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1.
Barrett食管的诊断及其与食管腺癌的关系   总被引:1,自引:0,他引:1  
Barrett食管(Barrett's esophagus,BE)是由英国心胸外科医生Barrett在1950年首次报道,并以他的名字命名的。BE是指食管下段的复层鳞状上皮被化生的单层柱状上皮所替代的一种病理现象,可伴肠化或无肠化,其中伴有特殊肠上皮化生者属于食管腺癌的癌前病变。BE的一般发生率为0.25%~3.90%,而反流性食管炎病人的发病率可高达10%~20%。BE最多见于白种人,黑人和亚洲人相对较少。BE与食管腺癌的发生率密切相关,是一种主要的食管腺癌的癌前病变。因此,提高对BE的认识和诊断率是食管癌早期防治的重要环节。  相似文献   

2.
背景与目的:近年来,食管腺癌的发生率急剧增高,而食管腺癌的发生与Barrett食管(BE)有关。由于诊断BE时需要应用上消化道内镜,所以一般人群中BE的发生率尚不确定。本研究目的是确定瑞典成人人群中BE的发生率及可能的相关危险因素。  相似文献   

3.
中国是食管癌发病大国,全世界每年死于食管癌约30万人,我国占其半数以上。近20年来,欧美食管腺癌的发病率呈明显上升趋势。我国原发食管腺癌的发生率较低,近年来有增加趋势。欧美国家的原发食管腺癌高达50.0%,这种高发生率主要与Barrett食管(以下简称BE)有关。本文主要介绍食管腺癌临床治疗的研究进展。  相似文献   

4.
Barrett食管(Barrett esophagus,BE)是指食管下段复层鳞状上皮被化生的柱状上皮所取代的一种病理现象。由于BE被认为是食管癌的癌前状态之一,与食管腺癌的发生有密切关系,随着BE及其相关的食管腺癌发病率不断增加,对这些患者进行定期的内镜监测非常必要。BE通过化生-异型增生-肿瘤的顺序导致食管腺癌的发生,内镜监测的目的是为了早期诊断和治疗异型增生及早期食管癌,  相似文献   

5.
现已明确Barrett氏食管(BE)与食管腺癌和部分贲门癌的发生密切相关,是一种癌前病变。BE在人群中发病率的增长已成为近年西方国家食管腺癌和贲门癌发病率大幅度增高的直接原因,因此近几十年来BE的研究在国外备受关注,在我国近年也有食管腺癌和贲门癌的发病率增高的报道。目前普遍认为胃食管反流是BE形成的主要原因,然而近年有学者提出,十二指肠液中的胆盐在BE的发生和发展中更重要。因此本实验采用24h食管内pH和Bilitec同步监测技术,对BE、反流性食管炎(RE)、非糜烂性反流性疾病(NERD)和对照组患者进行监测,比较各组患者的反流发生特点,并探讨影响BE黏膜长度的因素。  相似文献   

6.
Barrett食管(Barrett's esophagus,BE)是一种常见的胃食管反流病的并发症,是食管下端的鳞状上皮被特殊肠化生的柱状上皮所替代的一种病理改变。大量流行病学和病理学研究表明,BE是食管下端腺癌,是日前唯一公认的癌前病变,其发生食管癌的危险性较一般人群高30~60倍,约10%的BE患者可能发展为食管腺癌。然而,临床上无论是抑酸治疗还是抗反流折叠术都不能完全阻断粘膜上皮化生。  相似文献   

7.
1概况 Barrett食管(Barrett esophagus,BE)是胃食管反流病(Gastroesophageal Reflux Disease,GERD)最重要的一种并发症,其与食管腺癌的发生有着密切的关系。大量流行病学和病理学研究表明,食管下段腺癌唯一公认的癌前病变是BE,BE发展到食管腺癌的年发病率为0.5%~1.0%。  相似文献   

8.
Barrett食管(BE)是指食管粘膜在修复过程中,食管贲门交界处齿状线2cm以上的上皮细胞被胃内单层柱状上皮细胞替代的一种病理现象,是长期慢性胃食管反流病的严重并发症。由于本病与食管腺癌的关系密切而作为癌前病变引起高度关注,其腺癌发生率较正常成人高30~50倍。本文回顾我院自1998年1月至2005年1月经内镜及病理组织学诊断的BE患者33例,就其内镜特征、临床表现及病理特点进行分析。  相似文献   

