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Vascular activation in the histopathogenesis of Hodgkin's disease: Potential role of endothelial tissue factor in intravascular thrombosis and necrosis
Author(s) -
Ruco Luigi P.,
Pittiglio Marco,
Dejana Elisabetta,
Baroni Carlo D.
Publication year - 1993
Publication title -
the journal of pathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.964
H-Index - 184
eISSN - 1096-9896
pISSN - 0022-3417
DOI - 10.1002/path.1711710210
Subject(s) - pathology , disseminated intravascular coagulation , tissue factor , fibrin , coagulation , medicine , immunostaining , endothelial stem cell , endothelial activation , endothelium , immunology , immunohistochemistry , biology , biochemistry , in vitro
Endothelial cell activation and alterations of intravascular coagulation were investigated in 27 cases of Hodgkin's disease (HD), in five cases of anaplastic large cell lymphoma (ALCL), and in ten reactive lymph nodes. Lymph node sections were immunostained for E‐selectin, a molecule present on cytokine‐activated endothelial cells; for tissue factor (TF), a cellular initiator of the coagulation cascade; for glycoprotein (gp) II/III, a platelet‐specific antigen; and for fibrin. In HD, vascular activation was particularly prominent in the nodular sclerosis subtype, as indicated by a larger number of E‐selectin‐positive blood vessels (72 ± 49) compared with mixed cellularity (22 ± 37). High expression of E‐selectin was associated with alterations of intravascular coagulation, as indicated by immunostaining of some vascular endothelial cells for TF, by a higher incidence of intravascular thrombi, and by the extensive presence of areas of fibrin exudation and necrosis. In ALCL, the levels of endothelial cell activation and intravascular coagulation were comparable to those of HD nodular sclerosis. In reactive nodes, some E‐selectinpositive blood vessels were observed only in 3/10 cases; immunostaining for TF was not detected on endothelial cells; and alterations of intravascular coagulation were rarely observed.