隆起糜烂性胃炎脾胃湿热证与胃粘膜G细胞、D细胞、壁细胞的相关性研究
详细信息    本馆镜像全文|  推荐本文 |  |   获取CNKI官网全文
摘要
目的:通过观察隆起糜烂性胃炎(raised erosive gastritis, REG)脾胃湿热证、脾胃虚弱证及正常对照组胃粘膜G细胞、D细胞、壁细胞数目以及G、D细胞数目比值(G/D),研究三者之间上述指标的差异,初步探讨REG脾胃湿热证与胃酸分泌的关系,为中西医结合防治该病提供临床及理论依据。
     方法:选择REG患者65例,其中符合脾胃湿热证者30例,符合脾胃虚弱证者35例,并设正常对照组11例。所有受试者均空腹行胃镜检查,取胃窦部标本行快速尿素酶试验及组织染色法检测幽门螺旋杆菌(H.pylori,Hp),另取胃窦大弯、胃体大弯粘膜各1块用于免疫细胞化学染色及HE染色,观察G细胞、D细胞、壁细胞数目,计算G/D。
     结果:
     1 REG组、REG Hp阳性(Hp+)组、REG Hp阴性(Hp-)组较正常对照组的G、D细胞数目有下降趋势,但无统计学意义(均P>0.05),G/D比较无统计学意义(P>0.05),而壁细胞数目均非常显著的低于正常对照组(均P<0.01);REG Hp+组与REG Hp-组之间的G、D、壁细胞数目及G/D比较均无统计学意义(均P>0.05);
     2 REG萎缩组、REG非萎缩组较正常对照组的G、D细胞数目有下降趋势,但均无统计学意义(均P>0.05),G/D比较无统计学意义(P>0.05),而壁细胞数目则分别显著和非常显著的低于正常对照组(P<0.05,P<0.01);REG萎缩组与REG非萎缩组之间的G、D、壁细胞数目及G/D比较均无统计学意义(均P>0.05);
     3 REG50岁以上组、REG50岁以下组较正常对照组的G、D细胞数目有下降趋势,但均无统计学意义(均P>0.05),G/D比较无统计学意义(P>0.05),而壁细胞数目则均非常显著的低于正常对照组(均P<0.01);REG50岁以上组和REG50岁以下组之间的G、D、壁细胞数目及G/D比较均无统计学意义(均P>0.05);
     4 REG脾胃湿热证组、脾胃虚弱证组较正常对照组的G、D细胞数目有下降趋势,但均无统计学意义(均P>0.05),G/D比较无统计学意义(P>0.05),而壁细胞数目则分别显著和非常显著的低于正常对照组(P<0.05,P<0.01);脾胃湿热证组和脾胃虚弱证组之间的G、D、壁细胞数目比较均无统计学意义(均P>0.05),而脾胃湿热证组的G/D非常显著的高于脾胃虚弱证组(P<0.01);
     5 REG脾胃湿热证、脾胃虚弱证Hp+组与Hp-之间的G、D、壁细胞数目及G/D比较均无统计学意义(均P>0.05)。
     结论:
     1 REG组壁细胞数目较正常对照组低;
     2 REG组较正常对照组的G、D细胞数目有下降趋势,但无统计学意义;
     3 REG组较正常对照组的G/D无统计学意义;
     4 REG脾胃湿热证组的G/D较脾胃虚弱证组高,但无统计学意义;
     5 REG脾胃湿热证组与脾胃虚弱证组的G、D、壁细胞数目均无统计学意义;
     6针对REG可以尝试以保护胃粘膜为主进行治疗。
Objective:Through the observation of the number of gastric G cells, D cells and parietal cells and the ratio of the number of G and D cells (G/D ratio) in the raised erosive gastritis (REG) with spleen-stomach damp-heat syndrome(SSDHS) and spleen-stomach weakness syndrome(SSWS), as well as the control group, this study aims to investigate the differences among the three groups mentioned above, and explore the relationship between the REG with SSDHS and the gastric acid secretion, furthermore to provide clinical and theoretical bases for REG prevention and treatment with integrated traditional Chinese and Western Medicine.
