Soter N A
J Invest Dermatol. 1976 Sep;67(3):354-9. doi: 10.1111/1523-1747.ep12514705.
Cutaneous necrotizing angiitis may be present as either palpable purpura or less commonly as recurrent urticaria, and each clinical presentation may be associated with hypocomplementemia or a normal complement system. A variety of mechanisms may be operative in the production of necrotic vascular skin lesions that appear as similar, recognizable morphologic lesions. These mechanisms include immune complexes, cellular-type hypersensitivity reactions, and initiation or modulation by mast cells. Two cellular patterns have been recognized in the skin of patients with cutaneous necrotizing angiitis that can be correlated with the involvement of the complement system in serum. In patients with hypocomplementemia, there is an infiltrate of neutrophils that is consistent with a process involving immune complexes; in patients with normocomplementemia there are lymphocytes and activated lymphocytes consistent with participation in part by cellular mechanisms. In both the hypocomplementemic and normocomplementemic forms and as well as in a unique patient in whom the mast cell may initiate the venular damage, the mast cell, which its content of chemical mediators, has the capacity to initiate as well as modulate subacute and chronic vascular damage.
皮肤坏死性血管炎可表现为可触及的紫癜，较少见的表现为反复发作的荨麻疹，且每种临床表现可能与补体血症降低或补体系统正常有关。多种机制可能在坏死性血管性皮肤病变的产生过程中起作用，这些病变表现为相似的、可识别的形态学病变。这些机制包括免疫复合物、细胞型超敏反应以及肥大细胞的启动或调节作用。在皮肤坏死性血管炎患者的皮肤中已识别出两种细胞模式，这与血清中补体系统的参与情况相关。在补体血症降低的患者中，有中性粒细胞浸润，这与涉及免疫复合物的过程一致；在补体正常的患者中，有淋巴细胞和活化淋巴细胞，这部分与细胞机制的参与有关。在补体血症降低和补体正常的形式中，以及在肥大细胞可能引发小静脉损伤的一位独特患者中，肥大细胞因其化学介质的含量，有能力启动和调节亚急性和慢性血管损伤。
