中华消化内镜杂志
中華消化內鏡雜誌
중화소화내경잡지
CHINESE JOURNAL OF DIGESTIVE ENDOSCOPY
2009年
7期
348-352
,共5页
陈磊%房殿春%余欣%龙庆林
陳磊%房殿春%餘訢%龍慶林
진뢰%방전춘%여흔%룡경림
Barrett食管%胃黏膜异位%细胞角蛋白%螺杆菌,幽门%小凹
Barrett食管%胃黏膜異位%細胞角蛋白%螺桿菌,幽門%小凹
Barrett식관%위점막이위%세포각단백%라간균,유문%소요
Barrett esophagus%Heterotopic gastric mucosa%Cytokeratin%Helicohacter pylori%Pit pattern
目的 探讨食管高位胃黏膜异位(HGM)与Barrett食管(BE)患者在症状、内镜下表现、组织病理学、Hp感染以及细胞角蛋白染色方面的差异.方法 选择对2004年2月-2005年9月明确诊断的BE患者152例(BE组)、食管高位HGM患者52例(食管高位HGM组),收集两组患者临床资料,总结各组患者的症状特点、各型黏膜的常规内镜下和放大内镜下特点;比较各型黏膜的组织病理学结果,快速尿酶法及Warthin-Starry银染检测病灶部位及胃窦部Hp感染情况,免疫组化法检测细胞角蛋白CK7、CK20、CK13及CK19的表达情况.结果 BE组有反流症状者占64.5%(98/152),显著高于食管高位HGM组的(13.5%,7/52)(χ2=40.36,P<0.01).放大内镜下BE黏膜小凹表现为点状46例、条纹状65例、绒毛状41例,而食管异位胃黏膜的小凹全表现为条纹状.组织病理学分型上,152例BE患者中属胃底型56例、交界型39例、特殊肠化型57例;而52例食管高位HGM患者中31例为胃底型、16例为交界型、5例为胃窦腺型,无一例发现有杯状细胞.BE黏膜中中、重度炎症细胞浸润所占比例为63.2%(96/152),显著高于食管异位胃黏膜的28.8%(15/52)(P<0.01);而两组胃窦部中、重度炎症细胞浸润所占比例分别为44.7%(68/152)、51.9%(27/52),差异无统计学意义(P>0.05).BE黏膜Hp检出率为32.2%(49/152),BE组胃窦部黏膜Hp检出率为48.0%(73/152);食管异位胃黏膜Hp检出率为44.2%(23/52),食管高位HGM组胃窦部黏膜Hp检出率为40.4%(21/52);两组Hp感染检出率差异均无统计学意义(P>0.05).细胞角蛋白免疫组化检测中,食管异位胃黏膜以及正常的食管鳞状上皮中无CK7的阳性表达,而BE黏膜的3种类型的上皮中均有表达;CK20和CK19在BE黏膜和食管异位胃黏膜中均有阳性表达;CK13作为鳞状上皮特异性的标志,在部分胃型化生(55/95)和肠化型(29/57)的BE上皮中均可见阳性表达,而在食管异位胃黏膜中则不表达.结论 HGM与BE在有无反流症状、放大内镜下表现、组织病理学类型以及角蛋白染色上存在一定的差异,了解这些差异有利于两者的鉴别.
目的 探討食管高位胃黏膜異位(HGM)與Barrett食管(BE)患者在癥狀、內鏡下錶現、組織病理學、Hp感染以及細胞角蛋白染色方麵的差異.方法 選擇對2004年2月-2005年9月明確診斷的BE患者152例(BE組)、食管高位HGM患者52例(食管高位HGM組),收集兩組患者臨床資料,總結各組患者的癥狀特點、各型黏膜的常規內鏡下和放大內鏡下特點;比較各型黏膜的組織病理學結果,快速尿酶法及Warthin-Starry銀染檢測病竈部位及胃竇部Hp感染情況,免疫組化法檢測細胞角蛋白CK7、CK20、CK13及CK19的錶達情況.結果 BE組有反流癥狀者佔64.5%(98/152),顯著高于食管高位HGM組的(13.5%,7/52)(χ2=40.36,P<0.01).放大內鏡下BE黏膜小凹錶現為點狀46例、條紋狀65例、絨毛狀41例,而食管異位胃黏膜的小凹全錶現為條紋狀.組織病理學分型上,152例BE患者中屬胃底型56例、交界型39例、特殊腸化型57例;而52例食管高位HGM患者中31例為胃底型、16例為交界型、5例為胃竇腺型,無一例髮現有杯狀細胞.BE黏膜中中、重度炎癥細胞浸潤所佔比例為63.2%(96/152),顯著高于食管異位胃黏膜的28.8%(15/52)(P<0.01);而兩組胃竇部中、重度炎癥細胞浸潤所佔比例分彆為44.7%(68/152)、51.9%(27/52),差異無統計學意義(P>0.05).BE黏膜Hp檢齣率為32.2%(49/152),BE組胃竇部黏膜Hp檢齣率為48.0%(73/152);食管異位胃黏膜Hp檢齣率為44.2%(23/52),食管高位HGM組胃竇部黏膜Hp檢齣率為40.4%(21/52);兩組Hp感染檢齣率差異均無統計學意義(P>0.05).細胞角蛋白免疫組化檢測中,食管異位胃黏膜以及正常的食管鱗狀上皮中無CK7的暘性錶達,而BE黏膜的3種類型的上皮中均有錶達;CK20和CK19在BE黏膜和食管異位胃黏膜中均有暘性錶達;CK13作為鱗狀上皮特異性的標誌,在部分胃型化生(55/95)和腸化型(29/57)的BE上皮中均可見暘性錶達,而在食管異位胃黏膜中則不錶達.結論 HGM與BE在有無反流癥狀、放大內鏡下錶現、組織病理學類型以及角蛋白染色上存在一定的差異,瞭解這些差異有利于兩者的鑒彆.
