By N. F. Krasnov
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Fig. 6. , neutrophils) in vasculitis will lose their anti-coagulation function, including fibrinolysis and the reduction of platelet activation, resulting in the formation of fibrin thrombi at the luminal side of the damaged endothelial cell and eventually formation of fibrinoid necrosis at the damaged vessel wall. 28 Advances in the Diagnosis and Treatment of Vasculitis Fig. 7. Formation of fibrin thrombi at the very early stage of vasculitis. Fibrin thrombi (thick arrows) mixed with a few inflammatory cells are adhered to the affected intima, where loss of endothelial cells can be appreciated (long arrow).
A. Arteritis at the subacute stage. (Left) The inflammatory cells comprise a mixed infiltrate of neutrophils, lymphocytes, and histiocytes; however, there is no formation of fibrous proliferation and no neovascularization in and around the vessel wall. (Right) [elastic tissue stain] The fibrinous exudates can be seen discharging into the medial muscular layers throughout the disrupted internal elastic lamina (arrows). Histopathology of Cutaneous Vasculitis 33 Fig. 12. B. Another arteritis at the subacute stage (A) Arteritis at the subacute stage showing intimal concentric fibrinoid necrosis.
Fibrinoid necrosis of the vessel wall due to a direct vessel wall invasion by tumor cells can be identified in neoplastic lesions, as seen here in a case of NK/T cell lymphoma. (Right: elastic tissue stain) Histopathology of Cutaneous Vasculitis 43 Fig. 21. (A) A pitfall in overlooking vasculitis because of an inappropriate section cut in the wrong direction. Vasculitis occurs as a segmental lesion along the affected vessels. (B) If the lesion is cut in the wrong direction, the initial section may show no evidence of vasculitis.