Ciancio G, Nuti M, Orsini B, Iovi F, Ortolani M, Palomba A, Amorosi A, Surrenti E, Ilani S M, Surrenti C
Department of Clinical Pathophysiology, Institute of Pathology, University of Florence, Italy.
Dig Liver Dis. 2002 Jan;34(1):16-21. doi: 10.1016/s1590-8658(02)80054-8.
It is unclear whether the extent of duodenal gastric metaplasia is due to Helicobacter pylori and/or acid.
To investigate the role of Helicobacter pylori eradication in the regression of duodenal gastric metaplasia in patients with duodenal ulcer maintained in acid suppression conditions.
. Duodenal (anterior, superior inferior walls of first part of duodenum) and gastric antrum biopsies were obtained from 44 Helicobacter pylori positive duodenal ulcer patients. Helicobacter pylori infection was diagnosed by rapid urease test, histology and 13C-Urea Breath Test. Patients were treated with 20 mg omeprazole tid associated with 250 mg clarithromycin and 500 mg amoxycillin four times daily for 10 days and maintained with 20 mg omeprazole daily for 18 weeks. Control endoscopies were performed at 6 and 18 weeks after beginning treatment.
Duodenal gastric metaplasia regression was observed in all (32/32) patients in whom Helicobacter pylori was eradicated, but in only 3 out of 6 patients in whom eradication was not achieved (p<0. 001).
. The present results suggest that Helicobacter pylori eradication associated with prolonged acid suppression may represent a good therapeutic strategy to achieve duodenal gastric metaplasia regression and highlight the combined role of acid and Helicobacter pylori in the pathogenesis of duodenal gastric metaplasia.
十二指肠胃化生的程度是否由幽门螺杆菌和/或胃酸所致尚不清楚。
研究根除幽门螺杆菌在维持抑酸治疗的十二指肠溃疡患者十二指肠胃化生消退中的作用。
从44例幽门螺杆菌阳性的十二指肠溃疡患者获取十二指肠（十二指肠第一部的前壁、上壁和下壁）和胃窦活检组织。通过快速尿素酶试验、组织学检查和13C尿素呼气试验诊断幽门螺杆菌感染。患者接受20mg奥美拉唑每日3次，联合250mg克拉霉素和500mg阿莫西林每日4次治疗10天，随后以20mg奥美拉唑每日维持治疗18周。在开始治疗后6周和18周进行对照内镜检查。
在所有根除幽门螺杆菌的患者（32/32）中均观察到十二指肠胃化生消退，但在6例未实现根除的患者中仅有3例出现消退（p<0.001）。
目前的结果表明，根除幽门螺杆菌并延长抑酸治疗可能是实现十二指肠胃化生消退的良好治疗策略，并突出了胃酸和幽门螺杆菌在十二指肠胃化生发病机制中的联合作用。
