Clinical Image: Brachial arteritis on positron emission tomography/computed tomography in acute eosinophilic granulomatosis with polyangiitis

The patient, a 56-year-old man, was admitted with four weeks of bilateral ankle pain and swelling, lower limb dysesthesia, fatigue, night sweats, fevers, and 10 kg of subacute weight loss. On examination, there was bilateral ankle synovitis and a distal sensory peripheral neuropathy. History included asthma and eosinophilic chronic rhinosinusitis with polypectomy. Nerve conduction studies confirmed sensory neuropathy, and computed tomography (CT) chest demonstrated scattered pulmonary infiltrates. Laboratory tests revealed an elevated erythrocyte sedimentation rate of 91 mm/h (reference range 0–20 mm/h), C-reactive protein level of 215 mg/L (reference range <3 mg/L), peripheral eosinophilia level of 2.37 × 109/L, and negative antineutrophil cytoplasmic antibody (ANCA) result. Investigations for other causes of hypereosinophilia, including infection and hematologic malignancy, were negative. An 18F-fludeoyglucose–positron emission tomography (PET)/CT scan demonstrated increased metabolic activity in bilateral brachial arteries, more prominent on the right, consistent with active large vessel vasculitis (arrow). He had no vascular bruits or distal thrombotic changes. Temporal artery biopsy was negative. He was diagnosed with ANCA-negative eosinophilic granulomatosis with polyangiitis (EGPA) and commenced on prednisolone and rituximab. A right brachial artery ultrasound two weeks later was unremarkable, and his markers of inflammation and eosinophil count normalized. Eosinophilic disorders, including EGPA, are associated with arterial and venous thrombosis.1-3 This is thought to be secondary to the prothrombotic effects of eosinophilic granules on the coagulation cascade and endothelium.2 The PET/CT findings in this patient indicate that EGPA can also be associated with large vessel arterial inflammation, which has only rarely been reported. We hypothesize that this may be a contributing factor to the development of arterial thrombosis. Open access publishing facilitated by University of New South Wales, as part of the Wiley - University of New South Wales agreement via the Council of Australian University Librarians. Disclosure form Please note: The publisher is not responsible for the content or functionality of any supporting information supplied by the authors. Any queries (other than missing content) should be directed to the corresponding author for the article.