Balendra Vyshnavy, Amoroso Chiara, Galassi Barbara, Esposto Josephine, Bareggi Claudia, Luu Jennie, Scaramella Lucia, Ghidini Michele
Saint James School of Medicine, Park Ridge, IL 60068, USA.
Gastroenterology and Endoscopy Unit, Fondazione IRCCS Cà Granda, Ospedale Maggiore Policlinico, 20122 Milan, Italy.
J Pers Med. 2023 Aug 28;13(9):1325. doi: 10.3390/jpm13091325.
Gastric cancer ranks as the fifth-leading contributor to global cancer incidence and the fourth-highest in terms of cancer-related mortality. Helicobacter pylori () infection leads to inflammation and ulceration, atrophic and chronic gastritis, and eventually, increases the risk of developing gastric adenocarcinoma. In this paper, we delve into the combined impact of a high-salt diet (HSD) and concurrent infection, which act as predisposing factors for gastric malignancy. A multitude of mechanisms come into play, fostering the development of gastric adenocarcinoma due to the synergy between an HSD and colonization. These encompass the disruption of mucosal barriers, cellular integrity, modulation of gene expression, oxidative stress induction, and provocation of inflammatory responses. On the whole, gastric cancer patients were reported to have a higher median sodium intake with respect to healthy controls. infection constitutes an additional risk factor, with a particular impact on the population with the highest daily sodium intake. Consequently, drawing from epidemiological discoveries, substantial evidence suggests that diminishing salt intake and employing antibacterial therapeutics could potentially lower the susceptibility to gastric cancer among individuals.
胃癌是全球癌症发病率的第五大诱因,在癌症相关死亡率方面位列第四。幽门螺杆菌()感染会引发炎症和溃疡、萎缩性及慢性胃炎,并最终增加患胃腺癌的风险。在本文中,我们深入探讨高盐饮食(HSD)与同时感染幽门螺杆菌所产生的综合影响,这两者是胃部恶性肿瘤的诱发因素。多种机制发挥作用,由于高盐饮食与幽门螺杆菌定植之间的协同作用,促进了胃腺癌的发展。这些机制包括黏膜屏障的破坏、细胞完整性的破坏、幽门螺杆菌基因表达的调节、氧化应激的诱导以及炎症反应的激发。总体而言,据报道,与健康对照组相比,胃癌患者的钠摄入量中位数更高。幽门螺杆菌感染是另一个风险因素,对每日钠摄入量最高的人群影响尤为显著。因此,根据流行病学发现,大量证据表明,减少盐的摄入量并采用抗菌疗法可能会降低个体患胃癌的易感性。