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REVIEW ARTICLE
Year : 2015  |  Volume : 10  |  Issue : 5  |  Page : 11-21

Giant Cell Arteritis and Takayasu Arteritis: Are they a different spectrum of the same disease?


1 Nuffield Department of Orthopaedics Rheumatology and Musculoskeletal Sciences, Botnar Research Centre, University of Oxford, Oxford, United Kingdom
2 Nuffield Department of Orthopaedics Rheumatology and Musculoskeletal Sciences, Botnar Research Centre, University of Oxford, Oxford, United Kingdom; cDepartment of Internal Medicine, Jagiellonian University Medical College, Krakow, Poland
3 Nuffield Department of Orthopaedics Rheumatology and Musculoskeletal Sciences, Botnar Research Centre, University of Oxford, Oxford, United Kingdom; Department of Rheumatology, Hospital de Santa Maria, Lisbon Academic Medical Centre, Lisbon, Portugal;
4 Department of Internal Medicine, University of Jena, Germany; Nuffield Department of Orthopaedics Rheumatology and Musculoskeletal Sciences, Botnar Research Centre, University of Oxford, Oxford, United Kingdom

Correspondence Address:
Lorraine O'Neill
Nuffield Department of Orthopaedics Rheumatology and Musculoskeletal Sciences, Botnar Research Centre, University of Oxford, Oxford, United Kingdom

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Source of Support: None, Conflict of Interest: None


DOI: 10.1016/j.injr.2015.03.009

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Giant Cell Arteritis (GCA) and Takayasu Arteritis (TAK) are the two major forms of large vessel vasculitis (LVV). Traditionally GCA and TAK have been considered as two separate diseases based on a number of differences including age of onset, ethnicity, clinical features and vascular distribution. However, the realisation that large vessel involvement in GCA is more common than previously thought, has prompted the discussion that GCA and TAK may in fact represent a spectrum of the same disease. Greater understanding of the pathogenesis of GCA and TAK has highlighted striking similarities. Cell mediated immunity plays a critical role in the pathogenesis of large vessel vasculitis with T helper subsets 1 and 17 (Th1 & Th17) predominating.1,2 Interleukin 6 (IL 6) is upregulated in both GCA and TAK and promotes differentiation of T cells towards the Interleukin 17 producing (IL17), Th17 lineage, which directs the systemic inflammatory response. Interleukin 12 (IL 12) polarises T cells to differentiate into Th 1 cells, of which the signature cytokine is interferon gamma (IFN-g). IFN-g is responsible for driving vascular remodelling, intimal hyperplasia and ultimately luminal occlusion and increased expres- sion is found in patients with TAK vs. GCA,2 perhaps accounting for increased vessel stenosis in TAK. In GCA, the Th17 pathway appears to be important in early disease and is rapidly suppressed by glucocorticoid therapy, while the Th1 axis is responsible for ongoing vascular inflammation and is relatively steroid resistant.1,3 The opposite appears to be true for TAK, with Th17 cytokines persisting despite treatment, and the Th1 axis adequately suppressed by glucocorticoids. Therefore, while glucocorticoids are effective they do not fully eliminate the aberrant immune response and insights into the subtle differences in pathogenesis will help guide future targeted therapies. GCA itself could be considered to comprise of a number of clinical subtypes; PMR with systemic inflammation, myalgias, subclinical vasculitis with an IL 6 but not and IFN-g cytokine signature; uncomplicated cranial GCA with classical cranial symptoms, a systemic inflammatory response but without neuro-ophthalmic ischaemia; cranial GCA complicated by an ischaemic event such as blindness or stroke, often without a significant acute phase


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