal cancer

Ulcerative colitis (UC) is characterized by chronic inflammation in the colonic mucosa and submucosa with repeating relapse and remission, but the pathogenesis is unknown. Patients with long‐standing UC are at high risk of neoplasm development. The aim of the present study was to identify molecules whose expression is associated with UC and UC‐associated colorectal cancer (UCCA). Biopsy specimens from UC and normal colonic mucosae were analyzed using a proteomics approach, in which carbonic anhydrase 2 (CA2) was identified as a molecule downregulated in UC mucosae. Immunohistochemically, CA2 expression was detected in normal and diverticulitis mucosal epithelia, and its expression decreased as UC activity increased. CA2 expression was almost undetectable in UCCA. We also analyzed the expression of another carbonic anhydrase, CA9, and its upstream molecule, hypoxia‐inducible factor‐1α (HIF‐1α), both of which are induced under hypoxic conditions. It was revealed that CA9 expression was relatively low in normal, diverticulitis and UC mucosae, and was upregulated in UCCA. HIF‐1α expression was consistently low in all tissue types examined. In conclusion, these results suggest that CA2 and CA9 may be possible indicators of UC activity and UCCA development, respectively.     

Amelioration effect of bovine casein glycomacropeptide on ulcerative colitis in mice

To explore the mechanism for amelioration effect of bovine casein glycomacropeptide on oxazolone-induced ulcerative colitis in mice. BALB/c mice were divided into four groups as follows: (1) healthy control, (2) ulcerative colitis model control, (3) casein glycomacropeptide-supplemented ulcerative colitis model (CGMP group), and (4) sulfasalazine-supplemented ulcerative colitis model (SASP group). At the end of the administration period, serum IL-1β, IL-2, IL-4, IL-5, IFN-γ, TNF-α, and IL-10 were measured by cytometric bead array and enzyme-linked immunosorbent assay, and mitogen-activated protein kinase p38 and NF-κB p65 were determined by Western blotting. The results demonstrated the inactivation of NF-κB and MAPK signaling pathways and the downregulation of the serum levels of IL-1β, IL-5, IFN-γ, and TNF-α and upregulation of IL-10 production. These changes may be associated with amelioration of oxazolone-induced ulcerative colitis by bovine casein glycomacropeptide.     

Small cell neuroendocrine carcinoma of the rectum associated with chronic ulcerative colitis

A case of small cell carcinoma of the rectum in a patient with chronic ulcerative colitis is described. There was no evidence of enteroendocrine cell hyperplasia.     

Genetic markers in clinically well defined patients with ulcerative colitis (UC)

Results of genetic association studies in UC are conflicting. We propose that the power of candidate gene studies will increase when disease heterogeneity is taken into account. Phenotype frequencies of molecularly defined HLA-DR alleles, polymorphisms in the tumour necrosis factor-alpha (TNF-α), lymphotoxin-alpha (LT-α), IL-1 receptor antagonist (IL-1Ra) and IL-1β genes were determined in 98 clinically well characterized UC patients with a mean period of follow up of 10 years, and ethnically matched healthy controls (HC). The alleles HLA-DRB1*0103 (phenotype frequency 6% versus 0.2%; P = 0.0002; odds ratio (OR) 27.6) and DRB1*15 (41% versus 26%; P = 0.001; OR = 2.0, compared with HC) were associated with overall disease susceptibility. Subgroup analysis revealed that DRB1*15 was only increased in females (53% versus 24%; P < 0.0001; OR = 3.5), but not in males. With regard to disease localization, all DRB1*0103⁺ patients had extensive disease (P < 0.002; OR = 33.5), and DRB1*15 was found in 59% of females with extensive colitis (P < 0.0001; OR = 4.4). DRB1*0103 was significantly increased in patients undergoing colectomy (P < 0.0002; OR = 84). No association between overall disease susceptibility and the cytokine gene polymorphisms were found. Subgroup analysis revealed several significant associations, but most did not retain significance when corrected for multiple comparisons. However, a noticeable finding was that haplotype TNF-C was significantly associated with progression in extent of disease (P = 0.003, OR = 20.4). This study provides additional evidence for the role of DRB1 alleles in the susceptibility to UC, and supports the hypothesis that these alleles may determine the severity of the disease. The cytokine gene polymorphisms evaluated in this study do not seem to be strong risk factors for the overall disease susceptibility in UC, but may be involved in determining the severity of the disease.