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Correspondence
Many faces of the same myeloid neoplasm: a case of leukaemia cutis with mixed histiocytic and Langerhans cell differentiation
  1. Vignesh Shanmugam1,
  2. Elizabeth A Morgan1,
  3. Daniel J DeAngelo2,
  4. Annette S Kim1
  1. 1 Department of Pathology, Brigham and Women’s Hospital, Harvard Medical School, Boston, Massachusetts, USA
  2. 2 Department of Medical Oncology, Dana-Farber Center Institute, Harvard Medical School, Boston, MA, USA
  1. Correspondence to Dr Annette S Kim, Department of Pathology, Brigham and Women’s Hospital, Harvard Medical School, Boston, MA 02115, USA; askim{at}bwh.harvard.edu

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Cutaneous involvement by a myeloid neoplasm (myeloid leukaemia cutis), such as chronic myelomonocytic leukaemia (CMML) or acute myeloid leukaemia (AML), can show a spectrum of morphological features and maturation stages, with occasional evidence of histiocytic/dendritic cell differentiation.1 This has to be distinguished from de novo or clonally unrelated histiocytic/dendritic cell neoplasms, which may also arise in patients with underlying myeloid neoplasms. Here, we describe a patient with myeloid leukaemia cutis showing mixed histiocytic and Langerhans cell differentiation arising from underlying CMML/AML. This is an illustrative case of clonal evolution of a myeloid neoplasm that demonstrates at least three distinct constellations of clinical, pathological and molecular findings.

The patient is a 56-year-old man with a prior diagnosis of AML who now presents with a 5-month history of slowly progressive skin nodules. At the time of initial leukaemia diagnosis 10 months prior, the disease was characterised as AML, not otherwise specified with 80% myeloblasts (see legend of figure 1A for immunophenotype and cytochemical characterisation), background dysmegakaryopoiesis and a normal karyotype (figure 1A and B). A peripheral blood smear at the time was notable for a marked leucocytosis (white blood cell count 59.68 x 109/L) with 14% monocytes and 25% blasts, normochromic macrocytic anaemia (haemoglobin 9.0 g/dL, mean cell volume (MCV) 102.4 fL) with anisocytosis, and thrombocytopenia with unremarkable morphology (platelets 86 x 109/L). The only other available complete blood count (CBC) from 5 years prior was notable only for a platelet count of 106 x 109/L. Following standard induction and re-induction therapy, the patient appeared to be in morphological complete remission. One month after completion of induction therapy, CBCs revealed a persistent leucocytosis (up to 58.87 x 109/L) with monocytosis (up to 52%, 20.51 x 109/L), thrombocytopenia (50–90 x 109 …

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