放大内镜下胃黏膜微细结构形态与组织病理学的关系
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摘要
背景与目的：目前常规电子内镜检查对绝大部分消化道疾患均能作出准确的诊断，但对一些微细病变，则不易察觉，容易漏诊。放大内镜随着放大倍数的增加、清晰度的提高和可操作性的增强，近年已开始进入临床。放大内镜的放大倍数与实体显微镜相当，可以观察黏膜的腺体开口(小凹)、微小血管及绒毛等改变。目前，国外特别是日本有关放大内镜的临床应用研究已有较多报道，但主要集中在结肠和食管方面，而对胃的研究较少。国内有关放大内镜在胃方面的研究仅见个别报道。本文对140例慢性胃炎患者的放大内镜下胃黏膜微细结构形态与组织病理学及幽门螺杆菌(Hp)感染的相关性进行了研究，以探讨放大内镜对胃黏膜微细病变的临床诊断价值。
方法：随机选择2002年6月-2002年8月在我科内镜室行胃镜检查的140例慢性胃炎患者，用Olympus GIF Q-240Z新型放大内镜先行常规胃镜检查，再通过手动变焦进行放大观察，对胃小凹和胃体下部前壁集合静脉的形态进行分型。在放大观察的部位取活检作组织病理学检查和Hp检测。组织病理学检查除HE染色外，同时对肠化粘膜进行黏液组化(AB/PAS和AF/AB)染色和分型，并随机选取每型小凹组织各10例，采用PCNA抗体免疫组化方法测定细胞增殖指数。Hp检测采用快速尿素酶和Warthin-Starry银染色法。比较研究、分析放大内镜微细结构形态与组织病理学的相互关系。
结果：(1)胃黏膜小凹形态可分为A型(点状)、B型(短棒状)、C型(树枝状)、D型(斑块状)及E型(绒毛状)五种基本类型，A型仅出现于胃体和胃底，一般没有明显的炎症等病变；B型主要分布没有明显炎症等病变的胃窦部；C型见于有炎症、水肿及肠化等病变的黏膜；D型见于有明显炎症、水肿及肠化的区域，以及糜烂的周边；E型仅出现于肠化区域。小凹形态在以上五型基础上，可有相互重叠和交叉。
(2) 萎缩性胃炎在放大内镜下有比较明显的特征性改变：用较低放大倍数观察时，可见黏膜红白相间明显，再放大观察，可见白区增多，白区内小凹结构紊乱、数量减少甚至消失。放大内镜对萎缩性胃炎的检出率94.3%(33/35)明显高于未放大观察时的22.9%(8/35)(p<0.01)。
(3) 肠化生的小凹形态主要有C、D和E型。31例肠化C型小凹5例，D型8例，E型18例。其中，E型具有很高特异性，18例E型区标本病理证实均存在肠化。并
发现肠化的小凹分型与黏液组化分型之间有一定相关性。18例完全型肠化中有14例(77.8%)呈E型，而13例不完全型肠化则只有4例(30.8%)呈E型( P<0.01)。
(4) 胃体下部集合静脉形态可分为R型(规则型)、I型(不规则型)及D型(消失型)。三种类型的Hp感染率分别为12.2%(9/74)、60%(9/15)和84.3%(43/51)，D型和I型的Hp感染率明显增高(P<0.01)。
(5) 五型小凹对应的增殖指数(%)以均数±标准差(±SD)表示分别如下：A型 6.96±2.35；B型9.26±4.62；C型11.12±5.37；D型13.40±4.88；E型14.67±5.56。E型和D型小凹的增殖指数明显高于A型(P<0.05)。
结论：(1)放大内镜下的胃小凹形态与组织病理学密切相关，A型和B型小凹分别是正常胃体底和胃窦部小凹的表现，而C、D和E型小凹则多为有病变黏膜小凹的形态。
(2) 放大内镜下集合静脉形态与Hp感染密切相关，绝大多数无Hp感染的胃黏膜的集合静脉呈蜘蛛样规则性分布，而Hp感染后的集合静脉则呈不规则性分布或消失。
(3) 放大内镜对萎缩性胃炎有很高的检出率和准确性，黏膜萎缩表现为小凹减少、稀疏，甚至消失呈疤痕样改变。
(4) 不同类型小凹不仅反映其组织病理学背景的不同，而且也反映其黏液分泌功能和增殖能力的差异。E型小凹可能是完全型肠化的特征性表现，D型和E型小凹的增殖活性明显增加。
Background and Aims Recently, magnifying endoscope has been used clinically for its developments in amplifying power, definition and operational capability. Lots of international studies on clinical application of magnifying endoscope especially from Japan have been reported, but most of them were focused on colon and esophagus, only a few of them on gastric mucosa have been published. In this article, we reported our study on correlation of magnifying endoscopic patterns and histopathology, Helicobacter pylori (Hp) infection of the gastric mucosa in 140 patients with chronic gastritis to understand the value of magnifying endoscopy in diagnosing the minute lesions of gastric mucosa.
