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干燥综合征中广泛存在的克隆性B细胞紊乱易引发幽门螺杆菌相关胃淋巴瘤。

Widespread clonal B-cell disorder in Sjögren's syndrome predisposing to Helicobacter pylori-related gastric lymphoma.

作者信息

De Vita S, Ferraccioli G, Avellini C, Sorrentino D, Dolcetti R, Di Loreto C, Bartoli E, Boiocchi M, Beltrami C A

机构信息

Division of Experimental Oncology 1, Centro di Riferimento Oncologico, Aviano, Italy.

出版信息

Gastroenterology. 1996 Jun;110(6):1969-74. doi: 10.1053/gast.1996.v110.pm8964425.

DOI:10.1053/gast.1996.v110.pm8964425
PMID:8964425
Abstract

Helicobacter pylori has been identified as a critical antigenic stimulus to the development of gastric lymphoma, but additional factors should be required for such evolution. This topic is now of major importance to clarify the pathobiology of gastric lymphomagenesis. Peculiar autoimmune diseases, such as Sjögren's syndrome, are well known to predispose to B-cell lymphomas. We report on a patient with Sjögren's syndrome and a widespread B-cell lymphoproliferative disorder. A pathological picture of low-grade lymphoma was observed in the stomach, concomitantly with H. pylori infection. However, the B-cell disorder was definitely nonmalignant in the other tissues involved, i.e., the parotid gland and lymph nodes, which are the characteristic targets of Sjögren's syndrome-associated lymphoproliferation. After H. pylori eradication, a dramatic regression of gastric lymphoma into chronic gastritis was observed, but no amelioration occurred in the parotid and nodal involvement. Multiple molecular analyses showed the expansion of the same B-cell clone in synchronous and metachronous lymph node, parotid, and gastric lesions before and after H. pylori eradication. Thus, H. pylori played a crucial role in the local boosting of B-cell lymphoproliferation, but the underlying B-cell disorder was that associated with the autoimmune disease and was nonmalignant. The comprehensive clinical, pathological, and molecular approach allowed us to then distinguish the role of peculiar individual predisposing factors and of local infection in the pathobiology of mucosa-associated lymphoid tissue-associated lymphoproliferation.

摘要

幽门螺杆菌已被确认为胃淋巴瘤发生发展的关键抗原刺激因素,但这种演变还需要其他因素。阐明胃淋巴瘤发生的病理生物学,这一课题目前至关重要。众所周知,诸如干燥综合征等特殊自身免疫性疾病易引发B细胞淋巴瘤。我们报告了一例患有干燥综合征及广泛B细胞淋巴增殖性疾病的患者。在胃中观察到低度淋巴瘤的病理表现,同时伴有幽门螺杆菌感染。然而,在其他受累组织,即腮腺和淋巴结中,B细胞病变肯定是非恶性的,而腮腺和淋巴结是干燥综合征相关淋巴增殖的特征性靶器官。根除幽门螺杆菌后,观察到胃淋巴瘤显著消退为慢性胃炎,但腮腺和淋巴结受累情况未得到改善。多项分子分析表明,在根除幽门螺杆菌前后,同步和异时的淋巴结、腮腺及胃部病变中,相同的B细胞克隆发生了扩增。因此,幽门螺杆菌在局部促进B细胞淋巴增殖中起关键作用,但潜在的B细胞病变是与自身免疫性疾病相关的,且是非恶性的。综合临床、病理和分子方法,使我们能够区分特殊个体易感因素和局部感染在黏膜相关淋巴组织相关淋巴增殖病理生物学中的作用。

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