title: Bullous sweet syndrome in a patient with t(9;22)(q34;q11)-positive chronic myeloid leukemia treated with the tyrosine kinase inhibitor nilotinib: interphase cytogenetic detection of BCR-ABL- positive lesional cells.
abstract: BACKGROUND
  An association of Sweet syndrome with chronic myeloid leukemia (CML) has been recently observed in patients treated with tyrosine kinase inhibitors.
  
  
  METHODS
  We describe a 67-year-old patient with a 6-year history of Philadelphia chromosome translocation t(9;22)(q34;q11)-positive CML. The tyrosine kinase inhibitor AMN107 (nilotinib) kept the patient in chronic phase. After 10 months of taking nilotinib, he developed pneumonia with septic features. Seven days later, bullous skin infiltrations on the upper arms and a large, painful bullous swelling of the right neck occurred without any evidence of a viral, bacterial, or fungal blood infection. Findings from histologic examination showed massive infiltrations of the whole dermis with neutrophil granulocytes as well as with monocytoid histiocytic cells. Fluorescence in situ hybridization analysis of paraffin-embedded tissue revealed a BCR-ABL fusion, indicating the presence of t(9;22)(q34;q11). The addition of oral prednisolone to an adequate antibiotic treatment led to rapid resolution of the cutaneous infiltrations.
  
  
  CONCLUSIONS
  Skin infiltrations consistent with Sweet syndrome can occur in patients with septic CML during the treatment with tyrosine kinase inhibitors, including nilotinib. Skin infiltrations can include specific CML cells.
authors.affiliation: Department of Dermatology, Georg-August-University Goettingen, Von-Siebold-Strasse 3, 37075 Goettingen, Germany.
authors.forename: Kjell Matthias
authors.initials: KM
authors.lastname: Kaune
authors.forename: Mario
authors.initials: M
authors.lastname: Baumgart
authors.forename: Stefan
authors.initials: S
authors.lastname: Gesk
authors.forename: Christina
authors.initials: C
authors.lastname: Mitteldorf
authors.forename: Joerg
authors.initials: J
authors.lastname: Baesecke
authors.forename: Bertram
authors.initials: B
authors.lastname: Glass
authors.forename: Detlef
authors.initials: D
authors.lastname: Haase
authors.forename: Reiner
authors.initials: R
authors.lastname: Siebert
authors.forename: B Michael
authors.initials: BM
authors.lastname: Ghadimi
authors.forename: Christine
authors.initials: C
authors.lastname: Neumann
authors.forename: Steffen
authors.initials: S
authors.lastname: Emmert
mesh_terms: D000368:Aged; D000970:Antineoplastic Agents / Q000008:administration & dosage / Q000009:adverse effects*; D003937:Diagnosis, Differential; D016044:Fusion Proteins, bcr-abl / Q000032:analysis; D006801:Humans; D017404:In Situ Hybridization, Fluorescence; D015464:Leukemia, Myelogenous, Chronic, BCR-ABL Positive / Q000188:drug therapy* / Q000473:pathology; D008297:Male; D047428:Protein Kinase Inhibitors / Q000008:administration & dosage / Q000009:adverse effects*; D011505:Protein-Tyrosine Kinases / Q000037:antagonists & inhibitors*; D011743:Pyrimidines / Q000008:administration & dosage / Q000009:adverse effects*; D016463:Sweet Syndrome / Q000139:chemically induced / Q000175:diagnosis* / Q000473:pathology
chemical_list: D000970:Antineoplastic Agents; D047428:Protein Kinase Inhibitors; D011743:Pyrimidines; D011505:Protein-Tyrosine Kinases; D016044:Fusion Proteins, bcr-abl; C498826:nilotinib