脾脏恶性淋巴瘤。形态学和鉴别诊断的组织学和免疫组织化学研究]。

S Falk
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引用次数: 0

摘要

采用常规组织学和免疫组织化学方法研究了450例脾切除术标本,除少数罕见的恶性淋巴瘤(ML)外,其余所有恶性淋巴瘤(ML)均累及。该结果证实并增强了先前研究的结果,并有助于比较脾脏中不同ML的浸润模式。这些研究与肿瘤细胞的免疫组织化学检测相结合,因此可能有助于诊断最小的,即早期的ML脾浸润,以及鉴别ML伴晚期脾累及。最初,大多数低级别NHL导致脾脏白髓的结节性受累,可发展为更大的肿瘤结节和/或通过侵犯邻近红髓结构而弥漫性红髓受累。通常,浸润呈血管性,即肿瘤细胞在白色和红色牙髓的动脉和静脉血管附近积聚。鼻窦受累常与肿瘤的白血病广泛性有关。高级别NHL也主要局限于脾白髓。然而,脾内扩散的特点是形成大结节和/或弥漫性浸润,可破坏脾结构。相比之下,霍奇金淋巴瘤(HL)引起肿瘤结节,表现为扩张性生长,而不是脾实质的进行性浸润。脾脏ML的浸润模式是常见病。因此,结合肿瘤细胞的细胞学特征和免疫表型,它们构成了脾脏ML鉴别诊断的可靠标准,尽管其解剖学和功能基础尚未完全阐明。B细胞和T细胞淋巴瘤最初倾向于选择性地累及脾脏原有的B细胞和T细胞区域。大多数高级别ML表现出类似的行为,尽管脾脏病变的大小通常不能准确识别ML在脾脏的主要表现。因此,它们表现出一种“归巢现象”,即脾脏的两个大淋巴室,这是“类器官”ML(如CB-CC或T区淋巴瘤)最确凿的例证。这种行为被解释为反映了所研究的ML肿瘤细胞的组织发生。此外,特殊类型的辅助细胞,如CD35+ FDC和CD1/S100+ IDRC,似乎对分别适合B淋巴细胞和T淋巴细胞的条件的创造至关重要。肿瘤细胞的逐渐浸润会导致正常微环境的破坏,即FDC网络的改变。(摘要删节为400字)
本文章由计算机程序翻译,如有差异,请以英文原文为准。
[Malignant lymphoma of the spleen. Histological and immunohistochemical studies of morphology and differential diagnosis].

450 splenectomy specimens showing involvement by all save a few very infrequently occurring types of malignant lymphomas (ML) recognized by the updated Kiel classification of ML were investigated by conventional histologic and immunohistochemical methods. The results confirm and augment the findings of previous studies and facilitate a comparison of infiltration patterns of different ML in the spleen. These studies in conjunction with immunohistochemical detection of neoplastic cells may thus contribute to the diagnosis of minimal, i.e. early, splenic infiltration by ML and to the differential diagnosis of ML with advanced splenic involvement. Initially, most low grade NHL lead to nodular involvement of the splenic white pulp which may evolve into larger tumor nodules and/or diffuse red pulp involvement by invasion of adjacent red pulp structures. As a rule, the infiltrates are angiotropic, i.e. neoplastic cells accumulate in the vicinity of arterial and venous blood vessels both in the white and in the red pulp. Sinus involvement is frequently associated with leukemic generalisation of the neoplasm. High grade NHL are also localized predominantly in the splenic white pulp. However, their intrasplenic spread is characterized by the formation of large nodular and/or diffuse infiltrates which may efface the splenic architecture. Hodgkin lymphomas (HL), in contrast, cause coalescing tumor nodules which show expansive growth rather than progressive infiltration of the splenic parenchyma. These infiltration patterns of ML in the spleen are a constant finding. In conjunction with cytologic features and immunophenotype of the neoplastic cells they thus constitute reliable criteria for the differential diagnosis of ML in the spleen, although their anatomical and functional basis has not yet been fully elucidated. B and T cell lymphomas initially tend to show selective involvement of the original B and T cell areas of the spleen. Most high grade ML exhibit a similar behavior, although the size of the splenic lesions usually does not permit an exact identification of the ML's primary manifestation in the spleen. They thus exhibit a "homing phenomenon" to the two large lymphoid compartments of the spleen which is most conclusively illustrated by the "organoid" ML such as CB-CC or T zone lymphoma. This behavior has been interpreted to reflect the histogenesis of the neoplastic cells of the ML under study. In addition, specialised types of accessory cells such as CD35+ FDC and CD1/S100+ IDRC appear to be essential for the creation of conditions which are suitable for B and T lymphocytes, respectively. Progressive infiltration by neoplastic cells will lead to destruction of the normal microenvironment, i.e. alterations of FDC networks.(ABSTRACT TRUNCATED AT 400 WORDS)

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