门静脉高压性胃病病理分析

目的　探讨门脉高压性胃病 (portal hypertensive gastropathy,PHG)的病理特点 ,分析对 PHG的影响因素。方法　对 85例乙型肝炎后肝硬化 PHG患者 (PHG组 )的胃黏膜活检组织进行幽门螺杆菌 (Helico-bacter pylori,HP)特殊染色 ,乙型肝炎病毒 (hepatitis virus B;H BV)表面抗原 (HBs Ag)和核心抗原 (HBc Ag)免疫组织化学染色 ,光、电镜下观察 ;同时对 PHG组患者肝组织进行 HBs Ag和 HBc Ag免疫组织化学染色。对照组 4 0例慢性胃炎患者胃黏膜活检组织光、电镜下观察 ,幽门螺杆菌特殊染色。结果　胃黏膜血管扩张、内皮细胞连接松散、黏膜上皮和间质水肿等血管病变是 PHG共同的病理改变。PHG组幽门螺杆菌感染率为 77.8% (6 6 / 85 ) ,部分病例壁细胞增生 (2 4 / 85 ) ,胃黏膜乙型肝炎病毒 HBs Ag和 HBc Ag免疫组织化学染色均为阴性 ,肝组织免疫组织化学染色 ,HBs Ag阳性 80例 (94 % ) ,HBc Ag阳性 83例 (98% ) ;对照组幽门螺杆菌感染率为 30 % ,PHG组显著高于对照组 (P<0 .0 0 5 )。结论　 PH G有其较特征性的病理改变 ,幽门螺杆菌感染和高胃酸可能是影响 PHG的重要因素。 HBV感染对 PHG影响的证据不足 ,有待于进一步研究。

Pathological analysis of portal hypertensive gastropathy

Objective To explore the pathological characters of portal hypertensive gastropathy (PHG),and to analyse the affecting factors to PHG.Methods Gastric mucosal tissues from 85 patients with PHG (PHG group) were observed under light and electron microscopes,and immunohistochemical and special staining were also performed.In the meantime,all hepatic tissues from this group received immunohistochemical staining for HBsAg and HBcAg.In contrast with PHG group,gastric mucosal tissues from 40 cases with chronic gastritis (control grpup) were observed under light and electron microscopes,special staining was also performed.Results Vasodilatation of the gastric mucosa,loose connection of endotheliocytes,mucosa-epithelial and interstitial edema were the common pathological changes of PHG;Helicobacter pylori (HP) infection rate was 77.8% in PHG group;Some cases had oxyntic cell hyperplasia;Immunohistochemical staining of HBsAg and HBcAg was negative in the gastric mucosa;the positive rates of HBsAg and HBcAg by immunohistochemical staining in hepatic tissues were 94% and 98%,respectively.The HP infection rate of control group was 30%,but that of PHG group was obviously higher (P<0 05).Conclusion PHG has its own relative pathological characters,HP infection and hyperchlorhydria may be two important affecting factors to PHG.But there are no evidences to prove that hepatitis virus B (HBV) joined in the course of PHG.