胃癌前病变与幽门螺杆菌感染

Gastric preneoplastic lesions and Helicobacter pylori infection.

目的 了解胃癌前病变组织 Hp感染状况。方法 采用美蓝染色检测 12 6例慢性浅表性胃炎 ( CSG)、88例慢性萎缩性胃炎 ( CAG)、73例肠上皮化生 ( IM)、3 2例不典型增生 ( Dys)胃粘膜 Hp感染状况。观察胃粘膜炎症反应程度。结果 Hp感染率在 CAG( 65 .9% )、IM( 63 .0 % )、Dys( 62 .5 % )组显著高于 CSG ( 4 2 .1% )组 ( P<0 .0 5 ;P <0 .0 1,P<0 .0 1) ;轻度及中度 CAG( 78.9% ,70 .4 % )显著高于重度 CAG组 ( 3 9.1% ) ( P<0 .0 1,P<0 .0 5 ) ;轻度及中度 IM( 80 % ,69.6% )显著高于重度 IM组 ( 3 0 % ) ( P<0 .0 1)。胃粘膜单个核细胞、分叶核细胞浸润程度 Hp阳性组较 Hp阴性组显著增多 ( P<0 .0 1)。结论 Hp感染引起胃粘膜炎症反应 ,在胃癌前病变的发生中起着重要作用。随着胃粘膜萎缩和肠化的加重 ,Hp难于生存 ,其致病性减弱。

Objective To examine Helicobacter pylori(Hp)infection in gastric preneoplastic lesions tissues so as to study the relationship between Hp infection and gastric preneoplastic lesions.Methods Methylene blue staining was used to detect Hp in gastric mucosa from 126 cases of chronic superficial gastritis(CSG),88 cases of chronic atrophic gastritis(CAG),73 cases of intestinal metaplasia(IM) and 32 cases of dysplasia(Dys).Histopathological study was conducted to evaluate the level of inflammatory response.Results The rates of Hp infection in CAG(65.9%),IM(63%) and Dys(62.5%)were significantly higher than that in CSG(42.1%).The rates of Hp infection in mild and moderate CAG(78.9%,70.4%)were significantly higher than that in severe CAG(39.1%)( P <0 01, P <0 05).The rates of Hp infection in mild and moderate IM(80%,69.6%)were significantly higher than that in severe IM(30%)( P <0 01).Higher scores of mononuclear and polymorphonuclear cells in gastric mucosa were observed in Hp positiive group than in Hp negative group( P <0.01).Conclusion Hp infection can cause a more signficant inflammatory response,and this plays an important role in the genesis of gastric preneoplastic lesion.With the development of CAG and IM,Hp infection rates become lower and its pathogenicity is weakened.