Clinical presentations and mechanisms of necrotizing angitis of the skin.
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.
D000936:Antigen-Antibody Complex; D001167:Arteritis / Q000175:diagnosis* / Q000276:immunology / Q000473:pathology; D003165:Complement System Proteins / Q000172:deficiency; D006801:Humans; D006967:Hypersensitivity / Q000473:pathology; D008407:Mast Cells / Q000276:immunology; D009336:Necrosis; D011693:Purpura / Q000175:diagnosis; D012859:Sjogren's Syndrome / Q000097:blood; D012867:Skin / Q000098:blood supply; D012877:Skin Manifestations; D014581:Urticaria / Q000175:diagnosis
D000936:Antigen-Antibody Complex; D003165:Complement System Proteins