Materials and Methods Gastric mucosal patterns in 140 patients with chronic gastritis were studied using Olympus GIF-Q240Z magnifying endoscope. Histopathological examination,including mucin histochemistry and PCNA immunohistochemistry and Hp detection,including rapid urease test and Warthin-Starry staining were taken with biopsy samples from the magnified sites of stomach. The magnifying endoscopic patterns were compared with histopathological results and Hp detection.
Results The pit patterns of gastric mucosa were classified as follows: types A (round spot), B (short rod), C (branched), D (reticular) and E (villus). The detection rate of chronic atrophic gastritis by magnifying endoscopy was 94.3%(33/35), which was significantly higher than that by routine endoscopy (22.9%, 8/35)(P<0.01). The pit patterns of 31 cases with intestinal metaplasia (IM) appeared as type E in 18 cases (58.1%), type D in 8 cases (25.8%) and type C in 5 cases (16.1%). Fourteen of 18 cases (77.8%) with complete type of IM appeared as type E of pit patterns , whereas only 4 of 13 (30.8%)cases with incomplete type of IM appeared as the type E (P<0.05).Collecting venules in the anterior of lower part of gastric corpus were subgrouped into: type R(regular), I(irregular) and D(disappeared). Hp infection were found in 12.2%(9/74), 60%(9/15) and 84.3%(43/51) cases in these types respectively. Hp infection rate in type R was significantly lower than that of other two types (P<0.01). The percentage of PCNA-labeling proliferation index was found in type E (14.67±5.56) and type D (13.40±4.88) of gastric pits, which was significantly higher than that in
type A (6.96±2.35) (P<0.05).
Conclusion ①The classification of gastric pits by magnifying endoscopy reflects not only morphological features but also histological features. Type A and type B represent the normal pits of corpus and antrum respectively.The other three appear in abnormal mucosa, among them Type E only appears in the mucosa with IM. ②The architecture of collecting venules is closely related to Hp infection. Most mucosa without Hp infection have regular spider-like and jellyfish-like arrangement of collecting venules (type R).Whereas the mucosa with Hp infection appeared as irregular arrangement (type I) or disappearance (type D) of collecting venules.③ Under magnifying endoscopy, disordered structures, deficiency and even disappearance of gastric pits are of high detection rate and accuracy for atrophic gastritis.④Different types of gastric pits have difference not only in histological features but also in capability of mucus secretion and proliferation. Type E may be a characteristic appearance of the mucosa with complete IM. And pits of type D and type E may have higher activity of cell proliferation.
