肺黏膜相关淋巴组织边缘区B细胞淋巴瘤及良性淋巴组织增生性疾病的临床病理分析  

Clinieopathologie study of primary marginal zone B-cell iymphoma of MALT type and lymphoid hyperplasia of lung

作　　者：冯瑞娥[1] 田欣伦[2] 刘鸿瑞[1] 凌庆[1] 钟定荣[1] 罗玉凤[1] 曹金伶[1] 万建伟[1] 朱元珏[2] 

机构地区：[1]中国医学科学院北京协和医学院 北京协和医院病理科,100730 [2]中国医学科学院北京协和医学院 北京协和医院呼吸内科,100730

出　　处：《中华病理学杂志》2008年第3期155-159,共5页Chinese Journal of Pathology

摘　　要：目的研究肺原发性黏膜相关淋巴组织边缘区B细胞（MALT）淋巴瘤及良性淋巴组织增生性疾病的临床病理形态、免疫组织化学表型和B细胞重链基因重排，比较肺MALT淋巴瘤和良性淋巴组织增生性疾病的差异。方法回顾性的分析原发性肺MALT淋巴瘤13例，7例肺良性淋巴组织增生性疾病资料。对标本行常规HE染色，EnVision免疫组织化学染色（抗体包括AE1／AE3、CD20、CD79α、CD3、CD5、CD10、CD21、bcl-2、bcl-6、cyclinD-1）及免疫球蛋白重链IgH基因重排检测。结果13例肺MALT淋巴瘤，细胞成分多样，分别由不同比例的小淋巴细胞样细胞、中心细胞样细胞、单核样B细胞组成，常伴有浆细胞分化。肿瘤细胞以弥漫性和滤泡边缘区排列为主，常见反应性淋巴滤泡和滤泡中心的植入。肿瘤细胞呈串珠状直接侵犯肺泡间隔和沿支气管血管束向周边及肺膜扩散。MALT淋巴瘤中，均未见坏死。9例可见肿瘤细胞侵犯血管壁，6例可见胸膜累及，2例肺门淋巴结侵犯。9例肺MALT淋巴瘤可见淋巴上皮样病变，免疫组织化学显示上皮细胞内的淋巴细胞CD20阳性，CD3阴性。7例肺良性淋巴组织增生性疾病，2例可见淋巴上皮样病变，免疫组织化学显示，其淋巴上皮样病变内的淋巴细胞，部分CD20阳性，部分CD3阳性。9例肺MALT淋巴瘤进行了免疫球蛋白重链IgH基因重排，8例阳性；7例良性淋巴组织增生性疾病均为阴性。结论肺MALT淋巴瘤在细胞组成和排列上与其他部位结外MALT淋巴瘤相同，肿瘤细胞呈串珠状直接侵犯肺泡间隔和沿支气管血管束向周边及肺膜扩散。在肺内淋巴上皮样病变常见于MALT淋巴瘤，并有助于诊断，但并非其特异性病变，一些肺的反应性淋巴组织增生也可出现，用免疫组织化学有助于区别两种病变。免疫球蛋白重链IgH基因重排可以帮助鉴别肺MALT淋巴瘤和良性淋巴组织增生性Objective To study the clinicopathologic features, immunohistochemical findings and immunoglobulin heavy chain （IgH） gene rearrangement results of primary pulmonary mucosa-associated lymphoid tissue lymphoma （MALToma） and reactive lymphoid hyperplasia. Methods Twenty cases, included 13 cases of pulmonary MALToma and 7 cases of pulmonary lymphoid hyperplasia, encountered during the period from 1989 to 2007, were retrospectively analyzed. The samples were paraffin-embedded and stained with hematoxylin and eosin. Immunohistochemical study and semi-nested polymerase chain reaction for IgH gene rearrangement were performed. Results The 13 cases of primary pulmonary MALToma were composed of a spectrum of lymphoid cells, including lymphocyte-like cells, centrocyte-like cells and mononuclear B cells with plasmacytoid differentiation. They often had diffuse or marginal zone growth patterns. Lymphoid follicles with neoplastic colonization were apparent. The lymphoma cells spread along alveolar septa and bronchovascular bundles. Vascular invasion was noted in 9 cases, pleura involvement in 6 cases and nodal involvement in 2 cases. Lymphoepithelial lesions （LEL） were identified in 9 cases of pulmonary MALToma. Immunohistochemically, the lymphocytes in LEL were CD20-positive and CD3-negative. On the other hand, LEL was also present in 2 of the 7 cases of lymphoid hyperplasia studied, with a mixture of CD20-positive B cells and CD3-negative T cells. Eight of the 9 cases of primary pulmonary MALToma were positive for IgH gene rearrangement, while all of the 7 cases of lymphoid hyperplasia were negative. Conclusions Histologically, the cell population of primary pulmonary MALToma is similar to that of extranodal MALToma occurring in other organs. LEL, though commonly observed in pulmonary MALToma, are not specific and can also be seen in cases of reactive lymphoid hyperplasia. The immunophenotype of intraepithelial lymphocytes in pulmonary MALToma and reactive lymphoid hyperplasia is different. The presence of a mono

关 键 词：肺肿瘤 淋巴瘤 黏膜相关淋巴样组织 基因重排 

分 类 号：R686[医药卫生—骨科学]