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目的探讨幽门螺杆菌(Hp)、胃泌素、十二指肠胃化生之间的内在联系及其在溃疡形成中的作用机理。方法前瞻性调查十二指肠溃疡169例的 Hp 感染及十二指肠胃化生情况,检测部分患者的基础血清胃泌素,并与同期29例非溃疡性消化不良进行比较。结果 Hp 检出率、十二指肠炎及胃化生发生率,溃疡者(分别为94.0%,69.7%及75.5%)高于非溃疡者(分别为65.5%,10.3%及3.4%)(P<0.01);平均基础血清胃泌素,Hp 阳性 DU(244.23±68.15 ng/L)与 Hp 阳性非溃疡性消化不良(230.47±73.72 ng/L)无明显差异,但两者均高于 Hp 阴性非溃疡性消化不良(174。75±26.41 ng/L)(P<0.05),随着胃泌素水平增高胃化生有加重的趋势(r=0.573,P<0.05)。结论 Hp 感染、胃泌素释放增加、胃化生三者之间有内在联系,并可能在溃疡形成中起重要作用。
Objective To investigate the intrinsic relationship between Helicobacter pylori (Hp), gastrin and duodenal gasification and its mechanism of action in ulcer formation. Methods A prospective study was conducted on 169 cases of duodenal ulcer with Hp infection and gastroduodenal metaplasia. Serum gastrin levels were measured in some patients and compared with 29 cases of non-ulcer dyspepsia during the same period. Results The prevalence of Hp, duodenal and gastric metaplasia, ulcer (94.0%, 69.7% and 75.5%, respectively) were higher than those without ulcer (65.5%, 10.3% and 3.4%, P <0.01). The average basal serum gastrin, Hp positive DU (244.23 ± 68.15 ng / L) and Hp positive non-ulcer dyspepsia (230.47 ± 73.72 ng / L) had no significant difference, but both were higher than Hp negative Non-ulcer dyspepsia (174.75 ± 26.41 ng / L) (P <0.05), with the increase of gastrin levels, gastric metaplasia tended to aggravate (r = 0.573, P <0.05). Conclusions Hp infection, increased gastrin release and gastric metaplasia are intrinsically linked and may play an important role in ulcer formation.