AT1、Mas在反流性食管炎中的表达及意义

目的观察血管紧张素Ⅱ受体1亚型(AT1)及Mas在正常食管黏膜组织、反流性食管炎(reflux esophagitis,RE)、Barrett’s食管(Barrett’s esophagus,BE)组织中的表达水平,探讨AT1、Mas在RE发生与发展中表达的相互作用及意义。方法收集2014年12月至2016年9月就诊于内蒙古包钢医院消化内科符合胃镜下及病理标准的正常食管黏膜组织30例、RE组织45例、BE组织30例,采用免疫组化染色SP法检测AT1、Mas在不同食管组织中的表达水平。结果运用Krusral-wallis H方法检验AT1在正常食管黏膜、RE、BE组织中的表达秩均值分别为38.70、55.46、63.62,差异有统计学意义(P0.05),呈逐渐升高的趋势。Mas在正常食管黏膜、RE、BE组织中的表达秩均值分别为68.47、52.43、38.38,差异有统计学意义(P0.05),呈逐渐下降的趋势。Mas与AT1在RE及BE组织中的表达呈负相关(P0.05)。结论随着RE的发生及演化为BE的过程中,AT1表达强度升高,而Mas表达强度降低,且两者表达呈负相关,其与RE发病机制的关系值得进一步探讨。     

Ghrelin在食管腺癌、Barrett’s食管黏膜中的表达

目的:研究Ghrelin在食管腺癌、Barrett’s食管(barrett esophagus,BE)和正常食管黏膜中的表达.方法:选取30例食管腺癌患者、35例BE患者及35例健康对照,所有受试者均行胃镜检查,记录内镜下表现,在食管部位四象限活检取材,标本经10%甲醛固定,石蜡包埋,连续切片,分别用于改良HE染色及免疫组织化学,采用免疫组织化学方法检测Ghrelin在食管黏膜组织中的表达水平.结果:Ghrelin在食管腺癌组食管黏膜中的表达水平低于健康对照组和BE组,在BE组食管黏膜中的表达高于健康对照组,差异有统计学意义(1.34±0.51vs4.86±0.82vs3.54±0.79,F=27.21,P<0.05).食管腺癌组中,Ghrelin在中高分化腺癌患者食管黏膜的表达水平高于低分化腺癌,差异有统计学意义(Z=4.60,P<0.05).结论:Ghrelin在BE、食管腺癌黏膜中的表达不同,提示了Ghrelin在食管癌变前和癌变后的变化.食管腺癌组织恶变过程中其Ghrelin的分泌机制发生了改变,且与食管腺癌细胞分化程度有关.     

组织芯片研究胃食管黏膜病变中Ki67和C-erbB-2的表达及意义

目的:研究Ki67和C-erbB-2在各类胃食管黏膜病变中的表达及意义.方法:采用TMA制作140例各类胃食管黏膜病变的组织芯片,分成Barrett食管(BE)组、贲门癌(CA)组、食管腺癌(EA)组、和胃窦肠化(AIM)组、贲门肠上皮化生(CIM)组和正常对照(Control)组,共6组,采用免疫组织化学方法检测Ki67和C-erbB-2的表达.结果:BE组,EA组和CA组Ki67的阳性率均显著高于COntrol组(40.9%,69.6%,61.9% vs 0.0%,均P<0.01),明显高于CIM组11.5%(P<0.05);CIM组和AIM组以及EA组和CA组之间无显著性差异:EA和CA组中Ki67的阳性率高于BE组(P<0.05);BE组,EA组和CA组C-erbB-2的阳性率均显著高于Control组和CIM组(31.8%,52.1%,52.4% vs 0.0%,P<0.01),明显高于AIM组3.6%(P<0.05).C-rbB-2与Ki67在各类胃食管黏膜病变组织中的表达统计学上具有紧密关联性(P=0.001).结论:Ki67和C-erbB-2可能在Barrett食管和胃食管连接处腺癌的发生发展中起重要的促进作用.     

