Araújo-Filho Irami, Brandão-Neto José, Pinheiro Laíza Araújo Mohana, Azevedo Italo Medeiros, Freire Flávio Henrique Miranda Araújo, Medeiros Aldo Cunha
Postgraduate Program in Health Sciences, Federal University of Rio Grande do Norte, Natal, RN, Brazil.
Arq Gastroenterol. 2006 Oct-Dec;43(4):288-92. doi: 10.1590/s0004-28032006000400009.
[corrected] There is substantial evidence that infection with Helicobacter pylori plays a role in the development of gastric cancer and that it is rarely found in gastric biopsy of atrophic gastritis and gastric cancer. On advanced gastric tumors, the bacteria can be lost from the stomach.
To analyze the hypothesis that the prevalence of H.pylori in operated advanced gastric carcinomas and adjacent non-tumor tissues is high, comparing intestinal and diffuse tumors according to Lauren's classification
A prospective controlled study enrolled 56 patients from "Hospital Universitário", Federal University of Rio Grande do Norte, Natal, RN, Brazil, with advanced gastric cancer, treated from February 2000 to March 2003. Immediately after partial gastrectomy, the resected stomach was opened and several mucosal biopsy samples were taken from the gastric tumor and from the adjacent mucosa within 4 cm distance from the tumor margin. Tissue sections were stained with hematoxylin and eosin. Lauren's classification for gastric cancer was used, to analyse the prevalence of H. pylori in intestinal or diffuse carcinomas assessed by the urease rapid test, IgG by ELISA and Giemsa staining. H. pylori infected patients were treated with omeprazole, clarithromycin and amoxicillin for 7 days. Follow-up endoscopy and serology were performed 6 months after treatment to determine successful eradication of H. pylori in non-tumor tissue. Thereafter, follow-up endoscopies were scheduled annually. Chi-square and MacNemar tests with 0.05 significance were used.
Thirty-four tumors (60.7%) were intestinal-type and 22 (39.3%) diffuse type carcinomas. In adjacent non-tumor gastric mucosa, chronic gastritis were found in 53 cases (94.6%) and atrophic mucosa in 36 patients (64.3%). All the patients with atrophic mucosa were H. pylori positive. When examined by Giemsa and urease test, H. pylori positive rate in tumor tissue of intestinal type carcinomas was higher than that in diffuse carcinomas. In tumor tissues, 34 (60.7%) H. pylori-positive in gastric carcinomas were detected by Giemsa method. H. pylori was observed in 30 of 56 cases (53.5%) in tissues 4 cm adjacent to tumors. This difference was not significant. Eradication of H. pylori in non-tumor tissue of gastric remnant led to a complete negativity on the 12th postoperative month
The data confirmed the hypothesis of a high prevalence of H. pylori in tumor tissue of gastric advanced carcinomas and in adjacent non-tumor mucosa of operated stomachs. The presence of H. pylori was predominant in the intestinal-type carcinoma.
[已修正] 有大量证据表明,幽门螺杆菌感染在胃癌的发生发展中起作用,并且在萎缩性胃炎和胃癌的胃活检中很少发现该菌。在进展期胃肿瘤中,细菌可能会从胃中消失。
分析以下假说,即根据劳伦分类法比较肠型和弥漫型肿瘤,探讨进展期胃癌手术切除标本及其癌旁非肿瘤组织中幽门螺杆菌的感染率。
一项前瞻性对照研究纳入了巴西纳塔尔市北大河联邦大学“大学医院”的56例进展期胃癌患者,这些患者于2000年2月至2003年3月接受治疗。在部分胃切除术后,立即打开切除的胃,从胃肿瘤及距肿瘤边缘4厘米范围内的相邻黏膜处采集多个黏膜活检样本。组织切片用苏木精和伊红染色。采用胃癌的劳伦分类法,通过尿素酶快速试验、酶联免疫吸附测定法检测IgG以及吉姆萨染色来分析肠型或弥漫型癌中幽门螺杆菌的感染率。幽门螺杆菌感染患者接受奥美拉唑、克拉霉素和阿莫西林治疗7天。治疗6个月后进行随访内镜检查和血清学检测,以确定非肿瘤组织中幽门螺杆菌是否成功根除。此后,每年安排随访内镜检查。采用显著性水平为0.05的卡方检验和麦克尼马尔检验。
34例肿瘤(60.7%)为肠型癌,22例(39.3%)为弥漫型癌。在相邻的非肿瘤胃黏膜中,53例(94.6%)发现有慢性胃炎,36例(64.3%)发现有萎缩性黏膜。所有萎缩性黏膜患者的幽门螺杆菌均为阳性。通过吉姆萨染色和尿素酶试验检测发现,肠型癌肿瘤组织中幽门螺杆菌阳性率高于弥漫型癌。在肿瘤组织中,吉姆萨染色法检测到34例(60.7%)胃癌患者的幽门螺杆菌呈阳性。在距肿瘤4厘米范围内的组织中,56例中有30例(53.5%)观察到幽门螺杆菌。这一差异无统计学意义。胃残余非肿瘤组织中幽门螺杆菌的根除导致术后第12个月完全转阴。
数据证实了进展期胃癌肿瘤组织及其手术胃的相邻非肿瘤黏膜中幽门螺杆菌感染率较高这一假说。幽门螺杆菌在肠型癌中占主导。