Lord R V, Frommer D J, Inder S, Tran D, Ward R L
Department of Surgery, St. Vincent's Hospital, Sydney, New South Wales, Australia.
Aust N Z J Surg. 2000 Jan;70(1):26-33. doi: 10.1046/j.1440-1622.2000.01737.x.
The role of Helicobacter pylori infection in the development of Barrett's oesophagus and its complications is uncertain. The aim of the present study was to determine the importance of H. pylori infection in this disease by comparing the frequency of oesophageal and gastric H. pylori infection in a group of patients with Barrett's oesophagus or adenocarcinoma, with the frequency of infection in a control group without Barrett's disease.
The study group included 160 patients (123 male, 37 female; mean age: 61.2 years) who were classified (according to the highest grade pathological lesion in the oesophagus) as having Barrett's intestinal metaplasia (IM; 88 patients), Barrett's oesophagus with low-grade dysplasia (LGD; 28 patients), high-grade dysplasia (HGD; five patients), Barrett's indefinite for dysplasia (n = 4), and Barrett's adenocarcinoma (33 patients). A total of 91 of these patients had gastric antral specimens available for study. The control group consisted of 214 consecutive, prospectively enrolled symptomatic patients (122 male, 92 female; mean age: 57.2 years) who underwent upper gastrointestinal endoscopy and in whom Barrett's oesophagus or Barrett's adenocarcinoma was not found. A modified Warthin-Starry method was used to detect H. pylori infection.
Oesophageal H. pylori infection was found in eight of 160 (5%) patients with Barrett's oesophagus or Barrett's adenocarcinoma. Holicobacter pylori organisms in the oesophagus were found only on non-intestinalized cardiac or oxyntocardiac mucosa. All patients with oesophageal H. pylori infection and an antral biopsy available for study had antral H. pylori infection. Gastric antral H. pylori infection was significantly less prevalent in patients in the Barrett's study group (15/91, 16.5%) than in the non-Barrett's control group (67/214, 31.3%; Fisher's exact test, P = 0.01). Patients from the control group with an endoscopic diagnosis of duodenal ulcer, gastric ulcer, gastritis, or duodenitis had a significantly higher prevalence of infection compared with the Barrett's group, but there was no difference in the infection prevalence in patients in the Barrett's group and patients with reflux oesophagitis, hiatal hernia, no endoscopic abnormality, or any other diagnosis.
Oesophageal H. pylori infection is uncommon in patients with Barrett's IM, dysplasia, or adenocarcinoma, and may be restricted to non-intestinalized columnar epithelium. Gastric H. pylori infection may have a protective effect for the development of Barrett's oesophagus.
幽门螺杆菌感染在巴雷特食管的发生及其并发症中的作用尚不确定。本研究的目的是通过比较一组巴雷特食管或腺癌患者的食管和胃幽门螺杆菌感染频率与无巴雷特病的对照组的感染频率，来确定幽门螺杆菌感染在该疾病中的重要性。
研究组包括160例患者（男性123例，女性37例；平均年龄：61.2岁），根据食管中最高级别的病理病变分类，有巴雷特肠化生（IM；88例患者）、低级别异型增生的巴雷特食管（LGD；28例患者）、高级别异型增生（HGD；5例患者）、异型增生不明确的巴雷特食管（n = 4）和巴雷特腺癌（33例患者）。这些患者中共有91例有胃窦标本可供研究。对照组由214例连续的、前瞻性纳入的有症状患者组成（男性122例，女性92例；平均年龄：57.2岁），他们接受了上消化道内镜检查，未发现巴雷特食管或巴雷特腺癌。采用改良的Warthin-Starry方法检测幽门螺杆菌感染。
160例巴雷特食管或巴雷特腺癌患者中有8例（5%）发现食管幽门螺杆菌感染。食管中的幽门螺杆菌仅在未肠化生的贲门或胃贲门黏膜中发现。所有有食管幽门螺杆菌感染且有胃窦活检可供研究的患者均有胃窦幽门螺杆菌感染。巴雷特研究组患者的胃窦幽门螺杆菌感染患病率（15/91，16.5%）显著低于非巴雷特对照组（67/214，31.3%；Fisher精确检验，P = 0.01）。与巴雷特组相比，内镜诊断为十二指肠溃疡、胃溃疡、胃炎或十二指肠炎的对照组患者感染患病率显著更高，但巴雷特组患者与反流性食管炎、食管裂孔疝、无内镜异常或任何其他诊断的患者的感染患病率无差异。
食管幽门螺杆菌感染在巴雷特IM、异型增生或腺癌患者中不常见，可能仅限于未肠化生的柱状上皮。胃幽门螺杆菌感染可能对巴雷特食管的发生有保护作用。
