INTRODUCTION
The malignant transformation of hematopoietic cells leads to the manifestation of leukemia.1 Depending on the cell lineage and maturity, the main overarching subtypes of leukemia are acute myeloid leukemia (AML), acute lymphoblastic leukemia (ALL), chronic myeloid leukemia (CML), and chronic lymphoblastic leukemia (CLL).1
In addition to bone marrow and peripheral blood involvement, extramedullary forms of leukemia such as granulocytic sarcoma and leukemia cutis also exist.2 Leukemia cutis (LC) is the infiltration of leukemia cells in the skin, leading to clinically apparent lesions, and occurs in about 3% of leukemia patients.3 While the pathophysiology of LC remains unknown, there is speculation that the migration of leukemia cells to the skin is a result of an attraction between various expressed chemokines and adhesion molecules.4 Genetic variations have also been associated with this extramedullary involvement of AML such as the inversion of chromosome 16, rearrangement of chromosome 11q23, and NPM1 mutation.5 LC typically occurs concomitantly or after leukemia diagnosis, but can rarely precede it by months to years.6 Approximately 55-77% of LC patients are diagnosed with leukemia prior to presentation.6 Compared with the other leukemias, AML and CLL have a higher propensity to cause LC, specifically those with AML. Poorer prognosis of leukemia is suspected when there is cutaneous involvement.5 Wang et al conducted a retrospective study of matched AML subjects with or without LC and revealed the 5-year survival to be 8.6% and 23.8%, respectively.5
In addition to bone marrow and peripheral blood involvement, extramedullary forms of leukemia such as granulocytic sarcoma and leukemia cutis also exist.2 Leukemia cutis (LC) is the infiltration of leukemia cells in the skin, leading to clinically apparent lesions, and occurs in about 3% of leukemia patients.3 While the pathophysiology of LC remains unknown, there is speculation that the migration of leukemia cells to the skin is a result of an attraction between various expressed chemokines and adhesion molecules.4 Genetic variations have also been associated with this extramedullary involvement of AML such as the inversion of chromosome 16, rearrangement of chromosome 11q23, and NPM1 mutation.5 LC typically occurs concomitantly or after leukemia diagnosis, but can rarely precede it by months to years.6 Approximately 55-77% of LC patients are diagnosed with leukemia prior to presentation.6 Compared with the other leukemias, AML and CLL have a higher propensity to cause LC, specifically those with AML. Poorer prognosis of leukemia is suspected when there is cutaneous involvement.5 Wang et al conducted a retrospective study of matched AML subjects with or without LC and revealed the 5-year survival to be 8.6% and 23.8%, respectively.5
CASE
A 78-year-old African American female was referred to the dermatology clinic by her primary care physician due to a two-month history of raised, pruritic, dry lesions. The patient had a past medical history of untreated chronic myelomonocytic leukemia (CMML), Type II Diabetes Mellitus, Chronic Obstructive Pulmonary Disease, Hypertension, and Major Depressive Disorder. Her physical exam revealed multiple, indurated, pearly plaques and nodules on her eyelids and upper and lower extremities (Figure 1). There was no evidence of ulceration or scaling and the lesions were not tender to palpation. A right forearm biopsy was collected. She was prescribed a 14-day course of twice daily 0.1% triamcinolone cream to soothe her itch.