反流性食管炎、Barrett食管和食管腺癌的研究

背景:胃食管反流病(GERD)是一种常见疾病,包括非糜烂性反流病(NERD)、反流性食管炎(RE)和Barrett食管(BE),近年其发病率逐渐增高。目的:探讨RE、BE与各种因素的关系。方法:应用反流性疾病问卷筛选具有胃食管反流症状的患者,行胃镜检查检测RE、BE和食管腺癌的检出率,分析吸烟、饮酒、饮食、年龄、性别和民族与RE、BE的关系。结果:共纳入1834例具有胃食管反流症状的患者,其中RE患者234例(12.8%);BE患者213例(11.6%),包括特殊肠化生型BE 47例;食管腺癌5例(0.3%)。蒙古族RE、BE的检出率显著高于汉族和其他民族。饮酒者中RE和BE的比例明显升高。BE患者中-重度异型增生和食管腺癌的检出率升高。结论:蒙古族人群RE和BE的检出率较高,饮酒与食管反流致损伤的关系密切,BE为食管腺癌的癌前病变。     

一氧化氮合酶、环氧合酶-2在不同类型胃食管反流病中的表达及意义

背景非糜烂性胃食管反流病(non-erosive reflux disease,NERD)、反流性食管炎(refluxesophagitis,RE)、Barrett食管(barrettesophageal,BE)三种类型NERD转化少,独立性较强,临床表现和预后均有一定差异,其中NERD最为常见,但诊断难度最大.报道显示,NOS、COX-2在胃食管反流病(gastroesophageal reflux disease,GERD)呈高表达,但在不同类型GERD方面报道较少,推测一氧化氮合酶(nitric oxide synthetase,NOS)、环氧合酶-2(cyclooxygenase-2,COX-2)对NERD的诊断有一定价值.目的探究NOS、COX-2在不同类型胃食管反流病中的表达及意义.方法前瞻性选取2015-01/2019-12我院内科收治的GERD患者78例作为观察组,按照GERD不同类型分为NERD、RE、及BE3组;另选取同期在本院门急诊及体检中心进行胃镜检查的26例健康人群作为对照组.比较各组NOS mRNA、COX-2 mRNA表达,并分析两者相关性,以及NOS mRNA、COX-2 mRNA对NERD的诊断作用.结果内镜及组织病理学检查显示, 78例GERD患者中, RE组26例、NERD组28例、BE组24例;各组患者在性别年龄等一般资料比较无显著差异(P0.05), 3种不同类型GERD的NOS mRNA[神经元型一氧化氮合酶(neuronalnitricoxidesynthase,nNOS)mRNA、诱导型一氧化氮合酶(inducible nitric oxide synthase, iNOS)mRNA]、COX-2mRNA表达水平明显高于对照组,且BE组NOS mRNA、COX-2 mRNA表达水平明显高于RE组, RE组NOS mRNA、COX-2 mRNA表达水平明显高于NERD组,差异均有统计学意义(P0.05).nNOS mRNA、iNOS mRNA与COX-2mRNA均呈显著正相关(r=0.900、0.897, P0.05).受试者工作特征曲线分析显示, nNOS mRNA诊断NERD的曲线下面积(area under the curve, AUC)为0.662, iNOS mRNA诊断NERD的AUC为0.671,COX-2mRNA诊断NERD的AUC为0.613; Z检验AUC发现差异无统计学意义(P0.05),根据最佳临界值,当nNOS mRNA高于1.505时,其敏感度为65.8%,特异度为89.3%;当iNOS mRNA高于1.795时,其敏感度为63.2%,特异度为100%;当COX-2 mRNA高于1.895时,其敏感度为55.3%,特异度为92.9%.结论 NOS、COX-2在不同类型胃食管反流病中均呈高表达,其中在BE患者中表达最高, RE患者中表达次之,NERD患者中表达最少,并且对NERD的诊断有一定参考价值.     