     Method:This study chose 65 REG patients, which consisted of 30 REG patients with SSDHS and 35 REG patients with SSWS.In addition, a control group with 11 cases were found. All the subjects with fasting for 10 hours received a gastroscopy examination. During the examination, a piece of mucosa collected from the gastric antrum was used to do a rapid urease test and a histological staining, to detect the existence of H.Pylori (Hp). Two pieces of mucosa were also collected, one from the gastric antrum used for immunocytochemical staining, and the other from the gastric body used for HE staining. Finally, the number of gastric G cells, D cells and parietal cells, as well as the G/D ratio were computed.
     Results:
     1 Compared with the control group, the number of the gastric G and D cells in the overall REG group, the REG group with Hp (REG Hp+) and the REG group without Hp (REG Hp") fell.However, significant differences were not found (P>0.05). There were no significant differences in the G/D ratio (P>0.05), either. Whereas, the gastric parietal cells in the three groups mentioned above were significantly fewer than those in the control group (P <0.01). Significant differences were not found (P>0.05) in the number of the gastric G, D and parietal cells as well as the G/D ratio between the REG Hp- group and the REG Hp+ group.
     2 Compared with the control group, the number of the gastric G and D cells in the REG group with mucosa atrophy and the REG group without mucosa atrophy decreased. However, there were no significant differences (P>0.05). Significant differences were not found in the G/D ratio, either(P>0.05). Whereas, the gastric parietal cells in the REG group with mucosa atrophy and the REG group without mucosa atrophy were significantly fewer than those in the control group (P<0.01). There were no significant differences in the number of the gastric G, D and parietal cells as well as the G/D ratio (P>0.05) between the REG group with mucosa atrophy and the REG group without mucosa atrophy.
     3 Compared with the control group, the number of the gastric G and D cells in the over-50-year-old REG group and the under-50-year-old REG group declined. However, there were no significant differences (P>0.05). Significant differences were not found in the G/D ratio, either (P>0.05). Whereas, the gastric parietal cells in the over-50-year-old REG group and the under-50-year-old REG group were significantly fewer than those in the control group (P<0.01). There were no significant differences in the number of the gastric G, D and parietal cells as well as the G/D ratio (P>0.05) between the over-50-year-old REG group and the under-50-year-old REG group.
     4 Compared with the control group, the number of the gastric G and D cells in the REG group with SSDHS and the REG group with SSWS dropped. However, there were no significant differences (P>0.05). Significant differences were not found in the G/D ratio, either (P>0.05). Whereas, the gastric parietal cells in the two groups were significantly fewer than those in the control group (P<0.01). There were no significant differences in the number of the gastric G, D and parietal cells between the REG group with SSDHS and the REG group with SSWS (P>0.05). Nevertheless, the G/D ratio in the REG group with SSDHS was significantly higher than that in the REG group with SSWS (P<0.01).
     5 Significant differences were not found in the number of the gastric G, D and parietal cells,as well as the G/D ratio,between REG Hp+ group and REG Hp- group(P>0.05),both in REG with SSDHS and SSWS.
     Conclusion:
     1 The gastric parietal cells in REG are fewer than those in the control group.
     2 Compared with the the control group, the number of the gastric G and D cells in the REG group decreases. However, significant differences have not been found.
     3 Significant differences have not been found in the G/D ratio between the REG group and the control group.
     4 The G/D ratio in REG with SSDHS is higher than that in REG with SSWS. However, significant differences have not been found.
     5 Significant differences have not been found in the number of the gastric G, D and parietal cells between the REG with SSDHS and the REG with SSWS.
     6 To treat the REG may be implemented on the basis of protecting the gastric mucosa.
引文
[1]夏玉亭,余中麟主编.胃炎临床研究进展(M).第一版.上海科学技术出版社,2003:249.
