O40. BEWARE NEGATIVE FLUORODEOXYGLUCOSE POSITRON EMISSION TOMOGRAPHY/COMPUTED TOMOGRAPHY AND TEMPORAL ARTERY BIOPSY IN PYREXIA OF UNKNOWN ORIGIN: TWO CASES WITH DISCORDANT RESULTS

Abstract

Background: The use of FDG-PET/CT scanning is becoming more widespread in the investigation of pyrexia of unknown origin (PUO) with raised inflammatory markers to exclude rheumatological disorders. Methods: We report two cases of large vessel vasculitis fulfilling Petersdorf and Beeson criteria for PUO, where whole body FDG-PET/ CT scans were used successfully and unsuccessfully to diagnose vasculitis. Results: Case one is a 76 year old Caucasian male with stable seropositive ACPA positive rheumatoid arthritis on methotrexate monotherapy. Prednisolone 15mg was commenced in primary care for worsening arthritis. Weeks later he presented with recurrent fever, malaise, oral ulceration, fatigue and raised inflammatory markers (ESR 113mm/hr, CRP 283mg/l). Steroids were continued. Extensive microbiology, immunology, virology and imaging tests were unremarkable including CT of the thorax, abdomen and pelvis and MRI of the entire spine. An atypical right-sided headache developed without classic temporal tenderness, bruits or vascular signs. A 17mm inpatient temporal artery biopsy (TAB) was unremarkable. Subsequent negative tests included MRI, MRA, MRV of the brain; immunology; serial blood cultures; T-spot and lumbar puncture with cytology and virology. A FDG-PET/CT showed extensive large vessel vasculitis of the aorta, subclavian and right common carotid arteries. He was treated as giant cell arteritis (GCA), with IV methylprednisolone and oral corticosteroids. There was a rapid clinical improvement (CRP <4, ESR 5) at week 4. Case two is an 82 year old Caucasian male admitted with a one week history of fever, night sweats, malaise, hypoxia, with raised inflammatory markers (ESR of 132mm/hr, CRP 336). Following treatment for sepsis, he continued with fevers and abnormal tests. Opinions from infectious disease, microbiology, neurology, urology, and haematology were given. Investigations including unremarkable immunology; CT pulmonary angiogram; CT of the thorax, abdomen and pelvis; MRI of the entire spine; echocardiogram; lumbar puncture and extensive microbiology tests. He had no symptoms of headache, proximal limb girdle pain or features to suggest polymyalgia rheumatica. There were no bruits, temporal tenderness, or vascular signs. The FDG-PET/CT showed no evidence of vasculitis, occult sepsis, inflammation, or neoplasm. The malaise and fever settled with supportive therapy, inflammatory markers remained elevated. One month post discharge he presented with unilateral acute visual loss secondary to a central retinal artery occlusion, with acute headache. Treatment for GCA was commenced. Temporal artery biopsy (TAB) was confirmatory showing heavy trans-mural inflammation, internal elastic lamina disruption, and pathognomonic multinucleated giant cells. Conclusion: GCA can present as a PUO. These two cases highlight the utility and pitfalls of negative FDG-PET/CT and TAB when evaluating for large vessel vasculitis. Although steroids, and diabetes, can reduce the sensitivity of FDG-PET/CT, in case one where these factors were present, the scan was positive. In case two, without these factors, the scan was negative. Both FDG-PET/CT and TAB may be required in difficult cases.