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幽门螺杆菌相关胃病变中的嗜银核仁组织区

Argyrophilic nucleolar organizer regions in Helicobacter pylori-associated gastric lesions.

作者信息

Misra V, Bisht D, Misra S P, Dwivedi M, Bhatia R

机构信息

Department of Pathology, M.L.N. Medical College, Allahabad, India.

出版信息

APMIS. 2000 Jun;108(6):448-52. doi: 10.1034/j.1600-0463.2000.d01-81.x.

DOI:10.1034/j.1600-0463.2000.d01-81.x
PMID:11028808
Abstract

Three hundred and fifty biopsies from patients undergoing upper gastrointestinal endoscopy were studied for histopathological changes, H. pylori infection and argyrophilic nucleolar organizer region (AgNOR) counts. Histopathological examination revealed normal gastric mucosa in 10 (2.85%), gastritis in 254 (72.56%), intestinal metaplasia in 12 (4.0%), dysplasia in 13 (3.7%) and adenocarcinoma in 61 (17.4%). The mean (SD) AgNOR count was 1.66 (0.20) in normal, 2.43 (0.64) in gastritis, 3.09 (0.52) in intestinal metaplasia, 4.17 (0.31) in dysplasia, and 6.57 (0.98) in carcinoma. A statistically significant difference was observed between the AgNOR count of normal gastric mucosa and gastritis (p<0.001), gastritis and dysplasia (p<0.001), and dysplasia and adenocarcinoma (p<0.001). A statistically significant increase in mean AgNOR count was found with increase in H. pylori density in gastric biopsies (p<0.001) with gastritis. No significant difference was observed between mean AgNOR count of intestinal and diffuse type carcinomas. The AgNOR count in gastric biopsies with adenocarcinoma and H. pylori infection was 7.03 (0.85) as compared to 6.89 (0.73) in gastric biopsies with evidence of adenocarcinoma but without H. pylori infection. The difference was not statistically significant. The findings support the role of H. pylori as a promoting agent in gastric carcinogenesis by stimulating gastric epithelial cell proliferation at the stage of chronic inflammation, thereby making the cells more susceptible to endogenous or exogenous carcinogenic agents.

摘要

对350例接受上消化道内镜检查患者的活检样本进行了组织病理学变化、幽门螺杆菌感染及嗜银核仁组织区(AgNOR)计数研究。组织病理学检查显示,正常胃黏膜10例(2.85%),胃炎254例(72.56%),肠化生12例(4.0%),发育异常13例(3.7%),腺癌61例(17.4%)。正常样本中AgNOR计数的平均值(标准差)为1.66(0.20),胃炎样本中为2.43(0.64),肠化生样本中为3.09(0.52),发育异常样本中为4.17(0.31),癌组织样本中为6.57(0.98)。正常胃黏膜与胃炎的AgNOR计数之间、胃炎与发育异常之间以及发育异常与腺癌之间均观察到统计学显著差异(p<0.001)。胃炎患者胃活检样本中,随着幽门螺杆菌密度增加,平均AgNOR计数有统计学显著升高(p<0.001)。肠型和弥漫型癌的平均AgNOR计数之间未观察到显著差异。伴有腺癌和幽门螺杆菌感染的胃活检样本中AgNOR计数为7.03(0.85),而有腺癌证据但无幽门螺杆菌感染的胃活检样本中为6.89(0.73)。差异无统计学意义。这些发现支持幽门螺杆菌在胃癌发生过程中作为促进因子的作用,它通过在慢性炎症阶段刺激胃上皮细胞增殖,使细胞对内源性或外源性致癌剂更敏感。

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Helicobacter pylori and gastric cancer: Indian enigma.幽门螺杆菌与胃癌:印度谜团。
World J Gastroenterol. 2014 Feb 14;20(6):1503-9. doi: 10.3748/wjg.v20.i6.1503.