INVESTIGATIONS INTO THE PATHOGENESIS OF ACUTE CUTANEOUS ANGIITIS

Abstract

SUMMARY.– In this study of necrotizing (polymorphonuclear) angiitis, immunoglobulins and complement are often traceable in and about the superficial dermal blood vessels, serum immunoglobulins are raised, and during cropping of the lesions the serum complement may be low. The commoner lymphocytic angiitis differs in that abnormalities of serum immunoglobulins and of organ-specific and non-specific circulating antibodies are seldom found. Three experimental varieties of polymorphonuclear angiitis are considered in the pathogenesis of necrotizing angiitis: (1) The Arthus reaction with circulating antibodies of high specificity to the antigen; (2) The local Shwartzman reaction, probably a non-immune phenomenon but triggered by endotoxin release, immune complexes, and other non-specific materials; and (3) Circulating immune complexes sludging out in vessels where the flow of blood is sluggish. Clinical and experimental data implicate each of these. Some contributions of individual cell types other than polymorphonuclear cells and lymphocytes in the angiitic infiltrate are mentioned: the mast cell may not be degranulated; the red cell may be inert; the eosinophil's role remains mysterious; the platelet probably provides vasoactive substances and encourages early fibrin deposition. For the rash of necrotizing angiitis to develop, perhaps a specific Arthus type reaction initiates the process in the cutaneous vessels and then the inflammatory response is perpetuated by non-specific factors as in the local Shwartzman reaction.