方法：随机选择2002年6月-2002年8月在我科内镜室行胃镜检查的140例慢性胃炎患者，用Olympus GIF Q-240Z新型放大内镜先行常规胃镜检查，再通过手动变焦进行放大观察，对胃小凹和胃体下部前壁集合静脉的形态进行分型。在放大观察的部位取活检作组织病理学检查和Hp检测。组织病理学检查除HE染色外，同时对肠化粘膜进行黏液组化(AB/PAS和AF/AB)染色和分型，并随机选取每型小凹组织各10例，采用PCNA抗体免疫组化方法测定细胞增殖指数。Hp检测采用快速尿素酶和Warthin-Starry银染色法。比较研究、分析放大内镜微细结构形态与组织病理学的相互关系。
结果：(1)胃黏膜小凹形态可分为A型(点状)、B型(短棒状)、C型(树枝状)、D型(斑块状)及E型(绒毛状)五种基本类型，A型仅出现于胃体和胃底，一般没有明显的炎症等病变；B型主要分布没有明显炎症等病变的胃窦部；C型见于有炎症、水肿及肠化等病变的黏膜；D型见于有明显炎症、水肿及肠化的区域，以及糜烂的周边；E型仅出现于肠化区域。小凹形态在以上五型基础上，可有相互重叠和交叉。
(2) 萎缩性胃炎在放大内镜下有比较明显的特征性改变：用较低放大倍数观察时，可见黏膜红白相间明显，再放大观察，可见白区增多，白区内小凹结构紊乱、数量减少甚至消失。放大内镜对萎缩性胃炎的检出率94.3%(33/35)明显高于未放大观察时的22.9%(8/35)(p<0.01)。
(3) 肠化生的小凹形态主要有C、D和E型。31例肠化C型小凹5例，D型8例，E型18例。其中，E型具有很高特异性，18例E型区标本病理证实均存在肠化。并
发现肠化的小凹分型与黏液组化分型之间有一定相关性。18例完全型肠化中有14例(77.8%)呈E型，而13例不完全型肠化则只有4例(30.8%)呈E型( P<0.01)。
(4) 胃体下部集合静脉形态可分为R型(规则型)、I型(不规则型)及D型(消失型)。三种类型的Hp感染率分别为12.2%(9/74)、60%(9/15)和84.3%(43/51)，D型和I型的Hp感染率明显增高(P<0.01)。
(5) 五型小凹对应的增殖指数(%)以均数±标准差(±SD)表示分别如下：A型 6.96±2.35；B型9.26±4.62；C型11.12±5.37；D型13.40±4.88；E型14.67±5.56。E型和D型小凹的增殖指数明显高于A型(P<0.05)。
结论：(1)放大内镜下的胃小凹形态与组织病理学密切相关，A型和B型小凹分别是正常胃体底和胃窦部小凹的表现，而C、D和E型小凹则多为有病变黏膜小凹的形态。
(2) 放大内镜下集合静脉形态与Hp感染密切相关，绝大多数无Hp感染的胃黏膜的集合静脉呈蜘蛛样规则性分布，而Hp感染后的集合静脉则呈不规则性分布或消失。
(3) 放大内镜对萎缩性胃炎有很高的检出率和准确性，黏膜萎缩表现为小凹减少、稀疏，甚至消失呈疤痕样改变。
(4) 不同类型小凹不仅反映其组织病理学背景的不同，而且也反映其黏液分泌功能和增殖能力的差异。E型小凹可能是完全型肠化的特征性表现，D型和E型小凹的增殖活性明显增加。
Background and Aims Recently, magnifying endoscope has been used clinically for its developments in amplifying power, definition and operational capability. Lots of international studies on clinical application of magnifying endoscope especially from Japan have been reported, but most of them were focused on colon and esophagus, only a few of them on gastric mucosa have been published. In this article, we reported our study on correlation of magnifying endoscopic patterns and histopathology, Helicobacter pylori (Hp) infection of the gastric mucosa in 140 patients with chronic gastritis to understand the value of magnifying endoscopy in diagnosing the minute lesions of gastric mucosa.
Materials and Methods Gastric mucosal patterns in 140 patients with chronic gastritis were studied using Olympus GIF-Q240Z magnifying endoscope. Histopathological examination,including mucin histochemistry and PCNA immunohistochemistry and Hp detection,including rapid urease test and Warthin-Starry staining were taken with biopsy samples from the magnified sites of stomach. The magnifying endoscopic patterns were compared with histopathological results and Hp detection.