목적 탐토식관고위위점막이위(HGM)여Barrett식관(BE)환자재증상、내경하표현、조직병이학、Hp감염이급세포각단백염색방면적차이.방법 선택대2004년2월-2005년9월명학진단적BE환자152례(BE조)、식관고위HGM환자52례(식관고위HGM조),수집량조환자림상자료,총결각조환자적증상특점、각형점막적상규내경하화방대내경하특점;비교각형점막적조직병이학결과,쾌속뇨매법급Warthin-Starry은염검측병조부위급위두부Hp감염정황,면역조화법검측세포각단백CK7、CK20、CK13급CK19적표체정황.결과 BE조유반류증상자점64.5%(98/152),현저고우식관고위HGM조적(13.5%,7/52)(χ2=40.36,P<0.01).방대내경하BE점막소요표현위점상46례、조문상65례、융모상41례,이식관이위위점막적소요전표현위조문상.조직병이학분형상,152례BE환자중속위저형56례、교계형39례、특수장화형57례;이52례식관고위HGM환자중31례위위저형、16례위교계형、5례위위두선형,무일례발현유배상세포.BE점막중중、중도염증세포침윤소점비례위63.2%(96/152),현저고우식관이위위점막적28.8%(15/52)(P<0.01);이량조위두부중、중도염증세포침윤소점비례분별위44.7%(68/152)、51.9%(27/52),차이무통계학의의(P>0.05).BE점막Hp검출솔위32.2%(49/152),BE조위두부점막Hp검출솔위48.0%(73/152);식관이위위점막Hp검출솔위44.2%(23/52),식관고위HGM조위두부점막Hp검출솔위40.4%(21/52);량조Hp감염검출솔차이균무통계학의의(P>0.05).세포각단백면역조화검측중,식관이위위점막이급정상적식관린상상피중무CK7적양성표체,이BE점막적3충류형적상피중균유표체;CK20화CK19재BE점막화식관이위위점막중균유양성표체;CK13작위린상상피특이성적표지,재부분위형화생(55/95)화장화형(29/57)적BE상피중균가견양성표체,이재식관이위위점막중칙불표체.결론 HGM여BE재유무반류증상、방대내경하표현、조직병이학류형이급각단백염색상존재일정적차이,료해저사차이유리우량자적감별.
Objective To evaluate the differences, including clinical symptoms, endoscopic and histopathologic findings, status of Helicobacter pylori (Hp) infection and cytokeratin (CK) expressions, be-tween Barrett esophagus (BE) and heterotopic gastric mucosa (HGM) in upper esophagus. Methods Clinical data of 152 patients with BE and 52 patients with HGM in upper esophagus diagnosed from February 2004 to September 2005 were retrospectively studied. The parameters being compared include-ed clinical manifestations, conventional and magnifying endoscopic findings, histopathological findings, Hp infection determined by rapid urease test and Warthin-Starry staining and expression of CK phenotypes detec-ted by immunohistochemistry. Results Gastro-esophngeal reflux was observed in 64. 5% of patients with BE (98/152), higher than that in patients with HGM ( 13.5%, 7/52, χ2 = 40. 36, P < 0. 01 ). Endoscopic faveolus of BE mucosa included 46 cases of spot pattern, 65 striations and 41 villiform patterns, while those of HGM were all striation patterns. The histologic classification in BE included 56 cases of fundic type, 39 junction type and 57 specialized intestinal metaplasia, while in HGM mucesa, 31 cases of fundic type, 16 junction type and 5 antrum type were diagnosed, and no goblet cells were found. Moderate and severe infil-tration of inflammatory cells in BE mucosa was 63.2% (96/152), which was significantly higher than that in HGM mucosa (15/52, 28. 8%, P<0. 01). However, no difference was found in gastric antrum inflam-mation between the two groups (44.7%, 68/152, vs. 51.9%, 27/52, P>0.05). No difference was ob-served in prevalence of Hp infection between BE and HGM groups (P >0. 05 ), either in involved mucosa or in antrum. CK7 was not expressed in HGM or normal squamons mucosa, but was expressed in BE. CK20 and CK19 were expressed in both HGM and BE, and CK13 expression was found in some BE nmcosa including gas-tric metaplesia (55/95) and intestinal metaplasia (29/57) but not in HGM mucosa. Conclusion There are differences between HGM and BE, in regarding of reflux symptoms, magnifying endoscopic findings, histo-logical types and CKs expressions, which may be indicators to make differential diagnosis.
