Why the study?
Slightly elevated C-reactive protein during maintenance glucocorticoid therapy prompted whole-body [18F]-FDG PET/MRI to identify the activity and extent of suspected recurrent giant cell arteritis.
Does [18F]-FDG PET/MRI improve detection and therapy monitoring of active vasculitis compared to MRI alone and C-reactive protein in giant cell arteritis?
Case Report (n=1)
No
Does [18F]-FDG PET/MRI improve detection and therapy monitoring of active vasculitis compared to MRI alone and C-reactive protein in giant cell arteritis?
Hybrid [18F]-FDG PET/MRI can detect active large-vessel inflammation in giant cell arteritis when C-reactive protein and standalone MRI underestimate disease flare, while guiding effective immunosuppressive therapy.
May detect occult large-vessel vasculitis missed by MRI and CRP; leaves open whether PET/MRI improves monitoring or outcomes in giant cell arteritis.
A 68-year-old man with giant cell arteritis (GCA) was admitted to our hospital 1 year after diagnosis for reevaluation of disease status. Initially increased inflammatory biomarkers C-reactive protein (7.2 mg/dL; norm, <0.5 mg/dL) and blood sedimentation rate (80 mm/h; norm, <30 mm/h) disappeared within a few months during glucocorticoid treatment, which has been reduced to 5 mg/day as maintenance therapy. Due to slightly elevated C-reactive protein (0.8 mg/dL) suggesting low activity of GCA, [18F]-fludeoxyglucose ([18F]-FDG) positron emission tomography/magnetic resonance imaging (PET/MRI) was performed to identify activity and extent of suspected recurrent vasculitis. Positron emission tomography revealed extensive large vessel involvement with marked FDG vessel wall uptake in the aorta and its branches, indicative for active inflammation (Panel A: coronal PET, Panel D: fusion of PET and T2 STIR). Magnetic resonance imaging, however, did not show any vessel changes suggestive for active vasculitis (Panel E: axial T1 VIBE, Panel F: angiography). After changing the therapeutic regimen by adding methotrexate to ongoing glucocorticoid therapy, FDG vessel wall uptake decreased significantly and remained normal in 12- and 24-month follow-up PET/MRI studies (Panels B and C). Simultaneously, C-reactive protein disappeared and remained undetectable in further laboratory tests suggesting remission of GCA. This case emphasizes the important role of molecular imaging by PET in therapy monitoring of GCA, since biochemical evaluation of disease activity by C-reactive protein completely underestimated disease flare. Hybrid PET/MRI might be a useful approach for aiding in the management of GCA, given its high sensitivity based on PET and the reduced radiation exposure compared with well-established PET/CT.
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Einspieler et al. (2015) conducted a case report in Giant cell arteritis (n=1). Fully integrated whole-body [18F]-FDG PET/MRI and addition of methotrexate to glucocorticoid therapy vs. MRI alone and biochemical evaluation by C-reactive protein was evaluated on Detection of active large vessel inflammation and therapy monitoring (FDG vessel wall uptake and C-reactive protein levels).
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