缺血性肠病的诊断与治疗

缺血性肠病也称肠系膜血管病,是由于各种原因引起的肠道的急性或慢性血流灌注不良所致的肠壁缺血性疾病。按解剖分类,肠管的血液供应主要源于3支动脉:①腹腔动脉供应胃和十二指肠,侧支循环丰富,缺血性肠病罕见。②肠系膜上动脉供应小肠,右半结肠,横结肠至脾曲,因其分支的各动脉均为末梢动脉,一旦受阻易形成肠壁局部坏死。③肠系膜下动脉供应左半结肠及大部分直肠。静脉多与同名动脉伴行。缺血性肠病包括急性肠系膜缺血、慢性肠系膜缺血及结肠缺血。此病属少见病,但随着心血管病及糖尿病的日益增多,饮食结构的改变,以及诊疗技术的不断发展,发…     

肠脂肪酸结合蛋白在缺血性肠病中的研究进展

近年来随着社会人口的日益老龄化,动脉硬化所致的疾病发病率增加,缺血性肠病的患病率也有所增加.由于临床症状不典型,缺血性肠病的误诊率、漏诊率较高,关于缺血性肠病的早期诊断手段尚在研究中.肠脂肪酸结合蛋白富含于小肠粘膜组织中,具有以下特点：（1）存在于胞浆中的可溶性蛋白;（2）具有高组织特异性;（3）组织含量丰富;（4）分子质量低,易于检测.目前肠脂肪酸结合蛋白广泛用于缺血性肠病诊断的研究.本文综述了肠脂肪酸结合蛋白的定义以及作用机制,并且从动物实验和临床实验两方面总结了肠脂肪酸结合蛋白在缺血性肠病诊断中的研究进展.     

缺血性肠病新型生物标志物的研究进展

缺血性肠病（IBD）在临床上较为少见,由于其临床表现多样且缺乏特异性检查,故易误诊或漏诊而延误治疗,导致肠坏死及多器官功能障碍。IBD的病死率较高,及早确诊和治疗对于改善患者的预后至关重要。血清生物标志物的检测成本较低且为无创性检查,但目前临床上常用的血清生物标志物的特异度和敏感度均较低,亟需探索高效的新型生物标志物。该文就IBD新型生物标志物的研究进展作一综述,以期为IBD的临床诊治提供参考。     

缺血性肠病的回顾性分析

缺血性肠病是指由于肠系膜动脉或静脉阻塞导致的一种少见急腹症 ,多发生于老年人 ,早期诊断困难 ,病情发展迅速 ,病死率较高。随着人口的老龄化 ,该病的发病率有增高趋势 ,为减少误诊误治 ,现将 1985年～ 2 0 0 1年间在我院确诊的缺血性肠病患者 32例进行回顾性分析。一、临床资料1.一般资料 :本组 32例中 ,男 2 2例 ,女 10例 ,年龄 38～ 82岁 ,平均 6 5 .6岁。肠系膜上动脉缺血 2 2例 (6 8.8% ) :其中栓塞 13例 ,血栓形成 9例 ;合并有高血压、冠心病 15例 ,心瓣膜病 6例 ,同时伴心房纤颤 8例、脑梗死 3例。肠系膜静脉血栓形成 9例 (2 8.1% …     

老年缺血性肠病4例误诊分析

我院急诊科 1998年 9月至 1999年 9月收治老年人急性肠系膜血管闭塞症 4例 ,均因无法早期诊断 ,痛失抢救时机而死亡 ,报道如下。1　临床资料1.1　一般资料　死亡 4例中男女各 2例 ,平均年龄 69岁 (64～ 78岁 ) ,分别误诊为急性胃炎 1例 ,急性阑尾炎 1例 ,麻痹性肠梗阻 1例 ,腹膜炎休克 1例。最后确诊方法为剖腹探查 1例 ,广泛小肠切除 1例 ,肠系膜上动脉多普勒检查 1例 ,血便并腹穿血性液 1例。1.2　典型病例例 1,男 ,64岁 ,主因腹痛 2ｈ伴呕吐 1次来诊 ,既往高血压史 2 5年 ,5年前患脑梗死治愈 ,半年来间断发作的食后腹痛、腹胀 ,服助消化…     

纤维结肠镜诊断缺血性肠病3例报告

我院1996年至1999年用纤维结肠镜检查发现缺血性肠病3例,均属早期,给予相应治疗,预后较好。现分析报道如下。本组3例中,男2例,女1例,年龄分别为60、65、68岁,其中2例有高血压,1例有冠心病。3例均有突发性脐周部绞痛,继而排出鲜红色或暗红色血便,中等量,不与大便相混。2例有发热、1例腹泻。所     

