Ramírez Ramos Alberto, Sánchez Sánchez Rolando
Universidad Peruana Cayetano Heredia.
Rev Gastroenterol Peru. 2008 Jul-Sep;28(3):258-66.
Since its discovery and identification in gastric tissue by Marshall and Warren in 1983, our knowledge about the effects of Helicobacter pylori infection has grown considerably. Its role in the multifactorial pathology of peptic ulcer disease (gastrodudodenal ulcer disease), gastric adenocarcinoma, and MALT lymphoma is now widely accepted while its involvement in extraintestinal disease is still controversial.The correlation between the colonization of the stomach by H. pylori and gastric lymphoma has been demonstrated in multiple studies. Between 65 and 80% of distal gastric adenocarcinomas are attributed to H. pylori infection. However, gastric carcinogenesis cannot be explained by H. pylori infection alone. Among those individuals infected by this bacteria, only a small percentage (2-5%) ever develops gastric cancer, the majority exhibit benign lesions. There is a wide individual variation in the outcome of this infection in patients. This individual and population specific variation is due to the intricate relationship between genetics, the environment, bacterial virulence, diet, and socio-economic status and it explains the multiple outcomes of this infection. In this article, we conduct a review of the widely accepted theories regarding gastric cancer, Helicobacter pylori, the correlations and enigmas between them, the reported geographical variations, and the various proposed hypotheses on the carcinogenic mechanism of Helicobacter pylori.
自1983年马歇尔和沃伦在胃组织中发现并鉴定出幽门螺杆菌以来，我们对幽门螺杆菌感染影响的认识有了显著增长。它在消化性溃疡病（胃十二指肠溃疡病）、胃腺癌和黏膜相关淋巴组织淋巴瘤的多因素病理过程中的作用现已被广泛接受，而其在肠外疾病中的作用仍存在争议。多项研究已证实幽门螺杆菌在胃内定植与胃淋巴瘤之间的关联。65%至80%的远端胃腺癌归因于幽门螺杆菌感染。然而，胃癌的发生不能仅用幽门螺杆菌感染来解释。在感染这种细菌的个体中，只有一小部分（2%至5%）会患胃癌，大多数表现为良性病变。患者感染后的结果存在很大的个体差异。这种个体和群体的特异性差异是由于遗传、环境、细菌毒力、饮食以及社会经济地位之间的复杂关系所致，它解释了这种感染的多种结果。在本文中，我们对关于胃癌、幽门螺杆菌、它们之间的关联和谜团、报道的地理差异以及关于幽门螺杆菌致癌机制的各种提出的假说的广泛接受的理论进行综述。
