Ackermark Pernilla, Kuipers Ernst J, Wolf Claudia, Breumelhof Ronald, Seldenrijk Cornelis A, Timmer Robin, Segeren Katja C A, Kusters Johannes G, Smout André J P M
Department of Gastroenterology, St. Antonius Hospital, Nieuwegein, The Netherlands.
Am J Gastroenterol. 2003 Aug;98(8):1719-24. doi: 10.1111/j.1572-0241.2003.07585.x.
Recent studies indicate that colonization with cagA-positive Helicobacter pylori (H. pylori) strains may protect against gastroesophageal reflux disease (GERD) and its complications, but the role of cagA in the etiology of Barrett's esophagus has so far been poorly investigated. The pathogenesis of intestinal metaplasia (IM) at an endoscopically normal esophagogastric junction (EGJ) is still unclear, and the role of the H. pylori virulence factor cagA in it has not been investigated. The aim of our study was to assess the relationship between H. pylori and cagA-positive H. pylori in particular and IM at an endoscopically normal EGJ and Barrett's esophagus.
Serum samples were obtained from 62 patients without IM, 43 patients with IM at an endoscopically normal junction, and 51 patients with Barrett's esophagus. IM was defined as presence of goblet cells with positive staining with Alcian blue. The prevalence of H. pylori and cagA was investigated by assessment of IgG antibody levels as determined by ELISA.
The overall H. pylori prevalence was 59% (92/156), and the cagA prevalence was 29% (46/156). Although 63% (39/62) of IM negative subjects and 74% (32/43) of those with IM at the junction were H. pylori positive, only 41% (21/51) of Barrett's patients tested positive. The differences between the IM negative and the Barrett's group (p = 0.02) and between IM at the junction and Barrett's were significant (p = 0.002). The relative cagA prevalence (percentage with cagA positivity and H. pylori positivity) was 56% (22/39) in patients who were IM negative, 59% (19/32) in those with IM at the junction, and 24% (5/21) in those with Barrett's. The prevalence of anti-CagA was significantly lower in patients with Barrett's esophagus compared with patients who were IM negative (p = 0.002) and those who had IM at the junction (p < 0.001). No difference in cagA prevalence was seen between the latter groups.
These findings are in line with the concept that H. pylori and cagA-positive strains in particular protect against the development of Barrett's esophagus. In contrast, our findings do not support the theory that IM at an endoscopically normal esophagogastric junction is associated with H. pylori or cagA-positive strains. IM at the junction and Barrett's esophagus seem to have different etiologies.
近期研究表明，感染cagA阳性幽门螺杆菌（H. pylori）菌株可能预防胃食管反流病（GERD）及其并发症，但迄今为止，cagA在巴雷特食管病因学中的作用研究甚少。内镜检查正常的食管胃交界（EGJ）处肠化生（IM）的发病机制仍不清楚，H. pylori毒力因子cagA在其中的作用尚未得到研究。我们研究的目的是评估H. pylori特别是cagA阳性H. pylori与内镜检查正常的EGJ处IM以及巴雷特食管之间的关系。
采集62例无IM患者、43例内镜检查交界处有IM患者和51例巴雷特食管患者的血清样本。IM定义为存在对阿尔辛蓝染色呈阳性的杯状细胞。通过酶联免疫吸附测定（ELISA）法测定IgG抗体水平来研究H. pylori和cagA的流行率。
H. pylori总体流行率为59%（92/156），cagA流行率为29%（46/156）。虽然IM阴性受试者中有63%（39/62）以及交界处有IM的受试者中有74%（32/43）H. pylori呈阳性，但巴雷特食管患者中只有41%（21/51）检测呈阳性。IM阴性组与巴雷特食管组之间（p = 0.02）以及交界处有IM组与巴雷特食管组之间差异有统计学意义（p = 0.002）。IM阴性患者中相对cagA流行率（cagA阳性且H. pylori阳性的百分比）为56%（22/39），交界处有IM的患者中为59%（19/32），巴雷特食管患者中为24%（5/21）。与IM阴性患者（p = 0.002）和交界处有IM的患者（p < 0.001）相比，巴雷特食管患者中抗CagA的流行率显著更低。后两组之间cagA流行率无差异。
这些发现符合以下概念，即H. pylori特别是cagA阳性菌株可预防巴雷特食管的发生。相比之下，我们的发现不支持内镜检查正常的食管胃交界处IM与H. pylori或cagA阳性菌株有关的理论。交界处的IM和巴雷特食管似乎有不同的病因。