肝肠钙粘连蛋白在反流性食管炎、Barrett食管和食管腺癌中的表达及意义

目的研究肝肠钙粘连蛋白(LI-cadherin)在反流性食管炎(RE)、Barrett食管(BE)、食管腺癌(EA)、胃黏膜肠化生(GIM)中的表达,探讨BE和EA早期诊断的分子学标志物及BE伴肠化生(简称BE2)与GIM的关系。方法选取2013年8月至2014年12月就诊于内蒙古医学院附属医院,经胃镜或手术取得标本,组织学证实为RE、BE不伴有肠化生(简称BE1)、BE2、BE伴不典型增生(简称BE3)、EA患者各30例,选取同期GIM及正常人各20例为对照组。用免疫组织化学SP法、酶联免疫吸附法(ELISA)分别对入选者的组织、血清中的LI-cadherin进行检测,对获得的结果进行统计学分析。结果 LI-cadherin在组织、血清中检测显示:正常食管黏膜中不表达,在RE、BE1、BE2、BE3中的表达逐渐升高,而在EA低表达,在GIM表达为55.00%。在组织中,BE2、BE3组中的表达高于正常组、RE组、BE1组及EA组,差异均有统计学意义。BE1与GIM组中的表达差异有统计学意义。在血清中,BE1、BE2、BE3组中的表达高于正常组、RE组、EA组,在BE2、BE3组中的表达高于BE1组,差异均有统计学意义。在BE1组与GIM组中的表达差异有统计学意义。Spearman相关性分析,LI-cadherin血清中含量与组织中表达存在正相关关系。LI-cadherin在TNM分期Ⅲ+Ⅳ期的表达低于Ⅰ+Ⅱ期,差异有统计学意义。结论 (1)LI-cadherin为早期筛查BE及EA提供分子学诊断依据;(2)BE伴肠上皮化生为EA的癌前病变;(3)LI-cadherin表达与EA的TNM分期有关;(4)患者血清中LI-cadherin的含量可以反映其组织中的水平。     

不同类型胃食管反流病发病机制的差异

目的:比较不同类型胃食管反流病(GERD),即反流性食管炎(RE)、非糜烂性反流病(NERD)和Barrett食管(BE)发病机制的差异.方法:113例GERD患者,根据内镜下表现及病理情况分为RE、NERD、BE三组,比较三组患者内镜下表现、食管测压和24 h pH监测指标、合并食管裂孔疝(HH)情况的差异.结果:RE组较NERD组与BE组下食管括约肌压力减低,但无统计学差异.食管体部各段的收缩波幅比较,RE组减低最明显,NERD组减低最少,两组比较P<0.05;无效食管运功比较,RE组较另两组明显增多( P<0.05).RE、NERD、BE组24 h食管pH监测的DeMeester计分分别为90.2、55.2、48.8;RE组以重度酸暴露多见(43%),反流总时间阳性率较高;NERD组以轻度酸暴露多见(45.8%),反流频率阳性率较高;BE组以长反流时间阳性率较高.HH在RE、NERD、BE组中的检出率分别为50%、14.6%、25.7%( P = 0.003).结论:下食管括约肌及食管体部运动功能受损程度、酸反流情况的差异可能是造成三种不同类型GERD食管黏膜损伤表现不同的主要原因.     

趋化因子受体4在Barrett食管、食管腺癌和食管鳞状细胞癌中的表达及其意义

目的 了解趋化因子受体（CXCR4）在Barrett食管（BE）、食管腺癌和食管鳞状细胞癌中的表达,及其与病理分化程度、临床分期及淋巴结转移之间的关系.方法 应用免疫组织化学SP法对正常食管黏膜56例、BE 80例（其中伴多灶性异型增生22例）、食管腺癌25例和食管鳞状细胞癌组织48例标本中CXCR4的表达进行检测,并用仪器对表达结果进行图像分析,然后进行统计学分析.结果 （1）CXCR4在大部分BE、食管腺癌和食管鳞状细胞癌中呈阳性表达（其阳性率分别为78.8%、68.0%、83.3%）,3组间差异无统计学意义（P＞0.05）,而在正常食管黏膜组中呈阴性或弱阳性表达（阳性率为39.3%）,差异有统计学意义（P＜0.01）;（2）CXCR4在BE、食管腺癌和食管鳞状细胞癌的表达与性别、年龄、病变发生位置均无关（P＞0.05）;（3）CXCR4在BE无异型增生和BE伴多灶性异型增生组织标本中的表达差异无统计学意义（P＞0.05）;（4）CXCR4在食管腺癌高分化较中-低分化者、有淋巴结转移较无淋巴结转移者中的表达均高（P＜0.05）;（5）CXCR4在食管鳞状细胞癌表达水平在肿瘤TNM分期的Ⅲ-Ⅳ级较Ⅰ-Ⅱ级者、有淋巴结转移较无淋巴结转移者中的表达均高（P＜0.05）,高分化较中-低分化则明显更高（P＜0.01）.结论 CXCR4的表达上调可能是食管腺癌和鳞癌的一个普遍特征,与食管病理组织学类型无关,其表达在BE阶段就已上调,并与食管腺癌和鳞癌的分化程度,有无淋巴结转移和TNM分期有一定相关性.CXCR4的表达对BE、食管腺癌和鳞癌的诊断具有指导价值,有可能成为肿瘤治疗的一个新靶点.     

