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
Malone JC, Slone SP. Sweet Syndrome: A Disease in Histologic Evolution? Arch Dermatol. 2005;141(7):893–895. doi:10.1001/archderm.141.7.893
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