HP根治前后胃粘膜Gas、SS、SP变化及G、D、EC_1细胞图像定量研究

该研究旨在探讨HP感染的慢性胃炎和消化性溃疡患者HP根治前后胃粘膜中胃肠激素Gas、SS、SP及G、D、EC1细胞变化和其相关性。方法 :1997年 3月～ 1999年 12月对 10 2例HP感染的病人 ,HP根治前后分别用放射免疫法及免疫组化染色图像定量分析Gas、SS、SP含量和G、D、EC1细胞密度、灰度。结果 :HP阳性的三组病人经药物治疗根治后胃粘膜Gas含量均较治疗前明显降低 (P <0 .0 1) ,SS、SP含量较治疗前升高 (P<0 .0 1,P <0 .0 5 )。图像定量分析示HP根治前后胃粘膜G、D、EC1细胞密度显著降低 (P <0 .0 5 ) ,D、EC1细胞灰度增加 (P <0 .0 5 )。结论 :三组病人HP根除后胃粘膜Gas减少 ,G细胞灰度降低 ,SS、SP升高 ,D、EC1细胞灰度增加 ,细胞分泌颗粒变化与粘膜相应激素变化呈正相关。提示HP感染干扰了这些激素分泌释放的调控 ,可能是HP相关性胃炎和消化性溃疡的发病机制之一。根除HP后SS、SP升高 ,Gas降低纠正HP感染所致的这些激素分泌释放紊乱 ,可能是HP根除后溃疡复发率降低的原因之一。在HP根除前SP ,EC1细胞灰度降低 ,根除后升高 ,提示SP抑制胃泌素分泌释放 ,而对生长抑素无抑制作用 ,具有胃粘膜保护功能。

CHANGES OF GASTRIN,SOMATOSTATIN,AND SUBSTANCE P IN GASTRIC MUCOSA AND QUANTITATIVE STUDY ON CYTOGRAPHY OF G-,D-AND EC_1-CELL BEFORE AND AFTER THERAPY FOR HELICOBACTER PYLORI ERADICATION

Objective:To study changes of gastrin (Gas),somatostatin (SS) and substance P(SP) and cytography of G-,D-and EC 1-cell in Helicobacter Pylori(HP)-infected gastric muccosa of patients with chronic gastritis and peptic ulcer before and after theray for HP eradication and their correlations.Methods:Form March 1997 to December 1999,102 HP-infected patients were measured by radioimmunoassay for Gas,SS and SP content in gastric mucosa and quantitairely analyzed by immunochistochemistry for density and brightness of G-,D-and EC 1-cell of gastric mucosa before and after therapy for HP eradication.All patients were divided into 3 groups:35 cases of active chronic superficial gastritis (ACSG),35 active duodenal ulcer (DU) and active gastric ulcer (GU). Results:In the 3 groups,the Gas content after therapy was significantly lower than that before therapy(P<0.01),while SS,SP content increased after therapy (P<0.01 for SS,P<0.05 for SP).The respective density of G-,D-and EC 1-cell had no significant differernces before and after therapy.The brightness of D- and EC 1-cell increased significantly after therapy (P<0.05),while that of G-cell decreased after therapy (P<0.05).There were positve correlations between changes of cellular excretory granulae and levels of their respective hormone in gastric mucosa for all of the 3 groups.Conclusions:Pathocrinia of these hormone due to HP infection may be one of the pathogenic mechanisms of gastritis and peptic ulcer associated with HP infection.Rectification of the pathocrinia may contribute to the lowered recurrence rate of peptic ulcer after therapy for HP eradication.It is suggested that SP has a protective function for gastric mucosa by inhibitting the excretion of Gas instead of SS.