关键词: Helicobacter pylori gastric cancer intestinal metaplasia

Mesh : Humans Stomach Neoplasms / pathology microbiology etiology Metaplasia / pathology Helicobacter pylori Helicobacter Infections / complications pathology Precancerous Conditions / pathology microbiology Carcinogenesis / pathology Gastritis, Atrophic / pathology microbiology Gastric Mucosa / pathology microbiology Intestines / pathology microbiology

来  源:   DOI:10.2478/raon-2024-0028   PDF(Pubmed)

Abstract:
BACKGROUND: Non-cardia gastric cancer remains a major cause of cancer-related mortality worldwide, despite declining incidence rates in many industrialized countries. The development of intestinal-type gastric cancer occurs through a multistep process in which normal mucosa is sequentially transformed into hyperproliferative epithelium, followed by metaplastic processes leading to carcinogenesis. Chronic infection with Helicobacter pylori is the primary etiological agent that causes chronic inflammation of the gastric mucosa, induces atrophic gastritis, and can lead to intestinal metaplasia and dysplasia. Both intestinal metaplasia and dysplasia are precancerous lesions, in which gastric cancer is more likely to occur. Atrophic gastritis often improves after eradication of Helicobacter pylori; however, the occurrence of intestinal metaplasia has been traditionally regarded as \"the point of no return\" in the carcinogenesis sequence. Helicobacter pylori eradication heals non-atrophic chronic gastritis, may lead to regression of atrophic gastritis, and reduces the risk of gastric cancer in patients with these conditions. In this article, we discuss the pathogenesis, epigenomics, and reversibility of intestinal metaplasia and briefly touch upon potential treatment strategy.
CONCLUSIONS: Gastric intestinal metaplasia no longer appears to be an irreversible precancerous lesion. However, there are still many controversies regarding the improvement of intestinal metaplasia after Helicobacter pylori eradication.
摘要:
背景:非贲门胃癌仍然是全球癌症相关死亡的主要原因,尽管许多工业化国家的发病率下降。肠型胃癌的发展是通过多步骤过程发生的,其中正常粘膜依次转化为过度增生的上皮,其次是化生过程导致癌变。幽门螺杆菌的慢性感染是引起胃粘膜慢性炎症的主要病原体,诱发萎缩性胃炎,并可导致肠上皮化生和发育不良。肠上皮化生和异型增生都是癌前病变,其中胃癌更容易发生。根除幽门螺杆菌后,萎缩性胃炎通常会改善;然而,肠上皮化生的发生传统上被认为是癌变序列中的“不归点”。根除幽门螺杆菌治疗非萎缩性慢性胃炎,可能导致萎缩性胃炎的消退,并降低患有这些疾病的患者患胃癌的风险。在这篇文章中,我们讨论了发病机理,表观基因组学,肠化生的可逆性和潜在的治疗策略。
结论:胃肠上皮化生不再表现为不可逆的癌前病变。然而,关于根除幽门螺杆菌后肠上皮化生的改善仍存在许多争议。
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