十二指肠球部多发隆起病变与幽门螺杆菌和胃上皮化生的关系

目的探讨内镜下十二指肠球部多发隆起病变与幽门螺杆菌（Hp）感染和胃上皮化生等组织学异常关系.方法连续调查86例经胃镜检查证实十二指肠球部多发隆起病变患者,并以40例球部基本正常患者作为对照.病变组Hp阳性患者接受三联根除治疗（奥美拉唑20mg、克拉霉素250mg、甲硝唑400mg,每天2次）,疗程7 d,停药后随访6个月后复查胃镜;病变组Hp阴性者接受奥美拉唑20 mg,每天1次治疗,疗程4～6个月,停药后2周复查胃镜.比较2次胃镜检查结果,包括胃镜下隆起病变程度及球部黏膜胃上皮化生等组织学异常,分析Hp感染与上述胃镜下表现及组织学异常关系.结果对照组患者组织学仅部分发现轻度慢性炎症,未发现球部Hp感染.病变组患者Hp检出率为58.1%,胃上皮化生检出率为57.0%.Hp阳性与Hp阴性患者胃镜下隆起病变程度差异无统计学意义（P＞0.05）,但胃上皮化生检出率更高,程度更严重（P＜0.05）.76例患者复查胃镜,根除Hp或奥美拉唑治疗对Hp阳性或阴性患者球部多发隆起病变无明显作用,但根除Hp后6个月,53.6%（15/28）患者胃上皮化生消失,61.0%（25/41）患者绒毛萎缩恢复正常,所有患者淋巴滤泡完全消失（26/26）,杯状细胞减少完全恢复（25/25）,同时炎症和活动性显著减轻（P值均＜0.01）.奥美拉唑疗效不显著.结论十二指肠球部多发隆起病变患者半数以上有Hp感染.Hp感染与隆起病变伴随组织学炎症密切相关,而与其内镜下表现及严重程度无关.根除Hp可使炎症显著减轻,胃上皮化生范围缩小或消退.

The associations among diffuse nodularity, gastric metaplasia in the duodenal bulb and antral Helicobacter pylori infection

Objective To determine the associations among diffuse nodularity, gastric metaplasia in the duodenal bulb and antral Helicobacter pylori (H. pylori) infection. Methods Consecutive 86 patients with diffuse nodularity in the duodenal bulb verified by endoscopy were investigated. In addition, 40 patients were enrolled as the control group, in which no abnormalities were found in the duodenal bulb by endoscopy. The patients with antral H. pylori infection in the therapy group were administered with triple therapy consisting of omeprazole 20 mg plus clarithromycin 250 mg and metronidazole 400 mg twice daily for one week. The patients with no H. pylori infection in the therapy group received omeprazole 20 mg once daily for 4-6 months. Repeat endoscopy was performed 6 months after the anti-H. pylori therapy or 2 weeks after stopping of omeprazole. The endoscopic appearance of diffuse nodularity in the duodenal bulb and the accompanied histological alterations were evaluated. The associations among H. pylori infection in the antrum. endoscopic findings and the histological alterations in the duodenal bulb were analyzed. Results Only mild chronic inflammations were found in part of the controlled patients with normal endoscopic appearance of duodenal bulb, none with H. pylori infection in the duodenal bulb. The positive rate of antral H. pylori in the 86 patients with diffuse nodularity in the duodenal bulb was 58. 1%, and the positive rate of gastric metaplasia in the duodenal bulb was 57. 0%. There was no difference in the severity of diffuse nodularity in the duodenal bulb (P >0. 05) between patients with and without H. pylori infection. However, the positive rate and the degree of severity of gastric metaplasia were all higher in patients with H. pylori infection than in patients without H. pylori infection (both P <0. 05). Although no influence of H. pylori eradication or long-term acid inhibition therapy on the appearance of diffuse nodularity in the duodenal bulb was found, regression of gastric metaplasia in the duodenal bulb was observed in 53. 6% (15/28) of patients 6 months after eradication of H. pylori (P< 0.001), accompanied with recovery of duodenal villous atrophy (25/41) and regression of lymphoid follicles (25/25). and significant improvement of duodenal chronic inflammation and activity (both P< 0. 001). Conclusions More than half of the patients with diffuse nodularity in the duodenal bulb have H. pylori infection in the gastric antrum. The presence of H. pylori infection is related to histological duodenitis, but not to the endoscopic appearance or the severity of nodular duodenitis. Eradication of H. pylori leads to improvement of duodenal inflammation and diminution or regression of gastric metaplasia in the duodenal bulb.