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恶性和非恶性淋巴组织中的纤维蛋白原沉积及巨噬细胞相关纤维蛋白形成

Fibrinogen deposition and macrophage-associated fibrin formation in malignant and nonmalignant lymphoid tissue.

作者信息

Costantini V, Zacharski L R, Memoli V A, Kisiel W, Kudryk B J, Rousseau S M, Stump D C

机构信息

Department of Medicine, Veterans Administration Medical Center, White River Junction, VT 05001.

出版信息

J Lab Clin Med. 1992 Feb;119(2):124-31.

PMID:1740624
Abstract

Nonmalignant lymphoid tissue and tissue from patients with nodular sclerosis, Hodgkin's disease, and large cell lymphocytic lymphoma was examined by immunohistochemical techniques for the occurrence in situ of components of coagulation and fibrinolysis reaction pathways. Staining for material interpreted as fibrinogen was observed in abundance in both malignant and reactive lymphoid tissue. Fibrin also occurred to a variable extent but focally in all tissues. Components of coagulation pathways, including tissue factor, factor VII, factor X, and factor XIII ("a" subunit), were restricted to tissue macrophages. Double-labeling techniques revealed fibrin in direct apposition to tissue macrophages. We conclude that fibrinogen and fibrin occur in both benign and malignant lymphoid tissue and that the transformation of fibrinogen to fibrin is attributable to macrophage-initiated thrombin formation. We postulate that both systemic and local hypercoagulability associated with these disorders may be attributable to macrophage activation resulting in expression of procoagulant activity.

摘要

采用免疫组织化学技术对非恶性淋巴组织以及结节硬化型霍奇金病和大细胞淋巴细胞淋巴瘤患者的组织进行检查,以观察凝血和纤维蛋白溶解反应途径成分的原位发生情况。在恶性和反应性淋巴组织中均大量观察到被解释为纤维蛋白原的物质染色。纤维蛋白在所有组织中也有不同程度的出现,但呈局灶性。凝血途径的成分,包括组织因子、因子VII、因子X和因子XIII(“a”亚基),仅限于组织巨噬细胞。双重标记技术显示纤维蛋白与组织巨噬细胞直接并置。我们得出结论,纤维蛋白原和纤维蛋白存在于良性和恶性淋巴组织中,并且纤维蛋白原向纤维蛋白的转化归因于巨噬细胞启动的凝血酶形成。我们推测,与这些疾病相关的全身和局部高凝状态可能归因于巨噬细胞激活导致促凝血活性的表达。

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