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

Helicobacter pylori (HP) infection alone, but not HP-induced atrophic gastritis, increases the risk of gastric lymphoma: a case-control study in Japan
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DOI:
10.1007/s00277-019-03721-y
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发表时间:
2019-08-01
影响因子:
3.5
通讯作者:
Matsuo, Keitaro
Matsuo, Keitaro
中科院分区:
医学3区
文献类型:
--
作者:
Ishikura, Naoyo;Usui, Yoshiaki;Matsuo, Keitaro

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幽门螺杆菌(Helicobacter pylori,H. pylori)与胃恶性淋巴瘤风险增加相关。H.幽门螺杆菌感染诱发淋巴瘤发生。虽然这种慢性粘膜炎症也导致萎缩性胃炎,但支持萎缩性胃炎在胃淋巴瘤发生中可能意义的证据很少。在此,为了评估胃粘膜萎缩和胃淋巴瘤风险之间的关系,我们在爱知癌症中心进行了一项配对病例对照研究,重点关注H。幽门螺杆菌感染状况和血清胃蛋白酶原(PG)水平。共纳入86例胃淋巴瘤患者(包括49例粘膜相关淋巴组织结边缘区淋巴瘤(MALT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。通过条件Logistic回归分析评估比值比(OR)和95%置信区间(CI),并调整潜在混杂因素。结果未能显示萎缩性胃炎和胃淋巴瘤风险之间的统计学显著相关性。总体胃淋巴瘤、MALT淋巴瘤、DLBCL和其他淋巴瘤阳性萎缩性胃炎相对于阴性的校正OR分别为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)。相反,总体胃淋巴瘤和H。pylori感染(OR=2.14,95% CI 1.30-3.54)。观察到MALT淋巴瘤、DLBCL和其他淋巴瘤的一致相关性,OR分别为1.96(1.00-3.86)、1.92(0.74-4.95)和5.80(1.12-30.12)。这些结果表明,H.幽门螺杆菌感染诱发胃淋巴瘤,但萎缩性胃炎引起的上皮细胞变化本身并不影响胃淋巴瘤的发展。
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.