Giant cell arteritis (GCA) is a common granulomatous vasculitis affecting large to medium sized arteries. It may also be known as temporal arteritis or cranial arteritis, given its propensity to involve the extra-cranial carotid artery branches such as the temporal artery.
GCA is the most common primary systemic vasculitis. It has an incidence of 200 per million population per year 6. Typically affects older individuals (usually older than 50 years of age, with a peak age of 70-80 years 3). There is a recognised female predilection.
It is histologically similar to other large vessel vasculitides (such as Takayasu arteritis) showing granulomatous inflammation of arteries with infiltration predominantly by histiocytes, lymphocytes, and multinucleated giant cells. The characteristic multinucleated giant cells are only found in ~50% of cases 1.
Can potentially affect any large-to-medium sized vessels, affecting the aorta (~20% of cases 7) and its major branches, particularly the extracranial branches of the carotid artery 6.
- serum erythrocyte sedimentation rate (ESR): markedly raised
- serum C-reactive protein (CRP): often markedly raised
- polymyalgia rheumatica: seen in ~50% of cases
- increased diameter of the TA and hypoechoic wall thickening (halo)
- more specific for GCA if bilateral 8
- reversible under corticosteroid treatment
- stenosis may be present but is not a specific sign for GCA 8
- may be useful for assessing luminal abnormalities, such as stenoses, occlusions, dilations, and aneurysm formation
- may also show wall thickening of affected segments, calcification and mural thrombi
T1 C+ (Gd)
- the best sequence for assessment, and is reported to show mural inflammation very well 2,4
- mean wall thickness increased in the affected region
- luminal diameter decreased in the affected region
- reported approximate sensitivity and specificity is at 80 and 97% respectively 2
Treatment and prognosis
Often treated with corticosteroid therapy.
Imaging differential considerations include
- 1. Bau JL, Ly JQ, Borstad GC et-al. Giant cell arteritis. AJR Am J Roentgenol. 2003;181 (3): 742. AJR Am J Roentgenol (full text) - Pubmed citation
- 2. Bley TA, Uhl M, Carew J et-al. Diagnostic value of high-resolution MR imaging in giant cell arteritis. AJNR Am J Neuroradiol. 2007;28 (9): 1722-7. doi:10.3174/ajnr.A0638 - Pubmed citation
- 3. Bley TA, Wieben O, Uhl M et-al. High-resolution MRI in giant cell arteritis: imaging of the wall of the superficial temporal artery. AJR Am J Roentgenol. 2005;184 (1): 283-7. AJR Am J Roentgenol (full text) - Pubmed citation3
- 4. Bley TA, Weiben O, Uhl M et-al. Assessment of the cranial involvement pattern of giant cell arteritis with 3T magnetic resonance imaging. Arthritis Rheum. 2005;52 (8): 2470-7. doi:10.1002/art.21226 - Pubmed citation2
- 5. Markl M, Uhl M, Wieben O et-al. High resolution 3T MRI for the assessment of cervical and superficial cranial arteries in giant cell arteritis. J Magn Reson Imaging. 2006;24 (2): 423-7. doi:10.1002/jmri.20639 - Pubmed citation
- 6. Rubin GD, Rofsky NM. CT and MR angiography, comprehensive vascular assessment. Lippincott Williams & Wilkins. (2008) ISBN:078174525X. Read it at Google Books - Find it at Amazon
- 7. Martínez-Valle F, Solans-Laqué R, Bosch-Gil J et-al. Aortic involvement in giant cell arteritis. Autoimmun Rev. 2010;9 (7): 521-4. doi:10.1016/j.autrev.2010.02.014 - Pubmed citation
- 8. Karahaliou M, Vaiopoulos G, Papaspyrou S, Kanakis MA, Revenas K, Sfikakis PP. Colour duplex sonography of temporal arteries before decision for biopsy: a prospective study in 55 patients with suspected giant cell arteritis. Arthritis research & therapy. 8 (4): R116. doi:10.1186/ar2003 - Pubmed