P53、Bcl-2在正常食管黏膜、Barrett食管及食管腺癌中的表达及临床意义

[目的]通过免疫组织化学技术探讨P53、Bcl-2在正常食管黏膜、Barrett食管、食管腺癌中的表达探讨及临床意义及其相关性。[方法]收集我院2011~2013年内镜活检的明确诊断的Barrett食管、食管腺癌及正常食管黏膜组织标本各30例,并将Barrett食管根据异型增生程度分为不伴不典型增生、轻度不典型增生、中度不典型增生、重度不典型增生。应用免疫组织化学技术检测其p53及Bcl2的表达。[结果]90例患者中正常食管黏膜30例、11例不伴不典型增生、9例轻度不典型增生、5例中度不典型增生、5例重度不典型增生、30例食管腺癌各组中Bcl-2蛋白表达阳性率分别为3.3%、6.7%、9.1%、22.2%、40%、60%、70%;BCL2表达强度随Barrett食管不典型增生增生程度依呈递增趋势,各组间比较,差异有统计学意义。各组中p53蛋白表达阳性率则分别为6.7%、18.2%、33.3%、40%、80%、80.0%,除重度不典型增生与食管腺癌组间差异无显著性意义外,其它各组间差异有统计学意义(P0.05)。[结论]随着Barrett食管不典型增生程度的加重,Bcl-2、P53也随之升高。p53、Bcl-2过度表达与Barrett食管进展到食管腺癌有相关性。     

环氧合酶-2在不同病理类型非霍奇金淋巴瘤组织中的表达及其临床意义

目的:探讨环氧合酶-2(COX-2)在不同病理类型非霍奇金淋巴瘤(NHL)组织中的表达及其与患者临床特征的关系。方法:采用免疫组织化学EnVision二步法检测96例NHL和20例恶性肿瘤患者切除组织中未累及之淋巴结中COX-2的表达,回顾性分析患者的分期、分组、结外侵犯等临床特征。结果:COX-2在NHL中的阳性表达率为39%(37/96),对照组为15%(3/20),差异有统计学意义(P<0.05)。不同病理类型之间COX-2表达差异有统计学意义(P<0.01),其中鼻型结外NK/T细胞淋巴瘤、黏膜相关淋巴组织结外边缘区淋巴瘤(MALT淋巴瘤)、血管免疫母细胞T细胞淋巴瘤组织中COX-2阳性率分别为83%(10/12)、71%(5/7)和57%(4/7)。有结外侵犯的患者COX-2阳性率显著高于无结外侵犯者(P<0.01),有无B组症状的NHL患者之间COX-2阳性率差异有统计学意义(P<0.05)。结论:NHL中COX-2表达上调,但不同病理类型之间COX-2表达差异较大,高表达COX-2的NHL患者易于出现结外侵犯及B组症状。     

Cyclooxygenase 2 expression in Barrett's esophagus and adenocarcinoma: Ex vivo induction by bile salts and acid exposure

BACKGROUND & AIMS: Barrett's esophagus (BE) results from chronic, severe gastroesophageal reflux and predisposes to esophageal adenocarcinoma. Cyclooxygenase (COX)-2 is involved in chronic inflammation and epithelial cell growth. We investigated COX-2 expression in BE and esophageal adenocarcinoma to explore a potential relation between COX-2 expression and metaplasia or carcinogenesis. METHODS: Endoscopic mucosal biopsy specimens of Barrett's intestinal metaplasia (n = 30), Barrett's dysplasia (n = 11), and esophageal adenocarcinoma (n = 5) were compared with normal esophagus (n = 46) and duodenum (n = 46) and analyzed by Western blotting and immunohistochemistry. RESULTS: Immunoblots revealed constitutive expression of COX-2 in normal esophagus and duodenum. COX-2 protein expression was significantly higher in patients with Barrett's metaplasia, dysplasia, and adenocarcinoma compared with normal squamous esophageal or columnar duodenal epithelia and was heterogenous in different regions of the BE surface. Immunohistochemistry revealed prominent staining in the glands of BE, dysplasia, and adenocarcinoma and faint staining in the basal layers of squamous esophagus and the surface of the duodenum. In response to pulses of acid or bile salts in an ex vivo organ culture system, COX-2 expression increased significantly in BE tissues, and this effect was attenuated by the selective COX-2 inhibitor NS-398. CONCLUSIONS: The results show COX-2 expression in normal esophagus, which increases significantly in BE and esophageal adenocarcinoma. COX-2 is regulated ex vivo by exposure to acid or bile salts.     

