A Morphological Study of Evolution of Cutaneous Polyarteritis Nodosa
Masafumi Ishibashi, Ko‐Ron Chen
Abstract
Masafumi Ishibashi, Ko‐Ron Chen
Abstract
Morphologic changes including formation of vessel wall fibrinoid necrosis in evolution of cutaneous polyarteritis nodosa (C-PAN) have not been described in detail. Therefore, an investigation of 18 skin biopsy specimens from 14 cases of clinicohistologically proven C-PAN was performed. The results indicated that evolution of arteritis can be classified into 4 stages. Coexistence of different stages was common (50%) in the same or different specimens. The initial (acute) stage shows endothelial loss and fibrin thrombi with neutrophil infiltration without obvious internal elastic lamina disruption and medial fibrinoid necrosis. The second (subacute) stage has mixed cell infiltrates showing a unique intimal target-like fibrinoid necrosis with fibrinoid leakage extending through the disrupted sites of the internal elastic lamina to the media. The third (reparative) stage shows intimal fibroblastic proliferation and perivascular neovascularization with predominant infiltrates of histiocytes and lymphocytes. The final (healed) stage has minimal cellular inflammation with occlusive intimal thickening. Overall, our results show that there are 4 stages in the evolution of C-PAN. The initial change occurs in the intima, and the role of internal elastic lamina in preventing intimal fibrinoid necrosis from discharging into the media may account for the development of target-like fibrinoid necrosis in C-PAN.
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Morphologic changes including formation of vessel wall fibrinoid necrosis in evolution of cutaneous polyarteritis nodosa (C-PAN) have not been described in detail. Therefore, an investigation of 18 skin biopsy specimens from 14 cases of clinicohistologically proven C-PAN was performed. The results indicated that evolution of arteritis can be classified into 4 stages. Coexistence of different stages was common (50%) in the same or different specimens. The initial (acute) stage shows endothelial loss and fibrin thrombi with neutrophil infiltration without obvious internal elastic lamina disruption and medial fibrinoid necrosis. The second (subacute) stage has mixed cell infiltrates showing a unique intimal target-like fibrinoid necrosis with fibrinoid leakage extending through the disrupted sites of the internal elastic lamina to the media. The third (reparative) stage shows intimal fibroblastic proliferation and perivascular neovascularization with predominant infiltrates of histiocytes and lymphocytes. The final (healed) stage has minimal cellular inflammation with occlusive intimal thickening. Overall, our results show that there are 4 stages in the evolution of C-PAN. The initial change occurs in the intima, and the role of internal elastic lamina in preventing intimal fibrinoid necrosis from discharging into the media may account for the development of target-like fibrinoid necrosis in C-PAN.
Key concepts: Fibrinoid necrosis, Internal elastic lamina, Pathology, Necrosis, Polyarteritis nodosa, Fibrin, Histiocyte, Infiltration (HVAC)