Xia H H, Kalantar J S, Talley N J, Wyatt J M, Adams S, Chueng K, Mitchell H M
Department of Medicine, The University of Sydney, Nepean Hospital, Penrith, Australia.
Am J Gastroenterol. 2000 Jan;95(1):114-21. doi: 10.1111/j.1572-0241.2000.01609.x.
Helicobacter pylori is a carcinogen; gastric carcinoma involves a multistep process from chronic gastritis to atrophy, intestinal metaplasia, and dysplasia. The aims of this study were to determine the types of mucosa at different gastric sites in H. pylori-infected and uninfected patients, and whether the presence of antral-type mucosa in the incisura, body, and fundus is associated with gastric atrophy and intestinal metaplasia.
Two hundred and sixty-eight patients with dyspepsia were enrolled. Eight biopsies (i.e., antrum x3, body x2, fundus x2, and incisura x1) were obtained. One antral biopsy was used for the CLO-test. Three (each from the antrum, body, and fundus) were cultured. The remaining biopsies were examined histologically according to the updated Sydney System after staining with hematoxylin and eosin and Giemsa. A validated serological test was also applied.
Overall, 113 (42%) patients were infected with H. pylori. At the incisura, antral-type mucosa was more prevalent in infected than in uninfected patients (84% vs. 18%; odds ratio [OR] = 23.9, 95% confidence interval [CI] 12.5-45.8; p<0.001). Atrophic gastritis and intestinal metaplasia at the incisura was present in 19.5% and 13.3%, respectively, of infected, and 4.5% and 3.2%, respectively, of uninfected patients (both p<0.01). Moreover, atrophic gastritis at the incisura was associated with the presence of antral-type mucosa at the site (termed antralization); the prevalence of atrophic gastritis was 19.5% (24/123) in the presence of antralization, whereas the rate was 2.1% (3/145) without antralization (OR = 11.4, 95% CI 3.4-39.2; p<0.001). Similarly, at the incisura, 16.3% (20/123) of "antralized" cases and 1.4% (2/145) of "unantralized" cases had intestinal metaplasia (OR = 13.8, 95% CI, 3.2-60.7; p<0.001). The association between antralization at gastric body and fundus also appeared to be associated with atrophic gastritis and intestinal metaplasia at these sites.
Atrophic gastritis and intestinal metaplasia occurs predominantly at the gastric antrum and incisura with H. pylori infection. Antralization of the gastric incisura is a common event in H. pylori-infected patients, and appears to be associated with an increased risk of atrophic gastritis and intestinal metaplasia.
幽门螺杆菌是一种致癌物;胃癌是一个从慢性胃炎发展到萎缩、肠化生和发育异常的多步骤过程。本研究的目的是确定幽门螺杆菌感染和未感染患者不同胃部位的黏膜类型,以及胃切迹、胃体和胃底出现胃窦型黏膜是否与胃萎缩和肠化生相关。
纳入268例消化不良患者。获取8块活检组织(即胃窦3块、胃体2块、胃底2块和胃切迹1块)。1块胃窦活检组织用于快速尿素酶试验。3块组织(分别取自胃窦、胃体和胃底)进行培养。其余活检组织经苏木精-伊红和吉姆萨染色后,根据更新的悉尼系统进行组织学检查。还应用了一种经过验证的血清学检测方法。
总体而言,113例(42%)患者感染了幽门螺杆菌。在胃切迹处,感染患者中胃窦型黏膜比未感染患者更常见(84%对18%;优势比[OR]=23.9,95%置信区间[CI]12.5 - 45.8;p<0.001)。感染患者胃切迹处萎缩性胃炎和肠化生的发生率分别为19.5%和13.3%,未感染患者分别为4.5%和3.2%(均p<0.01)。此外,胃切迹处的萎缩性胃炎与该部位胃窦型黏膜的存在(称为胃窦化)相关;存在胃窦化时萎缩性胃炎的发生率为19.5%(24/123),无胃窦化时发生率为2.1%(3/145)(OR = 11.4,95% CI 3.4 - 39.2;p<0.001)。同样,在胃切迹处,“胃窦化”病例中有16.3%(20/123)发生肠化生,“未胃窦化”病例中有1.4%(2/145)发生肠化生(OR = 13.8,95% CI 3.2 - 60.7;p<0.001)。胃体和胃底的胃窦化与这些部位的萎缩性胃炎和肠化生之间也似乎存在关联。
幽门螺杆菌感染时,萎缩性胃炎和肠化生主要发生在胃窦和胃切迹处。胃切迹的胃窦化在幽门螺杆菌感染患者中很常见,并且似乎与萎缩性胃炎和肠化生风险增加相关。