反流性食管炎、Barrett食管和食管腺癌中上皮钙粘蛋白的表达

目的：研究反流性食管炎（ＲＥ）,Ｂａｒｒｅｔｔ食管（ＢＥ）及食管腺癌（ＥＡＣａ）中上皮钙粘蛋白（Ｅ－ｃａｄｈｅｒｉｎ）的表达及其意义。方法：运用免疫组化法ＡＢＣ法检测了１３例ＲＥ,１７例ＢＥ,１１例ＥＡＣａ以及３０例正常食管粘膜（ＮＥ）中Ｅ－ｃａｄｈｅｒｉｎ的表达。结果：Ｅ－ｃａｄｈｅｒｉｎ在ＮＥ,ＲＥ,ＢＥ,ＥＡＣａ中表达呈逐渐降低趋势。     

Toll-like receptor 4 activation in Barrett’s esophagus results in a strong increase in COX-2 expression

Background

Barrett’s esophagus (BE) is known to progress to esophageal adenocarcinoma in a setting of chronic inflammation. Toll-like receptor (TLR) 4 has been linked to inflammation-associated carcinogenesis. We aimed to determine the expression and functional activity of TLR4 in the esophagus and whether TLR4 activation in BE could promote carcinogenesis by inducing COX-2 expression.

Methods

TLR4 expression in esophageal adenocarcinoma, BE, duodenum, reflux esophagitis and normal squamous esophagus biopsies was assessed using real-time PCR and validated by in situ hybridization and immunohistochemistry. Ex vivo cultures of BE, duodenum and normal squamous esophagus biopsies and a BE cell line (BAR-T) were stimulated with the TLR4 agonist lipopolysaccharide (LPS). To evaluate the effect of TLR4 activation, NF-κB activation, IL8 secretion and expression and COX-2 expression were determined.

Results

TLR4 expression was significantly increased in esophageal adenocarcinoma, BE, duodenum and reflux esophagitis compared to normal squamous esophagus. LPS stimulation resulted in NF-κB activation and a dose-dependent increase of IL8 secretion and mRNA expression. The induction of IL8 was more evident in BE compared to normal squamous esophagus. Upon LPS stimulation, COX-2 expression increased significantly in ex vivo cultured BE biopsies, which was observed in both epithelium and lamina propria cells. However, no effect was found in duodenum and normal squamous esophagus biopsies.

Conclusion

TLR4 activation in BE results in a strong increase in COX-2 and may contribute to malignant transformation.     

Chemoprevention of esophageal adenocarcinoma by COX-2 inhibitors in an animal model of Barrett's esophagus

BACKGROUND & AIMS: Carcinogenesis in Barrett's esophagus (BE) is associated with an increased expression of cyclooxygenase (COX) 2. However, there has been no direct evidence that inhibition of COX-2 prevents cancer in BE. We studied the effect of MF-Tricyclic, a selective COX-2 inhibitor, on the development of BE and adenocarcinoma in a rat model. METHODS: Four weeks after esophagojejunostomy, 105 Sprague-Dawley rats were randomized to a chow containing MF-Tricyclic or Sulindac, or a placebo. Ninety-six (92%) rats completed the study and were sacrificed at 28 +/- 2 weeks. The animals were assessed for the presence of cancer, tumor volume, BE, degree of inflammation, and COX-2 expression and activity. RESULTS: MF-Tricyclic and Sulindac reduced the relative risk of development of esophageal cancer by 55% (95% confidence interval [CI] = 43%-66%, P < 0.008) and by 79% (95% CI = 68%-87%, P < 0.001), respectively, compared with controls. No significant differences were noted in the risk of esophageal cancer between the MF-Tricyclic and the Sulindac group (P = 0.34). The median tumor volume was not significantly different among the 3 groups (P = 0.081). Moderate to severe degree of inflammation was significantly more common (P = 0.005) in the control compared with the MF-Tricyclic and the Sulindac group; however, the prevalence of BE was not significantly different between groups (P = 0.98). Rats in the control group had higher tissue PGE2 level compared with the MF-Tricyclic and Sulindac groups (P = 0.038). CONCLUSIONS: Selective and nonselective COX-2 inhibitors can inhibit inflammation, COX-2 activity, and development of adenocarcinoma induced by reflux. This provides direct evidence that COX-2 inhibitors may have chemopreventive potential in BE.     

