Giant cell arteritis (GCA) is a non-necrotizing granulomatous vasculitis of large and middle-sized arteries that affects patients over 50 years of age. It is classically described as vasculitis with a particular tropism for the external carotid arterial branches and whose most recognizable manifestations are craniofacial ischemic symptoms.  However, current evidence shows that it is much more than a cranial disease, as it has a much broader and heterogeneous clinical spectrum than previously thought [1], [2], [3].

Generally, it exhibits a typical clinical picture consisting of classic cranial ischemic manifestations, but sometimes prevail non-specific clinical features related to the general inflammatory state (occult GCA presenting as fever of unknown origin) and/or the large-vessel involvement (aorta, supra-aortic trunks, and large peripheral arteries) [1], [2], [3]. There has been an increasing knowledge on the occurrence of the disease without the typical cranial symptoms [1], [2], [3], [4], [5] and its close relationship and overlap with polymyalgia rheumatica (PMR), which may be also the only clinical presentation of vasculitis (there are no well-defined clinical tools that can help identify “occult” vasculitis in those patients presenting an apparently isolated or “pure” PMR) [6,7].

Prompt diagnosis and treatment are essential to avoid irreversible damage in GCA. Although temporal artery biopsy (TAB) remains the gold standard, and color doppler ultrasound (CDUS) of the temporal arteries is being widely used, newer imaging techniques such as 18F-fluorodeoxyglucose positron emission tomography/computed tomography (18F-FDG PET-CT), CT angiography (CTA), or magnetic resonance angiography (MRA) are of valuable help to identify GCA, in particular in those cases with a predominance of extracranial large-vessel manifestations [8], [9], [10], [11], [12].

In this sense, 18F-FDG PET-CT has become increasingly recognized as an essential tool for rheumatologists in assessing large-vessel vasculitis (LVV) in GCA. Based on the ability to detect enhanced glucose uptake from high glycolytic activity, it can support the diagnosis of GCA identifying mural inflammation and/or luminal changes in extracranial arteries. Moreover, it can distinguish vasculitis from atherosclerotic lesions, as well as inflammation of the periarticular and extra-articular synovial structures in PMR [8]. The prevalence of LVV at GCA diagnosis, when systematically investigated with this technique, runs as high as 86% [13].

Glucocorticoids (GC) may reduce vascular wall uptake of 18-FDG and increase FDG uptake in the liver, thereby leading to an underestimation of vasculitis. Imfeld et al. showed 18F-FDG PET-CT to be significantly impactful as early as 3 days after treatment initiation in the abdominal aorta, and 10 days in the other examined arteries [14]. This is also exactly in line with the findings of Nielsen et al., who reported that the diagnostic accuracy of LVV with FDG-PET remained valid for 3 days following initiation of GC, after which the signal decreased significantly [15]. Thus, it appears that there may be a diagnostic window of opportunity within 3 days of initiating GC. After 10 days of treatment, FDG PET/CT sensitivity decreased significantly [15]. For this reason, it is recommended to perform the 18F-FDG PET-CT scan within the first 10 days of treatment using high-dose GC, and whenever possible within the first 3 days. However, due to waiting lists, this deadline is not always possible.

To further ascertain the impact of previous high-dose GC treatment, including the administration of intravenous (IV) methylprednisolone (MP) boluses, on the likelihood of obtaining a positive 18F-FDG PET-CT in patients with GCA, we reviewed our clinical experience in a consecutive cohort of 85 patients who received GC before PET/CT.