缺血性肠病介入治疗一例

正1病例介绍患者,男,63岁,因"反酸烧心1年,伴腹痛腹泻1周"于2016-09-26就诊于天津中医药大学第一附属医院。患者自诉近一年体重下降约15 kg。1周前因劳累、情绪波动出现脐周疼痛,餐后尤甚,大便5~6次/d,最多可达10次/d,大便质稀,无黏液脓     

缺血性肠病的诊断(附11例报告)

缺血性肠病是一种由于结肠肠壁血液灌注不良或回流受阻所致的结肠缺血性疾病,我科1999～2002年共收治11例,现将其诊断总结如下。1 资料与方法 全组11例,男7例,女4例,年龄35～82岁,平均65.6岁,有高血压、冠心病者5例,陈旧前壁心肌梗死史1例,心房颤动2例,糖尿病1例,脑梗死1     

急性缺血性肠病临床诊治分析

目的 了解缺血性肠病的发病因素、临床表现及诊断治疗方法,尽可能地降低对该病的误诊、漏诊率,以提高对本病的诊疗水平.方法 通过对33例临床诊断缺血性肠病患者的诊断治疗过程进行回顾性分析,找出其临床特点.结果 33例缺血性肠病患者,临床上表现为腹痛、血便、腹泻或黏液血便等非特异性症状,早期不易确诊.严重者病情发展迅速,可出...     

炎症性肠病与骨质疏松研究进展

骨质疏松是炎症性肠病(IBD)患者常见但易被忽视的并发症之一.炎症性肠病患者骨质疏松的发病机制尚未完全明了,皮质类固醇激素的应用、炎性细胞因子的增加、维生素D的缺乏及遗传等众多因素均可能参与骨质疏松的发生.对于炎症性肠病患者并发骨质疏松者应及早诊断及治疗,早期干预可减轻IBD患者骨质疏松的发生与发展.     

Update on ischemic heart disease

This article contains a review of the main developments reported in 2011 on the pathophysiology, prevention, prognosis and treatment of chronic coronary artery disease and acute coronary syndrome, with or without ST-segment elevation. It also discusses the recommendations of the latest clinical practice guidelines.     

螺旋CT检查急性缺血性肠病所致门静脉和肠壁积气的表现特点及其临床诊断价值研究*

目的 探讨急性缺血性肠病所致门静脉和肠壁积气CT表现特点,总结CT诊断的价值。方法 回顾性分析2014年6月~2017年6月我院收治的20例缺血性肠病所致门静脉和肠壁积气患者CT检查资料,使用德国西门子 Emotion 64层螺旋CT进行扫描。行纤维结肠镜检查,并取组织行病理学检查。结果 在20例患者中,缺血性肠病的病变部位在小肠者9例（空肠5例、回肠4例）,回盲部3例（累及回肠末端和升结肠）,结肠8例（横结肠3例、结肠肝曲2例、结肠脾曲1例、降结肠1例、乙状结肠1例）;所有患者均显示有门静脉积气,其中13例门静脉和肝静脉呈现广泛的积气,表现为树枝状气体影,另7例CT显示肝缘下肝静脉远端有气体影;所有患者CT均显示肠壁有积气,病变部位可见气泡状低密度影,10例为单气泡影、7例为多气泡影、3例为带状泡影;14例CT显示肠壁增厚和水肿,6例肠管扩张、肠壁变薄,4例腹腔积液;行增强CT检查10例,显示病变肠段的肠壁和肠系膜强化程度减弱,分层强化后显示为环形靶征和晕征;所有患者入院治疗后1~2 d进行CT复查,显示门静脉和肠壁积气有不同程度的吸收,其中门静脉积气完全吸收4例、明显吸收9例、少量吸收4例、无显著变化3例。肠壁积气完全吸收5例、明显吸收7例、少量吸收6例、无显著变化2例。结论 门静脉和肠壁积气的CT表现有特征性,使用 CT检查对急性缺血性肠病患者的诊断有较好的临床应用价值。     

Update on inflammatory bowel disease genetics

The idiopathic inflammatory bowel diseases (IBD), comprised of Crohn's disease (CD) and ulcerative colitis (UC), are related, complex genetic disorders. With the completion of the human genomic sequence, identification of genetic variants contributing to IBD susceptibility can now more systematically be identified. Significant genetic linkages have been observed on chromosomes 16, 12, 14, 19, 6, and 1, of which the linkage to CD on chromosome 16 is the most well-established. For many of the other regions, evidence for linkage has been observed for both CD and UC. Candidate gene association studies have largely focused on genes involved in inflammatory pathways, such as cytokines and cytokine receptors. With greater understanding of genetic differences underlying both disease susceptibility and response to medical therapy, the individualization of medical approaches based on this knowledge may soon be possible in patients with IBD.     

