Rugge M, Russo V, Busatto G, Genta R M, Di Mario F, Farinati F, Graham D Y
Department of Oncological and Surgical Sciences, Cattedra di Istochimica e Immunoistochimica Patologica, ULSS 15 del Veneto, Italia.
J Clin Pathol. 2001 Jun;54(6):456-60. doi: 10.1136/jcp.54.6.456.
BACKGROUND/AIMS: Barrett's oesophagus complicates the gastro-oesophageal acid reflux. Helicobacter pylori infection, particularly with cagA positive strains, induces inflammatory/atrophic lesions of the gastric mucosa, which may impair acid output. No systematic study has investigated the phenotype of the gastric mucosa coexisting with Barrett's oesophagus. This study was designed to identify the phenotype of gastric mucosa associated with Barrett's oesophagus.
In this retrospective case control study, the phenotype of the gastric mucosa was histologically characterised in 53 consecutive patients with Barrett's oesophagus and in 53 (sex and age matched) non-ulcer dyspeptic controls. Both patients and controls underwent extensive sampling of the gastric mucosa (two antral, one incisural, and two oxyntic biopsies). Intestinal metaplasia (IM) was categorised (type I, complete IM; types II and III, incomplete IM) by the high iron diamine stain; cagA status was ascertained by genotyping.
Helicobacter pylori was present in 19 of the 53 patients with Barrett's oesophagus and in 30 of the 53 controls (p < 0.02); eight of the 19 patients with Barrett's oesophagus and 28 of the 35 controls harboured cagA positive H pylori (p < 0.03). The histological severity of non-atrophic gastritis detected in the controls was significantly higher than that detected in the patients with Barrett's oesophagus (p < 0.0001). Multifocal atrophic gastritis was present in 4% of the patients with Barrett's oesophagus and in 23% of controls (p < 0.01). The odds ratio for the association between multifocal atrophic gastritis and Barrett's oesophagus was 0.20 (95% confidence interval, 0.006 to 0.60). Gastric IM was detected in 13.2% of the patients with Barrett's oesophagus and in 30.1% of the controls (p < 0.03). Type III IM at the gastric mucosa was only detected among controls.
Barrett's oesophagus is associated with a low prevalence of H pylori cagA positive infection and multifocal atrophic gastritis. This pathobiological pattern is considered to be associated with a low risk of distal gastric cancer.
背景/目的：巴雷特食管使胃食管酸反流复杂化。幽门螺杆菌感染，尤其是cagA阳性菌株感染，会引发胃黏膜的炎症/萎缩性病变，这可能会损害胃酸分泌。尚无系统性研究调查过与巴雷特食管共存的胃黏膜表型。本研究旨在确定与巴雷特食管相关的胃黏膜表型。
在这项回顾性病例对照研究中，对53例连续的巴雷特食管患者以及53例（性别和年龄匹配）非溃疡性消化不良对照者的胃黏膜表型进行了组织学特征分析。患者和对照者均接受了广泛的胃黏膜取样（两块胃窦活检、一块切迹活检和两块胃体活检）。通过高铁二胺染色对肠化生（IM）进行分类（I型，完全肠化生；II型和III型，不完全肠化生）；通过基因分型确定cagA状态。
53例巴雷特食管患者中有19例存在幽门螺杆菌感染，53例对照者中有30例存在幽门螺杆菌感染（p<0.02）；19例巴雷特食管患者中有8例以及35例对照者中有28例携带cagA阳性幽门螺杆菌（p<0.03）。对照者中检测到的非萎缩性胃炎的组织学严重程度显著高于巴雷特食管患者中检测到的（p<0.0001）。4%的巴雷特食管患者存在多灶性萎缩性胃炎，23%的对照者存在多灶性萎缩性胃炎（p<0.01）。多灶性萎缩性胃炎与巴雷特食管之间关联的比值比为0.20（95%置信区间，0.006至0.60）。13.2%的巴雷特食管患者检测到胃IM，30.1%的对照者检测到胃IM（p<0.03）。胃黏膜III型IM仅在对照者中检测到。
巴雷特食管与幽门螺杆菌cagA阳性感染及多灶性萎缩性胃炎的低患病率相关。这种病理生物学模式被认为与远端胃癌的低风险相关。