    [2]柯晓.隆起糜烂性胃炎病理分类和中医临床证候学的研究[C].第二十次全国中西结合消化系统疾病学术会议论文汇编.2008:73.
    [3]金海,於云燕.367例疣状胃炎与幽门螺杆菌及病理关系的探索[J].中华消化杂志,2005,25(8):495.
    [4]周庆南,梁运啸.幽门螺杆菌感染与慢性隆起糜烂性胃炎病理改变探讨.医学文选,2004,23(4):467-468.
    [5]樊代明,陈强.第十届世界胃肠病大会[J].中华消化杂志.1995,15:33.
    [6]邹尤宝,陈哲,潘海波,等.隆起糜烂性胃炎与幽门螺杆菌、胃泌素关系的研究[J].右江民族医学院学报,2004,26(1):15-17.
    [7]牛孝敏,施光亚.38例疣状胃炎临床分析[J].临床医学,2004,24(5):43.
    [8]徐三平,易粹琼,张锦坤.隆起糜烂性胃炎的临床及与酸相关性的研究[J].中华消化内镜杂志,1998,15(4):238.
    [9]RUDZINSKI J, KULA Z,JESA A. Gastric secretion in chronic erosive gastritis[J]. Przegl Lek.1992,49 (5):154.
    [10]杨春波,黄可成,肖丽春等.脾胃湿热证的临床研究--附400例资料分析[J].中医杂志1994,35(7):425-427.
    [11]徐远溪,王志荣.胃粘膜壁细胞功能及其泌酸机制研究进展[J].同济大学学报(医学版),2004,25(2):156-158.
    [12]徐光辉,柏乃运,石碧坚.隆起糜烂性胃炎患者幽门螺杆菌感染与高胃泌素血症的关系[J].中华消化杂志,2001,21(2):121-122.
    [13]王永华,郭荣斌,汪鸿志.疣状胃炎与幽门螺杆菌、胃泌素和表皮生长因子等相关的研究[J].中华消化杂志,1997,17(6):300.
    [14]徐三平,易粹琼.隆起糜烂性胃炎的抑酸及电凝治疗[J].中国内镜杂志,1996,2(3):46-48.
    [15]Arnold R, Eissele R, Frank M. Gastrin. Edited by J.H.Walsh:Raven press. Ltd.New fork,1993.
    [16]周凡,葛振华,王若愚.大鼠胃窦部胃泌素和生长抑素mRNA及其相关蛋白表达的研究[J].解剖学报.1998,29(3):289-292.
    [17]范玉林,杨建明,罗元辉,等.慢性萎缩性胃炎患者幽门螺旋杆菌根除后胃粘膜G细胞数量和血清胃泌素含量的变化[J].胃肠病学,2005,10:93-93.
    [18]Kent KC, Debas HT. Peripheral regulation of gastric acid secretion. In:Johnson LR,ed. Physiology of the gastrointestinal tract.3rd ed. New York:Raven Press,1994,1185-1226.
    [19]Zdon MJ, Ballantyne GH, Schafer DE, et al. Evidence for no gastrinmidiated somatostatin inhibition of parietal cell function. Surgery,1986,100:6954-6960.
    [20]周凡,葛振华,王若愚.大鼠胃窦部胃泌素和生长抑素mRNA及其相关蛋白表达的研究[J].解剖学报.1998,29(3):289-292.
    [21]Lamberts R, Stumnps D, Plumpe L, et al. Somatostatin cells in rat antral mucosa:quantitative ultrastructural analysis in different states of gastric acid secretion. Histochemistry,1991,95(4):373.
    [22]莫剑忠,王承党.胃肠激素对胃运动的调节作用[J].中华消化杂志,2005,25:379-381.
    [23]宋于刚,何燕萍,刘晓霞,等.幽门螺杆菌感染后胃窦部G、D细胞变化的研究[J].解放军医学杂志,2002,27(8):668-690.
    [24]武一曼,葛振华,周凡,等.幽门螺旋杆菌对慢性胃炎患者胃窦黏膜内G、D细胞的影响[J].解剖学报,2004,35(2):220-223.
