Ishibashi Masafumi, Chen Ko-Ron
Department of Dermatology, Saiseikai Central Hospital, Tokyo, Japan.
Am J Dermatopathol. 2008 Aug;30(4):319-26. doi: 10.1097/DAD.0b013e3181766190.
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.
皮肤结节性多动脉炎(C-PAN)演变过程中的形态学变化,包括血管壁纤维蛋白样坏死的形成,尚未得到详细描述。因此,我们对14例经临床组织学证实的C-PAN患者的18份皮肤活检标本进行了研究。结果表明,动脉炎的演变可分为4个阶段。不同阶段在同一或不同标本中同时存在的情况很常见(50%)。初始(急性)阶段表现为内皮细胞缺失、纤维蛋白血栓形成以及中性粒细胞浸润,无明显内弹力层破坏和中层纤维蛋白样坏死。第二(亚急性)阶段有混合细胞浸润,呈现独特的内膜靶样纤维蛋白样坏死,纤维蛋白样渗漏通过内弹力层的破损部位延伸至中层。第三(修复)阶段表现为内膜成纤维细胞增生和血管周围新生血管形成,主要浸润细胞为组织细胞和淋巴细胞。最后(愈合)阶段细胞炎症极少,内膜增厚并闭塞。总体而言,我们的结果表明C-PAN的演变有4个阶段。初始变化发生在内膜,内弹力层在防止内膜纤维蛋白样坏死扩散至中层方面的作用,可能是C-PAN中靶样纤维蛋白样坏死形成的原因。