Vasculitis allergica - a non-IgE-mediated hypersensitivity syndrome

Abstract

The diagnosis “Vasculitis allergica” suggests a classical allergic IgE-mediated genesis. However, this is not the case; rather, it is a highly complex mechanism that often prevents the antigen that actually triggers the antigen from being detected.

The current nomenclature for this dermatological disease pattern is cutaneous IgM or IgG immunocomplex vasculitis, which is leukocytoclastic vasculitis of the postcapillary venules [3]. This new classification discards the association associated with the original name with a typically IgE-mediated allergic disease.

Vasculitides are immunologically associated with immune complex diseases, the so-called type III reaction according to Coombs and Gell [14], [15], [16]. They are classified as “non-IgE-mediated allergic hypersensitivity syndrome” according to the underlying immunological process [14], [15], [16]. Many vasculitides are clinically first noticeable on the skin, e. g. by acute, rapidly progressive ulcerations, often associated with severe pain. They are therefore important in the clarification of the causes of venous leg ulcers, but here they rank among the rare diagnoses.

The long-standing term “leukocytoclastic vasculitis” for this disease no longer stands for a single disease pattern but rather for a histological pattern of a group of vasculitides, the so-called immune complex vasculitides [3]. Most of the vascular calibres are small vessel vasculitis, which can occur as single organ vasculitis (SOV) with sole manifestation on the skin or as a cutaneous partial symptom of another multi organ vasculitis (MOV), for example in the context of systemic lupus erythematosus [1]. Cutaneous IgM or IgG immunocomplex vasculitis shows the classic sudden, rapidly progressive course for vasculitis and is clinically characterized by a typical primary fluorescence, the palpable purpura, with high inflammation [2]. In the therapy concept, the first priority is to identify and eliminate the triggering agent [2], [42], [44]. Usually this type of vasculitis shows a predominantly residueless healing with low risk of recurrence, provided that the triggering agent is identified and eliminated [2], [41], [42], [44].

Key words

vasculitis - vasculitis allergica - leukocytoclastic vasculitis (LcV) - immune complex diseases - cutaneous IgM or IgG immune complex vasculitis

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