    [25]郭宏,邵润轩,李葆君,等.胃、十二指肠溃疡中幽门螺杆菌与生长抑素、胃泌素及G、D细胞密度的关系[J].白求恩医科大学学报,1998,24(2):165-166.
    [26]Konturek SJ, Kitler ME. Role of neuropetides in the control of gastric secretio[J]. Scand J Gastroenterol.1986,21:1153.
    [27]王承党,陈玉丽.幽门螺旋杆菌感染对十二指肠溃疡和功能性消化不良患者胃G细胞功能的影响[J].中华消化杂志,2000,20(3),188.
    [28]杨春波,柯晓,李秀娟,等.脾胃湿热证的临床研究[J].福建中医学院学报,1999,9(4):1-6.
    [29]张琳,杨连纹,杨李君.幽门螺旋杆菌与慢性萎缩性胃炎发病关系及防治研究[J].中国中西医结合杂志1992,12(9):621.
    [30]武一曼,葛振华,周凡,等.胃泌素、生长抑素与脾胃湿热证慢性浅表性胃炎的相关性研究[J].中医杂志,2004,45(3):215-216.
    [31]吴娟,田德禄.慢性浅表性胃炎脾胃湿热证胃粘膜G、D细胞变化及胃泌素、生长抑素的表达[J].世界华人消化杂志,2008,16(34):3840-384.
    [32]梁卫江,张万岱.脾虚证的消化吸收功能研究进展[J].中国中西医结合脾胃杂志,1999,7(3):191-192.
    [33]李燕舞,赵想法,王汝俊,等.脾虚大鼠壁细胞酸分泌机制的实验研究[J].中医药学刊,2005,23(6):997-999.
    [34]宋于刚,姚永莉,张万岱.脾虚证与体液胃泌素及生长抑素关系的实验研究[J].现代消化病及内镜杂志,1998,3(3):226-228.
    [35]张万岱,姚永莉,宋于刚.实验脾虚证组织中胃泌素及生长抑素含量变化及其意义[J].现代消化病及内镜杂志,1998,3(4):31-33.
    [36]魏彦明,宗瑞谦,杨孝朴.试验性脾虚证大鼠血浆胃泌素和胃动素含量变化及四君子汤对其调整作用[J].中国兽医学报,2001,21(3):381-382.
    [37]聂克,王汝俊,王建华.脾虚大鼠胃壁细胞胃泌素受体变化规律研究[J].中国中西医结合消化杂志,2002,10(3),157-158.
    [38]赵军宁,王建华,黄衡等.胃泌素受体在脾虚大鼠的异常表达与中药调控作用研究[J].中国中医基础医学杂志,2000,6(5):36-40.
    [39]马建伟,徐丽梅,孟如松,等.脾虚证与血浆和胃窦组织中生长抑素的关系[J].实用中西医结合杂志,1995,8(11):644-645.
    [40]马建伟,徐丽梅,孟如松,等.脾虚证与胃窦粘膜D细胞和G细胞关系的实验研究[J].辽宁中医杂志,1993,(5):41-43.
    [41]智发朝,张万岱,宋于刚.生长抑素与脾虚证关系的研究[J].新消化病学杂志,1993,1(T01):49.
    [42]钟振义.胃粘膜屏障与临床[J].衡阳医学院学报,1990,8(2):126-129.
    [43]徐彩朴,桂先勇,刘为纹,等.幽门螺旋菌对胃粘膜屏障的影响[J].内镜,1991,8(1):13-14.
    [1]崔海涛,常洁,姜孔英.疣状胃炎诊断与治疗的研究进展[J].医学创新研究,2008,5(6):24-26.
    [2]吴天安.九香散治疗疣状胃炎15例[J].实用中医药杂志,2002,18(1):61.
    [3]钱选华,陈慕廉.中药治疗疣状胃炎50例临床观察[J].河北中医,2001,23(11):825.
    [4]马桂香,周君宜.清热解毒为主辨治疣状胃炎101例[J].陕西中医,1995,16(1):5.
