LAUSR

these cells were strongly positive for CD123, CD138, CD33 and myeloperoxidase, which are markers that are frequently expressed on leukaemia blast cells (Fig. 2b–d). A bone marrow biopsy confirmed the suspected diagnosis of AML (subtype M2 of the French–American–British classification). A diagnosis of unusual LC in AML was made, and chemotherapy with 5-azacytidin was initiated, resulting in a rapid reduction of peripheral blood blast cells as well as clinical improvement of the leg ulcer. However, the patient died 2 months later because of progression of his AML. LC most frequently occurs in chronic lymphocytic leukaemia and AML. In a large study of 381 patients with AML, LC was found in 14 (3.7%), but only 1 had AML subtype M2. In the majority of cases, LC is observed in patients who already have a diagnosis of leukaemia, whereas simultaneous manifestation of cutaneous and systemic involvement is less frequent (approximately 25%). LC preceding haematological detection of leukaemia in the peripheral blood or bone marrow, as seen in our patient, is very rare. LC may present as localized or generalized lesions, with the latter occurring predominantly in acute types of leukaemia. Clinically, LC most frequently manifests as papules, nodules or plaques with a characteristic reddish or violaceous colour. Interestingly, specific leukaemic infiltrates also manifest at sites of previous trauma, within lesions of inflammatory skin diseases and in skin tumours. It has been reported that complex chemokine/chemokine-receptor interactions (e.g. CCR5, CXCR4, CXCR7, and CX3CR1) orchestrate the migration of leukaemic cells to the skin, a phenomenon called ‘skin selective homing’. Accordingly, local trauma and venous insufficiency might have been predisposing factors for homing and retention of AML blast cells in our patient’s leg ulcer. Prognosis of LC is usually poor, and it has been reported that up to 90% of patients will die within the first year after their diagnosis of LC, especially patients with AML.