thromboplastin and Sclerosis

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.

Topics: Adolescent; Adult; Aged; Factor VII; Factor VIII; Factor X; Female; Fibrin; Fibrinogen; Fibrinolysis; Hodgkin Disease; Humans; Immunohistochemistry; Leukemia, Lymphocytic, Chronic, B-Cell; Lymph Nodes; Lymphoid Tissue; Lymphoma, Large B-Cell, Diffuse; Macromolecular Substances; Macrophages; Male; Middle Aged; Sclerosis; Thromboplastin

Topics: Cardiovascular Diseases; Hematologic Diseases; Humans; Prothrombin Time; Research; Sclerosis; Thrombophilia; Thromboplastin