胃炎的组织病理学研究进展

H.M.T. El-Zimaity
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引用次数: 25

摘要

幽门螺杆菌现在被认为是胃炎和胃炎相关疾病(十二指肠溃疡、胃溃疡和胃癌)的病因。十二指肠溃疡通常伴有胃窦显性胃炎,很少/没有萎缩。胃溃疡和肠型胃癌通常伴有广泛的胃炎和广泛的肠化生。胃炎的模式是由一个人的胃酸分泌状态决定的,这是疾病结局的主要决定因素。幽门螺杆菌胃炎的自然历史是炎症从胃窦向邻近的体部进展,导致损伤前叶萎缩,导致酸分泌减少,壁细胞丢失,萎缩发展。与肠化生亚型相比,伴或不伴肠化生的萎缩的模式、程度和严重程度是更重要的萎缩预测因子。目前的挑战仍然是确定一种可靠的恶性肿瘤潜在标志物。
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Recent advances in the histopathology of gastritis

Helicobacter pylori is now accepted as the cause of gastritis and the gastritis-associated diseases (duodenal ulcer, gastric ulcer, and gastric carcinoma). Duodenal ulcer is typically associated with antral-predominant gastritis and little/no atrophy. Gastric ulcer and the intestinal type of gastric cancer are typically associated with extensive gastritis and widespread intestinal metaplasia. The gastritis pattern is determined by a person's acid secretory status, which is the major determinant of disease outcome(s). The natural history of H. pylori gastritis is for the inflammation to progress from the antrum into the adjacent corpus, resulting in an atrophic front of advancing injury, leading to a reduction in acid secretion, loss of parietal cells, and development of atrophy. The pattern, extent, and severity of atrophy with or without intestinal metaplasia are a far more important predictor of atrophy than the intestinal metaplasia subtype. The challenge remains to identify a reliable marker for malignancy potential.

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