反流性食管炎、Barrett食管的食管动力学研究

目的 探讨反流性食管炎(RE)、Barrett食管(BE)的动力学改变。方法 经内镜检查3 400例患者,分 RE、BE、对照组,进行症状调查、食管测压、食管24h pH检测,并行统计学分析。结果 RE与BE组间除吞咽不适外,烧心感、反酸及胸骨后疼痛的症状评分均为RE组大于BE组,且差异有显著性意义。部分RE、BE、对照组间食管运动功能比较,食管下括约肌静息压等差异均无显著性意义。食管24 h pH检测DeMeester评分、pH<4总时间、pH<4时间的百分比等 RE、BE组高于对照组,差异有显著性意义,但RE、BE组间差别无显著性意义。结论 食管反流症状与食管黏膜的内镜下表现不一致;食管组织化生与食管运动功能间无相关。     

Trends in Barrett's esophagus diagnosis in Southern Europe: implications for surveillance

The incidence of Barrett's esophagus (BE) and esophageal adenocarcinoma has increased in Western countries in recent decades. The aim of this study is to describe the changes in incidence and prevalence of BE diagnosis, dysplasia, and adenocarcinoma development in BE patients in a South‐European Mediterranean area. Retrospective population‐based analyses of endoscopy and pathology reports from 1976 to 2001 was performed. Data from patients with diagnosis of BE and/or esophageal carcinoma were collected. The study period was divided in four quartiles for statistical calculations; parametric and nonparametric tests were used. A 6.9‐fold increase was found in the diagnosis of long‐segment BE from the first to the fourth quartile, and a 9.3‐fold increase in short‐segment BE from 1995 to 2000, in contrast to a much smaller increase of 1.9‐fold increase in the number of upper gastrointestinal endoscopies. The adjusted incidence of BE diagnosis increased from 0.73 to 9.73 cases/100 000 (first to fourth quartile, respectively) and the adjusted prevalence from 6.51 to 76.04 cases/100 000 (1985–2001). The incidence of dysplasia was 2.13% per year (95% confidence interval: 0.05–11.3%) ? 1.78% for low‐grade dysplasia and 0.36% for high‐grade dysplasia – giving a total incidence of 1 per 47 patient‐years. The incidence of adenocarcinoma during follow‐up was 0.48% per year (95% confidence interval: 0.006–2.62%), for an incidence of 1 per 210 patient‐years. Nineteen patients with BE (14 long‐segment BE, 5 short‐segment BE) were diagnosed with esophageal adenocarcinoma, with eight being diagnosed during endoscopic surveillance. Only 14 (8%) adenocarcinoma patients diagnosed during the study period had a history of BE. BE diagnosis has dramatically increased over recent decades in our population, unrelated to an increase in endoscopies. Progression to low‐grade dysplasia and adenocarcinoma is rare. Surveillance may have a low impact on the survival of adenocarcinoma patients in Southern Europe.     

Barrett's esophagus and reflux esophagitis: is there a missing link?

OBJECTIVES: Barrett's esophagus (BE) is associated with esophageal reflux. The development stage of BE is not well described. Epidemiological evidence indicates that the columnar epithelium in BE is acquired and reaches its full length rapidly. We tested the hypothesis that BE might result from direct replacement of erosions in reflux esophagitis (RE). METHODS: At endoscopy, we compared the length and distribution of esophageal erosions in 50 patients with RE with the length and distribution of columnar epithelium in 50 patients with BE. RESULTS: The median length of erosions in RE was 2 cm, less than the median length of columnar epithelium in BE, 5 cm (p < 0.001). Erosions in RE were usually multiple and scattered, involving the entire circumference of the esophagus in only 10% of cases, but circumferential involvement by columnar epithelium was found in 68% of BE cases (p < 0.001). Circumferential involvement, 3 cm or longer, was found in 0% of cases of RE versus 56% of BE cases (p < 0.001). Two patients without RE or BE had large areas of epithelial loss of uncertain etiology. CONCLUSIONS: The length and distribution of erosions in RE differ greatly from the length and distribution of columnar epithelium in BE. It is unlikely that BE arises directly from areas of esophagitis. We suggest that BE may develop after loss of a long segment of squamous epithelium, with columnar replacement in the presence of continuing acid reflux.