摘要
活检证实的正常胃、十二指肠粘膜(NGDM),慢性活动性胃、十二指肠炎(CAGDI)和活动性十二指肠溃疡(ADU)各30例。胃窦部活检标本幽门螺杆菌尿素酶试验(HPUT)阳性者分别为16例,30例和30例。应用放免法测定上述3组空腹及餐后血清胃泌素发现,空腹水平3组之问或两两比较均无显著性差异(均为P>0.05),而餐后水平均有统计学意义(均为P<0.01)。在ADU组,经抗酸抗菌治疗后复查,HPUT转阴者溃疡愈合,升高的餐后血清胃泌素水平也降至正常,其余下降不显著(P>0.05)。这表明从CAGDI到ADU,通过胃酸调节胃泌素分泌的正常负反馈机制又可恢复正常。在十二指肠溃疡形成过程中,HP充当始动因子,血清胃泌素充当媒介因素。这些结果支持胃窦部HP感染通过血清胃泌素释放增加,而导致与HP相关的十二指肠溃疡形成的发病机理。
Fasting and postprandial serum gastrin levels were determined by radioimm-unoassay in each 30 cases of normal gastroduodenal mucosa (NGDM), chronic active gastroduodenitis (CAGDI), and active duodenal ulcer (ADU). All cases were confirmed by endoscopy with biopsy. H. pylori urease test (HPUT) results were positive in 16,30 and 30 cases respectively. Tlere were no significrct differences in tte fasting gastrin levels, but there were statistical differences strongly in postprandial levels. After antiacid and antimicrobial treatments tte ADU group was reexamin-ed, the gastrin levels of 23 cases with H. pylori eradication were reduced to normals but the levels of remainder 7 cases with HPUT-positive had 110 significant reduction. This indicated that following the H. pylori eradication, the ecid and pastrin regulating mechanism was recovered. The results supported tie lypotlesis that H. pylori infection of gastric antrum may lead to the development of duodenal ulcer through increasing gastrin release.
出处
《天津医药》
CAS
1994年第7期387-390,共4页
Tianjin Medical Journal
关键词
幽门螺杆菌
胃泌素
十二指肠溃疡
helicobacter pylori serum gas,trin duodenal ulcer pathogene- tic mechanism
