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Helicobacter pylori (HP) infection alone, but not HP-induced atrophic gastritis, increases the risk of gastric lymphoma: a case-control study in Japan

机译:单独幽门螺杆菌(HP)感染,但不是HP诱导的萎缩性胃炎,增加了胃淋巴瘤的风险:日本的病例对照研究

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Infection with Helicobacter pylori (H. pylori) is associated with an increased risk of gastric malignant lymphoma. The chronic inflammation of gastric mucosa by H. pylori infection induces lymphomagenesis. Although this chronic mucosal inflammation also results in atrophic gastritis, evidence supporting the possible significance of atrophic gastritis in gastric lymphomagenesis is scarce. Here, to evaluate the association between gastric mucosal atrophy and the risk of gastric lymphoma, we conducted a matched case-control study at Aichi Cancer Center focusing on the attribution of H. pylori infection status and pepsinogen (PG) serum levels. In total, 86 patients with gastric lymphoma (including 49 cases of extranodal marginal zone lymphoma of mucosa-associated lymphoid tissue (MALT lymphoma) and 24 cases of diffuse large B cell lymphoma (DLBCL)) and 1720 non-cancer controls were included. Odds ratios (ORs) and 95% confidence intervals (CIs) were assessed by conditional logistic regression analysis with adjustment for potential confounders. Results failed to show a statistically significant association between atrophic gastritis and the risk of gastric lymphoma. The adjusted ORs of positive atrophic gastritis relative to negative for overall gastric lymphoma, MALT lymphoma, DLBCL, and other lymphomas were 0.77 (95% CI 0.45-1.33), 0.65 (0.30-1.39), 1.03 (0.38-2.79), and 0.84 (0.22-3.29), respectively. In contrast, a positive association between overall gastric lymphoma and H. pylori infection was observed (OR=2.14, 95% CI 1.30-3.54). A consistent association was observed for MALT lymphoma, DLBCL, and other lymphomas with ORs of 1.96 (1.00-3.86), 1.92 (0.74-4.95), and 5.80 (1.12-30.12), respectively. These findings suggest that H. pylori infection triggers gastric lymphoma but that epithelial changes due to atrophic gastritis do not inherently affect the development of gastric lymphoma.
机译:用幽门螺杆菌(H.Pylori)感染与胃恶性淋巴瘤的风险增加有关。 H.幽门螺杆菌感染胃黏膜慢性炎症诱导淋巴瘤。虽然这种慢性粘膜炎症也导致萎缩性胃炎,但证据证据支持胃淋巴瘤中萎缩性胃炎可能意义稀缺。在这里,为了评估胃粘膜萎缩与胃淋巴瘤的风险之间的关联,我们在Aichi癌症中心进行了一项匹配的病例对照研究,这些研究专注于H.幽门螺杆菌感染状态和胃蛋白酶原(PG)血清水平的归因。包括总共86例胃淋巴瘤(包括粘膜相关淋巴组织(麦芽淋巴瘤)和24例弥漫性大B细胞淋巴瘤(DLBCL))和1720例非癌症对照的49例胃淋巴瘤患者。通过调整潜在混淆的条件逻辑回归分析评估了几率比率(或者)和95%的置信区间(CIs)。结果未能显示萎缩性胃炎与胃淋巴瘤风险之间的统计学意义关系。相对于整个胃淋巴瘤,麦芽淋巴瘤,DLBCL和其他淋巴瘤相对于阴性的调节或阳性萎缩性胃炎为0.77(95%CI 0.45-1.33),0.65(0.30-1.39),1.03(0.38-2.79)和0.84 (0.22-3.29)分别。相反,观察到整个胃淋巴瘤和H.幽门螺杆菌感染之间的阳性关系(或= 2.14,95%CI 1.30-3.54)。对于麦芽淋巴瘤,DLBCL和其他具有1.96(1.00-3.86),1.92(0.74-4.95)和5.80(1.12-30.12)的淋巴瘤的其他淋巴瘤分别观察到一致的关联。这些发现表明H. Pylori感染触发胃液淋巴瘤,但由于萎缩性胃炎引起的上皮变化并不具有胃淋巴瘤的发育。

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