9.
Barrett食管(Barrett′s esophagus,BE)是胃食管反流病(gastro-esophageal reflux disease,GERD)的一种特殊类型,在蒙特利尔GERD定义和分类的全球专家共识中BE也被认为是GERD的一种并发症.流行病学调查显示GERD中约有5%~10%患者是BE,约2%~5% BE患者最终可发展为食管腺癌[1].目前研究认为,BE是食管腺癌的癌前病变.近年来中国和西方国家食管腺癌的发病率呈上升趋势,因此,BE的及时诊断对预防和减少食管腺癌发生有重要的意义[2].  相似文献   

10.
常英  刘斌  龚均 《陕西医学杂志》2004,33(9):807-809
近年来,美国和西欧国家的食管及胃食管连接处腺癌发病率逐渐增高,Barrett食管(Barrett’s esophagus,BE)被认为是其发生的重要危险因素而倍受关注。亦有研究发现,位置正常的胃食管连接处也可出现肠上皮化生,它是否也增加胃食管连接处腺癌发生的危险性,目前看法不一。本文旨在将BE和贲门肠上皮化生(Cardla intestinal metaplasia,CIM)的最新研究进展做一综述。  相似文献   

11.
Barrett esophagus (BE) is intestinal metaplasia (MI) within the distal tubular esophagus. The BE results in replacement of the normal squamous-lined epithelium with a columnar type epithelium. This metaplastic lesion is a clearly defined risk factor for the development of esophageal adenocarcinoma (ADC). In the western countries the incidence of adenocarcinoma of the lower esophagus and the gastro-esophagus junction have rapidly increased during the past twenty years. The 5-year survival is very poor. Although the relative risk of individuals in the United States with BE developing esophageal adenocarcinoma is very high, the absolute risk is extremely low due to the small number of cases. This lesion is caused by a persistent gastro-esophageal reflux. The nature of the reflux liquid is mixed acid and alkaline in the big majority of cases. A familial aggregation of BE and esophageal adenocarcinoma are present in 14% of patients with BE and esophageal adenocarcinoma. The diagnosis, the surveillance, the new tools of characterization of BE and the therapy remain an actual problem. We present 2 cases of endobrachyesophagus associated to an adenocarcinoma of the lower esophagus and a review of the main actual problem.  相似文献   

12.
The rising incidence of esophageal adenocarcinoma(EAC) in the world has led to continued interest in its precursor lesion,Barrett’s esophagus(BE). This review endeavors to summarize the recent advances in the therapy of BE with an emphasis on novel endoscopic therapies.  相似文献   

13.
Shaheen N  Ransohoff DF 《JAMA》2002,287(15):1972-1981
CONTEXT: Gastroesophageal reflux disease (GERD) is a risk factor for adenocarcinoma of the esophagus, a rare cancer whose incidence is increasing. Adenocarcinoma may develop from Barrett esophagus, a metaplastic change of the esophageal epithelium from squamous to intestinalized columnar mucosa, which is associated with chronic reflux. Some have recommended that patients with chronic reflux symptoms undergo upper endoscopy to assess for Barrett esophagus and to screen for cancer. OBJECTIVES: To review the evidence linking GERD and Barrett esophagus to esophageal adenocarcinoma and to examine the utility of upper endoscopy as a screening tool in adenocarcinoma of the esophagus among individuals with GERD. DATA SOURCES: A MEDLINE search was performed to identify all pertinent English-language reports about GERD, adenocarcinoma, and Barrett esophagus from 1968 through 2001. Reports were of randomized controlled clinical trials if available, case-control data if trials were unavailable, and cohort studies if case-control data were unavailable. Pertinent bibliographies were also reviewed to find reports not otherwise identified. STUDY SELECTION AND DATA EXTRACTION: Studies were selected by using the search terms gastroesophageal reflux, adenocarcinoma, and Barrett's esophagus, with subheadings for classification, complications, drug therapy, economics, epidemiology, mortality, surgery, and prevention and control. Clinical guidelines for the care of subjects with GERD and Barrett esophagus were retrieved and abstracted. DATA SYNTHESIS: Cohort studies demonstrate that symptoms of GERD occur monthly in almost 50% of US adults and weekly in almost 20%. Three large case-control studies demonstrate a positive association between reflux symptoms and risk of adenocarcinoma of the esophagus, with more prolonged and severe symptoms accentuating this risk. However, because of the low incidence of adenocarcinoma of the esophagus and the ubiquity of reflux symptoms, the risk of cancer in any given individual with reflux symptoms is low. No randomized trial data are available to demonstrate either decreased cancer incidence or increased life expectancy in subjects with GERD who undergo screening endoscopy. CONCLUSIONS: Strong evidence supports the association of GERD and adenocarcinoma of the esophagus; however, the risk of cancer in any given individual with GERD is low. Barrett esophagus appears to be a common precursor lesion to this cancer. Given the low absolute risk of cancer in those with GERD and the lack of demonstrated efficacy of endoscopic screening, insufficient evidence exists to endorse routine endoscopic screening of patients with chronic GERD symptoms.  相似文献   

