images in haematology
Pyoderma gangrenosum secondary to azacitidine in myelodysplastic syndrome
A 66-year-old female was diagnosed with myelodysplastic syndrome (MDS), specifically refractory cytopenia with multilineage dysplasia. Her bone marrow demonstrated 3% blasts with a complex karyotype and she had transfusion-dependent anaemia and thrombocytopenia. She was started on azacitidine for very high-risk MDS, as determined by her Revised International Prognostic Scoring System score. The first cycle of azacitidine was well tolerated. Three days into her second cycle, multiple erythematous, painful pustular plaques with a violaceous border and central haemorrhagic crusting appeared on her lips, inner nose and upper arms (top). Empirical ciprofloxacin and clindamycin had no clinical benefit and the lesions then progressed to involve her forearms, with three dominant lesions 3–4 cm in diameter. A skin biopsy demonstrated a neutrophilic infiltrate with marked acute inflammation and reactive changes (bottom); microbiological studies were negative. The clinical and pathological presentation was in keeping with pyoderma gangrenosum (PG). She was treated with prednisone and colchicine, and the azacitidine was withheld for 2 months with subsequent healing of the lesions. The forearm lesions recurred when re-challenged with azacitidine, but promptly responded to a second course of prednisone. Neutrophilic dermatoses, including Sweet syndrome and PG, are uncommon but well-documented dermatological sequalae of MDS. However, given the recurrence of skin lesions with therapy, the clinical and pathological picture was most in keeping with PG secondary to azacitidine, rather than to the underlying disease. PG in MDS has also been linked to the administration of granulocyte colony-stimulating factor. While our patient’s skin lesions were controlled with concurrent colchicine and corticosteroids, her MDS did not improve with azacitidine and as a result, this drug was stopped after five cycles.
ª 2015 John Wiley & Sons Ltd British Journal of Haematology, 2015, 169, 461
Eric Tseng1, Raed Alhusayen1, Shachar Sade1, Rena Buckstein1 and Anca Prica2 1
Sunnybrook Health Sciences Centre, University of Toronto, and
2
Princess Margaret Cancer Centre, University of Toronto, Toronto, ON,
Canada. E-mail: [email protected]
First published online 12 March 2015 doi: 10.1111/bjh.13341
Pyoderma gangrenosum secondary to azacitidine in myelodysplastic syndrome
A 66-year-old female was diagnosed with myelodysplastic syndrome (MDS), specifically refractory cytopenia with multilineage dysplasia. Her bone marrow demonstrated 3% blasts with a complex karyotype and she had transfusion-dependent anaemia and thrombocytopenia. She was started on azacitidine for very high-risk MDS, as determined by her Revised International Prognostic Scoring System score. The first cycle of azacitidine was well tolerated. Three days into her second cycle, multiple erythematous, painful pustular plaques with a violaceous border and central haemorrhagic crusting appeared on her lips, inner nose and upper arms (top). Empirical ciprofloxacin and clindamycin had no clinical benefit and the lesions then progressed to involve her forearms, with three dominant lesions 3–4 cm in diameter. A skin biopsy demonstrated a neutrophilic infiltrate with marked acute inflammation and reactive changes (bottom); microbiological studies were negative. The clinical and pathological presentation was in keeping with pyoderma gangrenosum (PG). She was treated with prednisone and colchicine, and the azacitidine was withheld for 2 months with subsequent healing of the lesions. The forearm lesions recurred when re-challenged with azacitidine, but promptly responded to a second course of prednisone. Neutrophilic dermatoses, including Sweet syndrome and PG, are uncommon but well-documented dermatological sequalae of MDS. However, given the recurrence of skin lesions with therapy, the clinical and pathological picture was most in keeping with PG secondary to azacitidine, rather than to the underlying disease. PG in MDS has also been linked to the administration of granulocyte colony-stimulating factor. While our patient’s skin lesions were controlled with concurrent colchicine and corticosteroids, her MDS did not improve with azacitidine and as a result, this drug was stopped after five cycles.
ª 2015 John Wiley & Sons Ltd British Journal of Haematology, 2015, 169, 461
Eric Tseng1, Raed Alhusayen1, Shachar Sade1, Rena Buckstein1 and Anca Prica2 1
Sunnybrook Health Sciences Centre, University of Toronto, and
2
Princess Margaret Cancer Centre, University of Toronto, Toronto, ON,
Canada. E-mail: [email protected]
First published online 12 March 2015 doi: 10.1111/bjh.13341