经腹超声联合肠镜检查在老年人缺血性肠病诊断及治疗中的应用

目的：探讨老年缺血性肠病的超声声像图特征及其临床应用价值。方法对2007年10月至2012年10月解放军空军总医院门、急诊及住院治疗的23例急性腹痛、便血老年患者先行经腹肠道超声检查,并结合临床及肠镜所见分析其声像图特征。结果全部病例均经结肠镜和临床证实,超声定位符合率82.6%（19/23）,其中病变累及左半结肠12例（占52.2%）,降结肠5例（占21.7%）,乙状结肠3例（占13.0%）,脾曲3例（占13.0%）。肠壁增厚0.61～1.91cm,病变累及范围10～19cm,病变肠壁呈均匀性及全周性增厚,正常肠壁结构层次模糊或消失,代之以不规则的低回声,受累肠腔稍变窄,肠壁蠕动不同程度减弱或消失。8例腹腔可见少量积液。9例于腹腔腹膜后区可见稍大淋巴结（长径＞0.6cm）。12例病变肠壁无明显血流显像,11例仅见稀疏点、短条状血流信号。结论经腹肠道超声有助于缺血性肠病的早期诊断,联合肠镜能明确病变的性质、部位、范围,对临床治疗具有指导意义。     

Update on the genetics of inflammatory bowel disease

There is a general consensus that interplay of genetic and environmental factors leads to an overactive mucosal immune response, which mediates the tissue damage in inflammatory bowel disease. Ethnic aggregation of inflammatory bowel disease (particularly, increased incidence and prevalence in the Ashkenazim), familial aggregation of inflammatory bowel disease, and greater concordance for inflammatory bowel disease in monozygotic twins than dizygotic twins are 3 lines of evidence for a central role of genetic factors in the pathogenesis. The genetics of inflammatory bowel disease cannot be explained by simple Mendelian genetics; it is characterized by incomplete penetrance, multiple susceptibility loci and genetic heterogeneity. Unraveling the complex genetics of inflammatory bowel disease is a daunting challenge, but the perseverance of inflammatory bowel disease gene hunters has produced commendable results in recent years. Since 1996, the field of inflammatory bowel disease genetics has progressed from publication of the first systematic genome searches for inflammatory bowel disease susceptibility loci to the identification of Crohn disease-associated genetic variants in CARD15/NOD2. Strategies for finding additional inflammatory bowel disease genes include taking advantage of the greater resolution and power of linkage disequilibrium mapping, mapping by admixture disequilibrium in African-American and Hispanic-American populations, stratifying genetic analyses by genotypes at known inflammatory bowel disease loci, and refining inflammatory bowel disease phenotypes to reduce genetic heterogeneity and simplify the search for additional inflammatory bowel disease genes.     

Update on the genetics of inflammatory bowel disease

Crohn’s disease and ulcerative colitis are related genetic disorders. Epidemiologic studies suggest that both disorders are caused by a complex interplay of genetic and environmental factors. Genetic linkage studies identify the general chromosomal locations of disease susceptibility genes, and a number of genetic linkages have been reported in inflammatory bowel disease (IBD). Most notable among these linkage regions has been the linkage in the pericentromeric region of chromosome 16, IBD1, among families multiply affected with Crohn’s disease. Recent studies have established that at least three coding region variants in the Nod2 gene are responsible for the linkage findings here, and Nod2 therefore represents the first definitively established gene contributing to the pathogenesis of IBD. The implications of these findings for advancing our understanding of Crohn’s disease are discussed.     

Update of fecal markers of inflammation in inflammatory bowel disease

The diagnosis, prognosis, and assessment of disease activity of inflammatory bowel disease (IBD) require investigating clinical, radiological, and histological criteria, as well as serum inflammatory markers. However, a range of fecal inflammatory markers now appears to have the potential to greatly assist in these processes. Calprotectin, a prominent neutrophil protein, was identified two decades ago as a potentially revolutionary marker for IBD. Following this discovery, numerous additional markers, including S100A12, lactoferrin, and M2-pyruvate kinase, have also been suggested as novel markers of IBD. In the present study, we provide an up-to-date review of fecal markers of IBD, and further, provide a novel analysis of each of these fecal markers in severe ulcerative colitis and compare their expression pattern in contrast to calprotectin.