14.
目的 探讨30 例Barrett 食管(Barrett esophagus, BE) 的内镜下特点及与幽门螺杆菌(Helicobacter pylori, Hp) 感染的关系。方法 采用胃镜检查结合病理检查结果对30 例BE 患者进行分析,同时选取反流性食管炎及正常食管黏膜各50 例作为对照组,采用快速尿素酶法及Warthin-Starry 银染两种方法检测Hp 感染。结果 30 例BE 中,以短段、舌型发病率最高,分别占83.33% 和66.67% ;组织学上,胃底型12 例(40%),贲门型10 例(33.33%),特殊肠化生型8 例(26.67%)。食管部Hp 的检出率,BE 组阳性率明显高于反流性食管炎组和正常食管黏膜组(P < 0.05)。胃窦部Hp 的检出率,BE 组显著低于反流性食管炎组和正常食管黏膜组(P < 0.05)。结论 本组BE 病例内镜下以短段、舌型为主,Hp 对BE 可能有保护作用。  相似文献   

15.
赵志飞  朱晓娟 《医学综述》2012,18(12):1858-1860
肥胖是Barrett食管(BE)发生、发展的危险因素,然而肥胖是否是BE发生的独立危险因素还存在争论。有研究证明,腹型肥胖,尤其是内脏肥胖是BE发生的独立危险因素。肥胖作为BE发生的危险因素,其机制尚不明确。腹型肥胖导致胃内压力增加,胃酸反流入食管,导致食管长期暴露于酸性环境,发生食管炎进而发展为BE;肥胖者体内脂肪组织代谢增加,血浆中脂肪素、瘦素水平增加,脂联素水平降低,这些都可能与BE以及食管腺癌的发病有关。  相似文献   

16.
目的观察反流性食管炎、Barrett食管和食管腺癌中食管上皮细胞过氧化物酶体增殖物激活受体γ(PPARγ)的表达及细胞增殖的变化特点。方法胃镜下取20例反流性食管炎(RE组)、20例Barrett食管(BE组)和6例食管腺癌(EA组)和20例慢性浅表性胃炎(正常对照组)的食管黏膜组织进行活检,免疫组化法和免疫印迹法测定各组黏膜组织食管上皮细胞PPARγ和增殖细胞核抗原(PCNA)的蛋白表达。结果免疫组化法显示RE、BE、EA组PPARγ的阳性表达率分别为25%、30%、33%,均高于正常对照组的10%(P<0.05);免疫印迹法显示RE、BE、EA组的PPARγ蛋白吸光度比值分别为0.28±0.15、0.21±0.18、0.32±0.13,均高于正常对照组的0.08±0.06(P<0.05);RE、BE、EA组3组间的PPARγ表达差异无统计学意义(P>0.05)。免疫组化法显示正常对照组、RE组、BE组、EA组PCNA的阳性表达率分别为25%、60%、75%、100%。结论从正常食管到反流性食管炎、Barrett食管、食管腺癌,食管上皮的细胞增殖明显增加,伴随着PPARγ蛋白的表达增加,提示PPARγ可能参与了反流性食管炎、Barrett食管、食管腺癌发病过程中细胞增殖的调控。  相似文献   

