摘要
探讨乙型肝炎后肝硬化胃粘膜病变发病因素。 10 2例肝病或非肝病因伴有胃病行胃镜检查的患者 ,取胃窦小弯距幽门周围 ( 2 - 3 )cm处粘膜 3块 ,分别做快速尿素酶试验及嗜伊红、品红染色 ,并行免疫组化检测幽门螺旋杆菌HPlgG型抗原。发现肝硬化组 (LC组 )与慢性肝炎组 (HB组 )有不同程度胃粘膜炎症达 95 5 % ( 42 / 44 )、5 3 6% ( 15 / 2 8) ;前者萎缩、肠化多于后者 (P <0 0 5 )。上述两组乙型肝炎病毒 (HBV)抗原表达率分别为 81 8% ( 3 6/44 )、5 3 6% ( 15 / 2 8) ;前者多于后者 (P <0 0 5 )。与非肝病胃病患者 3 0例相比 ,LC组、HB组HP阳性率无明显差别(P >0 0 5 )。
To investigate the etiology of chronic hepatitis B(HB)post cirrhosis gastritic mucosal lesion.In 102 patients diagnostic endoscopy was performed.Three gastric biopsies were taken within 2-3cm around the pylorus of gastric antra,urease detection,HE fuchsin staining and immunohistochemical analysis of Helicobacter pylori(HP) IgG antigen,HBsAg and HBcAg were performed separately.In cirrhosis group,95.5% of 44 patients (42/44) showed different extent of chronic inflammation of gastric mucosa 92.9%(26/28)in chronic hepatitis B group.In addition to chronic gastric mucous inflammation,the date of existence of gland atrophy or/and intestinal epithelialization is 33.3%(14/42) and 11.5%(3/26)respectively(P<0.05).The positivity of HBVAg in these two groups is 81.8%(36/44)and 53.6%(15/28)respectively(P<0.05).In these two groups the positive rate of HP in inflammatory gastric mucous is 69.0%(29/42)and 76.9%(20/26)respecctively,there is no obvious defference between them. Among the 42 patients with cirrhosis associated gastritis,19 were found to be esophageales varicosis positive,but the other 23 were not,the positivity of HP of these two groups was 73.7%(14/19)and 65.3%(15/23)(P>0.05).The result of analysis of the severity of HB associated gastritis indicated that the portal hypertensive cirrhosis in later stage of liver disease plays an important role in the development of this disease.The relationship between hepatitis B virus and this disease needs further investigation.HP is not the pathogeny of this disease.
出处
《临床肝胆病杂志》
CAS
北大核心
2003年第3期185-187,共3页
Journal of Clinical Hepatology
基金
北京军区重点资助课题 ( 95B0 0 8)
关键词
乙型肝炎
肝硬化
胃粘膜病变
病因
幽门螺杆菌
门脉高压
Hepatitis B virus
Portal hypertension
Gastric mucosa
Cirrhosis
Helicobater pylori.