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A Disease in Histologic Evolution?

Arch Dermatol. 2005;141:893-895.

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

Sweet syndrome (SS) occurs in several predictable clinical settings: those with inflammatory conditions, perhaps most commonly following upper respiratory tract infection; those with hematologic dyscrasias and malignancies, most commonly involving cells of myeloid lineage; and in a variety of other settings. Sweet syndrome occurring in the setting of myeloid malignancy may histologically and clinically appear atypical for a number of reasons: clinically, some of these lesions appear purpuric owing to associated thrombocytopenia; SS occurring as a manifestation of myeloid dyscrasia does not exhibit a predominance in women, unlike the other forms of the disease; and histologically, some of these cases exhibit mononuclear cells compatible with leukemic granulocytic precursors combined with mature neutrophils.¹

Histopathologically, SS is less predictable. The histologic characteristics of this neutrophil-predominant dermatosis have been considered fairly uniform but have been called into question in the literature recently. There has been much controversy regarding the presence of fibrinoid degeneration . . . [Full Text of this Article]

AUTHOR INFORMATION
Janine C. Malone, MD; Stephen P. Slone, MD

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