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Effect of Helicobacter pylori infection and its eradication on cell proliferation DNA status and oncogene expression in patients with chronic gastritis

机译：幽门螺杆菌感染及其根除对慢性胃炎患者细胞增殖DNA状态和癌基因表达的影响

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摘要

BACKGROUND—Helicobacter pylori, the main cause of chronic gastritis, is a class I gastric carcinogen. Chronic gastritis progresses to cancer through atrophy, metaplasia, and dysplasia. Precancerous phenotypic expression is generally associated with acquired genomic instability.
AIM—To evaluate the effect of H pylori infection and its eradication on gastric histology, cell proliferation, DNA status, and oncogene expression.
METHODS/SUBJECTS—Morphometric and immunohistochemical techniques were used to examine gastric mucosal biopsy specimens from eight controls, 10 patients with H pylori negative chronic gastritis, 53 with H pylori positive chronic gastritis, and 11 with gastric cancer.
RESULTS—All patients with chronic gastritis were in a hyperproliferative state related to mucosal inflammation, regardless of H pylori infection. Atrophy was present in three of 10 patients with H pylori negative chronic gastritis and in 26 of 53 with H pylori positive chronic gastritis, associated in 18 with intestinal metaplasia. DNA content was abnormal in only 11 patients with atrophy and H pylori infection; eight of these also had c-Myc expression, associated in six cases with p53 expression. Fifty three patients with H pylori positive chronic gastritis were monitored for 12 months after antibiotic treatment: three dropped out; infection was eradicated in 45, in whom cell proliferation decreased in parallel with the reduction in gastritis activity; atrophy previously detected in 21/45 disappeared in five, regressed from moderate to mild in nine, and remained unchanged in seven; complete metaplasia disappeared in 4/14, and markers of genomic instability disappeared where previously present. In the five patients in whom H pylori persisted, atrophy, metaplasia, dysplasia, and markers of genomic instability remained unchanged.
CONCLUSIONS—Chronic H pylori infection seems to be responsible for genomic instability in a subset of cases of H pylori positive chronic atrophic gastritis; eradication of H pylori infection can reverse inflammation and the related atrophy, metaplasia, and genomic instability.


Keywords: H pylori infection; atrophic gastritis; genomic instability; eradication therapy
机译：背景—幽门螺杆菌是慢性胃炎的主要原因，是I类胃癌致癌物。慢性胃炎会通过萎缩，化生和发育异常发展为癌症。癌前表型表达通常与获得性基因组不稳定性有关。
目标：评估幽门螺杆菌感染及其根除对胃组织学，细胞增殖，DNA状态和癌基因表达的影响。
方法/主题—使用形态计量学和免疫组化技术检查了来自8个对照组，10例幽门螺杆菌阴性慢性胃炎，53例幽门螺杆菌阳性慢性胃炎和11例胃癌的胃黏膜活检标本。
结果—所有慢性胃炎患者不论幽门螺杆菌感染如何，均处于与粘膜炎症相关的过度增殖状态。在10例幽门螺杆菌阴性慢性胃炎患者中有3名萎缩，在53例幽门螺杆菌阳性慢性胃炎患者中有26例出现萎缩，其中18例伴有肠上皮化生。仅11名萎缩和幽门螺杆菌感染患者的DNA含量异常;其中有8个也有c-Myc表达，在6例中与p53表达有关。抗生素治疗后监测了53例幽门螺杆菌阳性慢性胃炎患者，持续12个月。在45个地方消除了感染，其中细胞增殖减少与胃炎活性减少同时发生;先前在21/45中检测到的萎缩在五分中消失，在九分中度至轻度下降，在七分中保持不变。完全的化生在4/14中消失，而基因组不稳定性的标记在先前存在的位置消失。在5例幽门螺杆菌持续存在的患者中，萎缩，化生，异型增生和基因组不稳定的标志物保持不变。
结论—慢性幽门螺杆菌感染似乎是部分病例的基因组不稳定的原因。幽门螺杆菌阳性慢性萎缩性胃炎；根除幽门螺杆菌感染可逆转炎症反应及相关的萎缩，化生和基因组不稳定。


关键词：幽门螺杆菌感染;萎缩性胃炎；基因组不稳定根除疗法

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