LAUSR

filled bulla on the left lower abdomen. He had just administered six of his seven injections in his ninth cycle of azacitidine. The lesion on the abdomen corresponded with the site of the azacitidine injection. His past medical history included a previous diagnosis of classic Sweet syndrome to which he was responding to a course of prednisolone (15 mg mane) and dapsone (25 mg mane). Despite broad spectrum antibiotic therapy, he experienced ongoing fevers and over the next 2 days the lesion on his left abdomen become haemorrhagic with concentric rings (Fig. 4). Histopathology demonstrated a florid neutrophilic infiltrate in the epidermis, dermis and subcutis, with spongiosis and pustule formation, and without evidence of vasculitis, necrosis or infection. His dose of prednisolone was increased, and the azacitidine was withheld, with a rapid resolution of his fever. One week later, he, too, was left with only residual bruising. Azacitidine is an antineoplastic agent used in the treatment of high-risk myelodysplastic syndromes, chronic myelomonocytic leukaemia and acute myeloid leukaemia. There are 13 reports of azacitidine-induced Sweet syndrome in the literature (Table S1). In two cases there are reports of disease activity at the injection site, with one patient reporting associated widespread disease and the other reporting oedema of the affected limb. None, apart from the two we present here, report localised haemorrhagic concentric rings at the site of the injection. It has been well documented that pathergy and surgery can precipitate Sweet syndrome. However, in the above patients there was an absence of lesions at other sites of trauma, implicating azacitidine as the causative agent.