17.
Barrett食管(BE)诊断主要依赖于内镜及组织病理学检查。提高BE的诊断水平,为及早治疗及干预其向食管腺癌的发展具有重要的意义。近年来,BE诊断技术得到进一步发展,普通内镜、胶囊内镜、染色内镜、染色放大内镜、增强放大内镜、荧光内镜技术、超声内镜、共聚焦荧光内镜、窄带光照内镜技术在诊断BE中具有不同特点。现对BE诊断标准、不同内镜诊断技术特点进行综述。  相似文献   

18.
Rising incidence of adenocarcinoma of the esophagus and gastric cardia   总被引:48,自引:1,他引:47  
W J Blot  S S Devesa  R W Kneller  J F Fraumeni 《JAMA》1991,265(10):1287-1289
Analyses of cancer incidence data from nine areas of the United States revealed steadily rising rates from 1976 to 1987 of adenocarcinomas of the esophagus and gastric cardia. The increases among men in this period ranged from 4% to 10% per year, and thus exceeded those of any other type of cancer. In contrast, there were relatively stable trends for squamous cell carcinoma of the esophagus and slight declines for adenocarcinoma of more distal portions of the stomach. Adenocarcinomas of the esophagus and gastric cardia disproportionately affected white men and rarely occurred among women. By the mid-1980s, among white men, adenocarcinomas accounted for about one third of all esophageal cancers, while cardia cancers accounted for about one half of all stomach cancers with specified subsites. The rising incidence rates and similar demographic patterns point to the need for investigation into the causes of these poorly understood cancers.  相似文献   

19.
目的对了解食管癌病人的病理类型及变化趋势。方法查阅32年间胃镜检查记录,对检出食管癌病人性别、年龄、民族、病变部位及病理类型,按诊断时间分为四组,进行分析。结果B、C、D组食管癌检出率比较差异有统计学意义(χ^2=7.126,P〈0.05);B、C组食管癌检出率比较无统计学意义(χ^2=0.078,P〉0.05);食管癌男女比例为2.58∶1,以40-65岁之间的病人为多(占59.65%);病变在食管中段的占70.7%;食管鳞癌占88.2%,腺癌占11.8%;汉族、回族、蒙古族食管鳞癌和腺癌构成比之间比较,差异无统计学意义(χ^2=0.038,P=0.981〉0.05);B、C、D组食管下段腺癌构成比比较差异无统计学意义(χ^2=2.767,P〉0.05)。结论32年间食管癌检出率无明显变化;食管癌发病有老年化趋势。  相似文献   

20.
姜志茹  郑爱萍  郭海  陈静  孙亮 《现代医学》2012,40(4):433-436
目的:观察反流性食管炎(RE)、Barrett食管(BE)、食管腺癌(EA)中食管上皮细胞的P38表达与细胞增殖凋亡的变化特点.方法:胃镜下取食管黏膜活检,免疫组化法和免疫印迹法测定RE组、BE组、EA组及正常对照组的P38和Ki-67的蛋白表达,TUNEL法测定细胞凋亡.结果:免疫组化法测定正常对照组、RE组、BE组、EA组的Ki-67表达率分别为10%、55%、60%、83.3%.TUNEL法测定正常对照组、RE组、BE组、EA组的细胞凋亡指数分别为(1.51±1.06)%、(8.12±1.55)%、(7.25±1.87)%、(3.63±1.70)%.免疫印迹法测定RE组、BE组的磷酸化P38蛋白吸光度比值分别为0.09±0.03、0.11±0.04,EA组和正常对照组无磷酸化P38蛋白表达.结论:与食管腺癌组相比,反流性食管炎、Barrett食管的细胞增殖率下降,细胞凋亡指数增加,伴随着磷酸化P38蛋白的表达增加,提示P38信号通路可能参与了反流性食管炎、Barrett食管发病过程中细胞增殖凋亡的调控.  相似文献   

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