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	Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings.

We read with interest the article by Irvine et al¹ in a recent issue of the ARCHIVES that describes a "cutaneous-limited variant of microscopic polyangiitis associated with antimyeloperoxidase autoantibody."

The authors describe a 34-year-old man with a 22-year history of cutaneous purpuric generalized lesions. Several skin biopsy specimens showed a neutrophilic perivascular inflammatory infiltrate with leukocytoclasis, but evidence of dermal vessel necrosis was not demonstrated. Direct immunofluorescence revealed no vascular deposit of immunoreactants. Extracutaneous involvement other than myalgia, fever, anorexia, and synovitis was not documented (although neither electromyography nor angiography were performed). Antimyeloperoxidase titers closely correlated with disease activity.

Although the authors propose that such biopsy specimens represent a "histologically typical leukocytoclastic vasculitis," true vasculitic changes, such as fibrinoid necrosis of the dermal vessels, inflammatory infiltration of vascular walls, or red blood cell extravasation, were never documented.^2-3 In our opinion, since cutaneous leukocytoclastic angiitis and microscopic polyangiitis are both considered . . . [Full Text of this Article]

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