Department of Clinical Hematology, Institut Curie, 26 rue d'Ulm, Paris cedex 05, France.
Am J Hematol. 2010 Sep;85(9):645-9. doi: 10.1002/ajh.21765.
There is a causal association between Helicobacter pylori (Hp) gastric infection and the development of gastric MALT lymphoma. In contrast, the link between Hp gastric infection and the development of extragastric lymphoma has not been thoroughly investigated. We, therefore, studied the prevalence of gastric Hp infection at initial diagnosis of ophthalmologic and nonophthalmologic extragastric lymphoma patients. Three cohorts of patients were studied: a first one of 83 patients with OAL, a second one of 101 patients with extraophthalmologic extragastric lymphoma, and a third one of 156 control individuals (control) without malignant lymphoma. Gastric Hp infection was investigated by histopathological analysis and Hp-specific PCR assay on gastric biopsy tissue samples. We found gastric Hp infection in 37 OAL patients (45%), in 25 extraophthalmologic extragastric lymphoma cases (25%), and in 18 controls individuals (12%) (P < 0.0001 OAL/C and P < 0.01 OAL/extra-OAL cases). Gastritis was found in 51% and 9% of Hp-positive and Hp-negative lymphoma patients, respectively (P < 10(-4)). Gastric Hp infection only correlated with MALT/LPL lymphoma (P = 0.03). There is a significant association between gastric Hp infection and MALT/LPL OAL. This suggests a novel mechanism of indirect infection-associated lymphomagenesis whereby chronic local antigen stimulation would lead to the emergence of ectopic B-cell lymphoma.
幽门螺杆菌（Hp）胃感染与胃黏膜相关淋巴组织（MALT）淋巴瘤的发展之间存在因果关系。相比之下，Hp 胃感染与胃外淋巴瘤的发展之间的联系尚未得到彻底研究。因此，我们研究了初诊眼科和非眼科胃外淋巴瘤患者中胃 Hp 感染的流行情况。研究了三组患者：第一组 83 例 OAL 患者，第二组 101 例非眼外胃外淋巴瘤患者，第三组 156 例无恶性淋巴瘤的对照个体（对照）。通过组织病理学分析和胃活检组织样本中的 Hp 特异性 PCR 检测研究了胃 Hp 感染。我们发现 37 例 OAL 患者（45%）、25 例非眼外胃外淋巴瘤病例（25%）和 18 例对照个体（12%）存在胃 Hp 感染（P < 0.0001 OAL/C 和 P < 0.01 OAL/extra-OAL 病例）。Hp 阳性和 Hp 阴性淋巴瘤患者的胃炎分别为 51%和 9%（P < 10(-4)）。胃 Hp 感染仅与 MALT/LPL 淋巴瘤相关（P = 0.03）。胃 Hp 感染与 MALT/LPL OAL 之间存在显著相关性。这表明了一种新的间接感染相关淋巴瘤发生机制，即慢性局部抗原刺激会导致异位 B 细胞淋巴瘤的出现。