Results The pit patterns of gastric mucosa were classified as follows: types A (round spot), B (short rod), C (branched), D (reticular) and E (villus). The detection rate of chronic atrophic gastritis by magnifying endoscopy was 94.3%(33/35), which was significantly higher than that by routine endoscopy (22.9%, 8/35)(P<0.01). The pit patterns of 31 cases with intestinal metaplasia (IM) appeared as type E in 18 cases (58.1%), type D in 8 cases (25.8%) and type C in 5 cases (16.1%). Fourteen of 18 cases (77.8%) with complete type of IM appeared as type E of pit patterns , whereas only 4 of 13 (30.8%)cases with incomplete type of IM appeared as the type E (P<0.05).Collecting venules in the anterior of lower part of gastric corpus were subgrouped into: type R(regular), I(irregular) and D(disappeared). Hp infection were found in 12.2%(9/74), 60%(9/15) and 84.3%(43/51) cases in these types respectively. Hp infection rate in type R was significantly lower than that of other two types (P<0.01). The percentage of PCNA-labeling proliferation index was found in type E (14.67±5.56) and type D (13.40±4.88) of gastric pits, which was significantly higher than that in
type A (6.96±2.35) (P<0.05).
Conclusion ①The classification of gastric pits by magnifying endoscopy reflects not only morphological features but also histological features. Type A and type B represent the normal pits of corpus and antrum respectively.The other three appear in abnormal mucosa, among them Type E only appears in the mucosa with IM. ②The architecture of collecting venules is closely related to Hp infection. Most mucosa without Hp infection have regular spider-like and jellyfish-like arrangement of collecting venules (type R).Whereas the mucosa with Hp infection appeared as irregular arrangement (type I) or disappearance (type D) of collecting venules.③ Under magnifying endoscopy, disordered structures, deficiency and even disappearance of gastric pits are of high detection rate and accuracy for atrophic gastritis.④Different types of gastric pits have difference not only in histological features but also in capability of mucus secretion and proliferation. Type E may be a characteristic appearance of the mucosa with complete IM. And pits of type D and type E may have higher activity of cell proliferation.
引文
1. Guelrud M,Herrera I,Essenfeld H,et al.Intestinal Metaplasia of the Gastric Cardia:A Prospective Study With Enhanced Magnification Endoscopy. Am J Gastroenterol,2002;97:584-589.
2. 周丽雅,李建辉,林三仁,等.胃黏膜肠上皮化生的内镜分析.中华消化内镜杂志 2001;18(2 ):84-86.
3. 金宣真,春间贤,伊藤工训，等.上消化管扩大内视镜检查组织学的胃炎の诊断に有用でする-Helicobacter pylori除菌判定の试み.Gastroenterol Endosc,2001;43(suppl.1):633.
4. 中川,宗一,加藤,等.扩大内视镜观察にょる胃炎の诊断. Gastroenterol Endosc , 2001; 43 (suppl.1):633.
5. Sakaki N, Iida Y, Okazaki Y et al. Magnifying endoscopic observation of gastric mucosa, particularly in patients with atrophic gastritis. Endosc 1978;10:269-74.
6. Sakaki N, Iida Y, Saito M et al. New magnifying endoscopic classification of the fine gastric mucosa pattern. Gastroenterol.Endosc. 1980; 22: 377-83.
7. Niwa Y, Goto H, Ohmiya N, et al.Magnifying endoscopy for the diagnosis of early gastric cancer. Dig Endosc.2002;14 (Suppl):70-71.
8. Endo T,Awakawa T,Takahashi H,et al. Classification of Barrett's epithelium by magnifying endoscopy. Gastrointest Endosc.2002;55(6): 641-7.
9. 王崇文,谢勇,吕农华,等.慢性胃炎的胃镜表现与黏膜组织学改变相关性的研究.中华消化内镜杂志.2002;19(1):24-26.
10. 郑京华,魏虹,杨海燕,等.胃黏膜萎缩及伴肠化的可视性诊断.潍坊医学院学报 2001;23(2 ):116-117.
11. Jass JR.Role of intestinal metaplasia in the histogenesis of gastric carcinoma. J Clin Pathol;1980,33:801.
12. Kumagai Y,Inoue H,Nagai K,et al. Magnifying endoscopy, stereoscopic microscopy, and the microvascular architecture of superficial esophageal carcinoma. Endoscopy, 2002;34(5):369-75.
