INTRODUCTION
A 22-year-old male presented to his physician with a two-
week history of fevers, night sweats, and a new tender
erythematous plaque on the left buttock (Figure 1). He
was treated with dicloxacillin without improvement. Subsequent evaluation revealed a severe leukocytosis, anemia, and
thrombocytopenia suspicious for Acute Myelogenous Leukemia (AML). Dermatology was consulted for evaluation of his
skin lesions. Examination revealed a single 7 cm, non-tender,
slightly indurated erythematous plaque on the left buttock with
two shallow central erosions.
Punch biopsies revealed dermal infiltrates with numerous
large, weakly, and strongly positive CD117, CD163, and CD 34
cells consistent with leukemia cutis (Figure 2). Bone marrow
biopsy, peripheral blood smears, and karyotype analysis confirmed the diagnosis of AML subtype M4eos with chromosome
16 inversion.
DISCUSSION
Leukemia cutis (LC) is defined as disseminated or localized skin
lesions that result from neoplastic leukocytes infiltrating into
the dermis, epidermis, or subcutaneous tissues.1 Leukemia
Cutis can present in many ways, including single or multiple
violaceous, reddish, brownish, or hemorrhagic ulcers, nodules,
papules, or plaques of varying sizes.1
Leukemia cutis can arise in various leukemic or dysplastic conditions, most commonly in AML with 3% to 15% of patients
having cutaneous lesions.1,2 Generally, development of LC in
AML portends a poor prognosis.1
Histopathology shows infiltration of the neoplastic cells into the
dermis and occasionally into the epidermis, with extension into
the subcutaneous tissues. Periadnexal or perivascular involvement may be prominent.2,3 The pattern of infiltration can vary
as well with the most frequently observed pattern being diffuse and nodular.2 Less common patterns include single-filing
of cells through collagen bundles and a granuloma annulare-
like pattern.2 The World Health Organization (WHO) recognizes
four main categories of AML: AML with recurrent genetic abnormalities; AML with multilineage dysplasia; therapy-related AML; and AML not otherwise specified.4 Classification by WHO
includes genetic, immunophenotypic, biologic, and clinical
features to define specific disease entities and their associated
prognosis and potential treatments.
Though WHO classification is the standard for today, the French-
American-British classification (FAB) is still commonly used.
The FAB divides AML into subtypes from M0-M7 based on cellular morphology and histochemical activity.5 In some instances,
those morphologic characteristics attributed to each subtype
can actually predict the genetic abnormalities. M4 subtype of
AML occasionally exhibits increased numbers of abnormal
marrow eosinophils making it M4Eo variant. Chromosome 16
inversion is associated with this particular morphologic variant.6 Our patient was diagnosed with AML M4Eo based on the
bone marrow biopsy with karyotyping significant for inv(16).
Chromosome 16 aberrations account for approximately 6% of
all AML diagnoses and 20% of AML M4.7 An inversion of this
chromosome can establish AML diagnosis without any other
cell counts and predicts a favorable prognosis.7
