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© Dirk Biddle
Kossard (1) pointed out: “Vasculitis can be defined as vascular inflammation which is usually immune mediated, leading to structural and functional damage to the vessel wall. Our concept of vasculitis has been built around the events surrounding immune-complex-triggered leukocytoclastic vasculitis, while the role of lymphocyte mediated vasculitis remains largely undefined. This may be due to maintaining a stereotypic image of lymphocytic vasculitis as one associated with vascular necrosis, fibrin deposition and haemorrhage and merely substituting lymphocytes for neutrophils. Our understanding of lymphocytic vasculitis may be advanced by identifying the clinical settings in which such reactions may occur, such as autoimmune skin diseases sharing features with graft vs. host disease, as well as recognizing that lymphocyte mediated inflammation may lead to a morphologically distinct group of vasculitides, apart from those associated with angio-destruction.
Lymphocytic endovasculitis, lymphocytic lichenoid vasculitis and granulomatous vasculitis are potential examples of lymphocytic vasculitis that differ from the histological pattern seen in association with immune complex leukocytoclastic vasculitis. Ultimately, the proof that these vasculitides are examples of lymphocytic vasculitis will rest on new techniques emerging in molecular pathology that have the capacity of analysing the immunological events beyond the current limitations posed by routine histopathology.” (1)
Smoller, McNutt and Contreras (1990) also contended: “While histopathologic analysis may offer some clues as to the pathogenesis of vasculitis, observations must be interpreted with caution, as there is considerable overlap in the histologic pattern. In most cases, a predominantly neutrophilic vasculitis affecting small dermal venules suggests a relatively acute, immune complex-mediated reaction. Less commonly, this histologic pattern may be seen in non-immunologically mediated processes, such as in the presence of bacterial toxins or malignant hypertension, or in more chronic disease states, such as granuloma faciale or erythema elevatum diutinum. A predominantly lymphocytic vasculitis may represent several pathogenetic mechanisms. In lesions more than 24 to 48 hours old, a lymphocytic vasculitis may represent a resolving phase of an immune complex-mediated neutrophilic vasculitis. Alternatively, this histologic pattern may be seen de novo in conditions with a presumed cell-mediated immunologic pathogenesis. Lymphocytic vasculitis may also be seen in rickettsial infections such as Rocky Mountain spotted fever. The pathogenesis of granulomatous vasculitis remains poorly understood and is thought to be induced by a combination of circulating immune complexes and a cell-mediated immune response.” (2)
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1. Kossard, S. (2000) Defining lymphocytic vasculitis. Australasion journal of Dermatology. 41(3), 149-155.
2. Smoller, B., McNutt, N., & Contreras, F. (1990) The natural history of vasculitis. What the histology tells us about pathogenesis. Archives of Dermatology. 126(1).
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