13. Haruhiro I. Magnification endoscopy in the esophagus and stomach. Dig Endosc. 2001;13(Suppl.):40-41.
Yagi K,Nakamura A,Sekine A，et al.Comparison Between Magnifying Endoscopy and Histological,Culture and Urease Test Findings from the Gastric Mucosa of the
14. Corpus.Endoscopy 2002;34:376-381.
15. 于永征,王青釭,于中麟. 高清晰放大内镜对幽门螺杆菌相关性胃炎胃黏膜表现的临床研究. 中华消化内镜杂志 2002;19(5):274-277.
16. Tobita K. Study on minute surface structure of the depressed-type early gastric cancer with magnifying endoscopy.Dig Endosc,2001;13:121-6.
17. Yao K,Oishi T. Microgastroscopic findings of mucosal microvascular architecture as visualized by magnifying endoscopy. Dig Endosc,2001;13 (Suppl): 27-33.
18. Yagi K, Nakamura A, Sekine A. et al. Characteristic endoscopic and magnified endoscopic findings in the normal stomach without Helicobacter pylori infection.J Gastroenterol Hepatol. 2002 ;17(1):39-45.
2. 周丽雅,李建辉,林三仁,等.胃黏膜肠上皮化生的内镜分析.中华消化内镜杂志 2001;18(2 ):84-86.
3. 金宣真,春间贤,伊藤工训，等.上消化管扩大内视镜检查组织学的胃炎の诊断に有用でする-Helicobacter pylori除菌判定の试み.Gastroenterol Endosc,2001;43(suppl.1):633.
4. 中川,宗一,加藤,等.扩大内视镜观察にょる胃炎の诊断. Gastroenterol Endosc , 2001; 43 (suppl.1):633.
5. Sakaki N, Iida Y, Okazaki Y et al. Magnifying endoscopic observation of gastric mucosa, particularly in patients with atrophic gastritis. Endosc 1978;10:269-74.
6. Sakaki N, Iida Y, Saito M et al. New magnifying endoscopic classification of the fine gastric mucosa pattern. Gastroenterol.Endosc. 1980; 22: 377-83.
7. Niwa Y, Goto H, Ohmiya N, et al.Magnifying endoscopy for the diagnosis of early gastric cancer. Dig Endosc.2002;14 (Suppl):70-71.
8. Endo T,Awakawa T,Takahashi H,et al. Classification of Barrett's epithelium by magnifying endoscopy. Gastrointest Endosc.2002;55(6): 641-7.
9. 王崇文,谢勇,吕农华,等.慢性胃炎的胃镜表现与黏膜组织学改变相关性的研究.中华消化内镜杂志.2002;19(1):24-26.
10. 郑京华,魏虹,杨海燕,等.胃黏膜萎缩及伴肠化的可视性诊断.潍坊医学院学报 2001;23(2 ):116-117.
11. Jass JR.Role of intestinal metaplasia in the histogenesis of gastric carcinoma. J Clin Pathol;1980,33:801.
12. Kumagai Y,Inoue H,Nagai K,et al. Magnifying endoscopy, stereoscopic microscopy, and the microvascular architecture of superficial esophageal carcinoma. Endoscopy, 2002;34(5):369-75.
13. Haruhiro I. Magnification endoscopy in the esophagus and stomach. Dig Endosc. 2001;13(Suppl.):40-41.
Yagi K,Nakamura A,Sekine A，et al.Comparison Between Magnifying Endoscopy and Histological,Culture and Urease Test Findings from the Gastric Mucosa of the
14. Corpus.Endoscopy 2002;34:376-381.
15. 于永征,王青釭,于中麟. 高清晰放大内镜对幽门螺杆菌相关性胃炎胃黏膜表现的临床研究. 中华消化内镜杂志 2002;19(5):274-277.
16. Tobita K. Study on minute surface structure of the depressed-type early gastric cancer with magnifying endoscopy.Dig Endosc,2001;13:121-6.
17. Yao K,Oishi T. Microgastroscopic findings of mucosal microvascular architecture as visualized by magnifying endoscopy. Dig Endosc,2001;13 (Suppl): 27-33.
18. Yagi K, Nakamura A, Sekine A. et al. Characteristic endoscopic and magnified endoscopic findings in the normal stomach without Helicobacter pylori infection.J Gastroenterol Hepatol. 2002 ;17(1):39-45.