Abstract
Giant cell arteritis (GCA) is the most common vasculitis among elderly people. The clinical spectrum of the disease is heterogeneous, with a classic/cranial phenotype, and another extracranial or large vessel phenotype as the two more characteristic patterns. Permanent visual loss is the main short-term complication. Glucocorticoids (GC) remain the cornerstone of treatment. However, the percentage of relapses with GC alone is high, and the rate of adverse events affects more than 80% of patients, so it is necessary to have alternative therapeutic options, especially in patients with worse prognostic factors or high comorbidity. MTX is the only DMARD that has shown to reduce the cumulative dose of GC, while tocilizumab is the first biologic agent approved due to its ability to decrease the relapse rate and lower the cumulative GC doses. However, apart from the IL-6 pathway, there are other pro-inflammatory cytokines and growth factors involved in the typical intima hyperplasia and vascular remodeling of GCA. Among them, the more promising targets in GCA treatment are the IL12/IL23 axis antagonists, IL17 inhibitors, modulators of T lymphocytes, and inhibitors of either the JAK/STAT pathway, the granulocyte-macrophage colony-stimulating factor, or the endothelin, all of which are updated in this review.
Highlights
Giant cell arteritis (GCA) is the most common vasculitis among elderly people
Branches), which is manifested by limb claudication or subclavian steal syndrome, carrying an increased risk of long-term vascular complications such as aortic aneurysm, vascular stenosis, and the dissection of the aorta; (iii) fever of unknown origin (9%), characterized by persistent fever, constitutional symptoms and elevated inflammatory markers; (iv) a picture mainly characterized by symptoms of polymyalgia rheumatica (PMR), in which asymptomatic vasculitis is accidentally found by a temporal artery biopsy (TAB), or by imaging examinations [6,7]
GCA and/or with unacceptable GC-related side effects, respectively [60,61], TCZ had to be withdrawn in 3 patients each, due to serious adverse event (AE) (SAEs) and one death occurred in each study, all possibly drug-related (Table 1) [12,13,39,60–66]
Summary
Giant cell arteritis (GCA) is an idiopathic granulomatous vasculitis involving medium and large caliber arteries that causes the inflammation of the vascular wall, with cellular infiltration and thickening of its layers, leading to vascular remodeling and occlusion. Branches), which is manifested by limb claudication or subclavian steal syndrome, carrying an increased risk of long-term vascular complications such as aortic aneurysm, vascular stenosis, and the dissection of the aorta; (iii) fever of unknown origin (9%), characterized by persistent fever, constitutional symptoms and elevated inflammatory markers; (iv) a picture mainly characterized by symptoms of polymyalgia rheumatica (PMR), in which asymptomatic vasculitis is accidentally found by a temporal artery biopsy (TAB), or by imaging examinations [6,7] These phenotypes are not mutually exclusive, and overlapping patterns can often exist [6]. Certain imaging techniques, especially ultrasound (US), magnetic resonance imaging (MRI), and positron emission tomography (PET)/computed tomography (CT) with 18Ffluorodeoxyglucose (18F-FDG), have been postulated as very sensitive and useful methods for the diagnosis of GCA (see “Imaging tests in the early diagnosis of GCA” in another section of this issue) In this regard, a group of experts from the European League Against. For a better understanding of the new therapeutic targets, it is positive to know the main molecular mechanisms, cell populations, and pathogenic pathways on which the pathophysiology of GCA is based
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