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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。
Biopsy confirmed normal stomach, duodenal mucosa (NGDM), chronic active stomach, duodenitis (CAGDI) and active duodenal ulcer (ADU) in 30 cases. Antral biopsy specimens H. pylori urease test (HPUT) positive were 16 cases, 30 cases and 30 cases. The application of radioimmunoassay in determining the above three groups of fasting and postprandial serum gastrin found no significant difference (P> 0.05) between the three groups of fasting levels or any pairwise comparison, and the postprandial levels were statistically significant ( All P <0.01). In ADU group, after anti-acid antibacterial therapy review, HPUT negative ulcer healed, elevated postprandial serum gastrin levels also dropped to normal, the rest did not decline significantly (P> 0.05). This suggests that the normal negative feedback mechanism of regulating gastrin secretion by gastric acid from CAGDI to ADU may return to normal. In the process of duodenal ulcer formation, HP acts as a starting factor and serum gastrin acts as a mediator. These results support the pathogenesis of HP-associated duodenal ulcer formation by HP infection of the gastric antrum through increased serum gastrin release.