    [5]李国安,徐兆山,徐大龙.牡贝消疣汤治疗疣状胃炎68例[J].四川中医,2000,18(2):29.
    [6]葛桂萍.活血化痰散结法治疗疣状胃炎30例[J].山西中医,1999,15(6):14.
    [7]顾庆华.从胃痈论治疣状胃炎[J].中医药研究,1995,5(6):15.
    [8]吴建一.隆起糜烂性胃炎372例中医辨证分析[J].甘肃中医,2004,17(3):11-12.
    [9]于正龙.幽门螺杆菌感染与疣状胃炎100例[J].新消化病学杂志,1997,5(1):64.
    [10]白歌,胡伏莲.疣状胃炎与幽门螺杆菌的关系及其治疗的研究[J].中国内镜杂志,1997,3(1):14-15.
    [11]谭至柔,黄雪.幽门螺杆菌与疣状胃炎关系探讨[J].1临床荟萃,2002,17(21):1259-1260.
    [12]王永华,郭荣斌,汪鸿志.疣状胃炎与幽门螺杆菌、胃泌素和表皮生长因子等相关的研究[J].中华消化杂志,1997,17(5):300.
    [13]徐光辉,柏乃运,石碧坚.隆起糜烂性胃炎患者幽门螺杆菌感染与高胃泌素血症的关系[J].中华消化杂志,2001,21(2):121-122.
    [14]牛孝敏,施光亚.38例疣状胃炎临床分析[J].临床医学,2004,24(5):43.
    [15]邹尤宝,陈哲,潘海波,等.隆起糜烂性胃炎与幽门螺杆菌、胃泌素关系的研究[J].右江民族医学院学报,2004,26(1):15-17.
    [16]徐三平,易粹琼,张锦坤.隆起糜烂性胃炎的临床及与酸相关性的研究[J].中华消化内镜杂志,1998,15(4):238.
    [17]RUDZINSKI J,KULA Z,JESA A.Gastric secretion in chronic erosive gastritis[J]. Przegl Lek.1992,49(5):154.
    [18]ANDRE C,GILLON J,MOULINIER B,et al. Randomised placebo-controlled double-blind trial of two dosages of sodium cromoglycate in treatment of varioliform gastritis: comparison with cimetidine[J].Gut,1982,23(4):348.
    [19]丁西平,王巧民,郑帮海,等.疣状胃炎外周血T淋巴细胞亚群检测及其临床意义[J].临床消化病杂志,2003,15(3):111.
    [20]杨卫文,杨景林.腹型过敏性紫癜15例内镜观察及其与疣状胃炎的关系[J].中国内镜杂志,1997,3(4):74.
    [21]USTUNDAG Y, OKSOZOGLU G, TATAR G, et al. Atopy and food allergy in varioliform gastritis[J]. Clin Gastroenterol,1998,27(3):275.
    [22]李益农,陆星华.消化内镜学[M].北京:科学出版杜,1995:214.
    [23]KOLARSKI V, PETROVA-SHOPOVA K, VASILEVA E, et al. Erosive gastritis and gastroduodenitis-clinical, diagnostic and therapeutic studies[J]. Vutr Boles,1987,26 (3):56-59.
    [24]何国章,贺玉华.136例疣状胃炎临床及相关因素分析[J].中国当代医学,2005,4(5):21-22.
    [25]芦红,建新,景艺.隆起糜烂性胃炎的临床及与幽门螺杆菌感染的相关性研究[J].中国医药指南,2008,6(2):170-171.
    [26]徐洁萍,陆和平,郑银宝,等.胃癌和糜烂性胃炎中细胞增殖、凋亡的改变[J].中华现代临床医学杂志,2005,3(19):1983-1984.

© 2004-2018 中国地质图书馆版权所有 京ICP备05064691号 京公网安备11010802017129号

地址:北京市海淀区学院路29号 邮编:100083

电话:办公室:(+86 10)66554848;文献借阅、咨询服务、科技查新:66554700