Giant Cell Arteritis

Abstract

This review summarizes the diagnosis, clinical manifestations and management of giant cell arteritis. Giant cell arteritis is an immune-mediated vasculitis of medium to large sized arteries that affects individuals older than the age of 50. Patients typically present with signs of vascular insufficiency of the extracranial arteries of the head and systemic inflammation. Temporal artery biopsy remains the hallmark of diagnosis. Specific treatment regimens must be tailored to each individual, but steroids remain the backbone of therapy.

Temporal Artery Biopsy for Diagnosing Giant Cell Arteritis: A Ten-year Review

“…[5] The presence of at least three of these five criteria carries a sensitivity of 93.5% and a specificity of 91.2% for GCA. [5,6] In 2016, a new and more extensive set of criteria for early diagnosis of the GCA was proposed. [7] Table 1 shows the 2016 revised ACR (rACR) criteria for early diagnosis of GCA (previously called temporal arteritis).…”

Giant Cell Arteritis and Angiogenesis: A Review

“…25 The recruited macrophages then release proinflammatory cytokines Il-1 and Il-5 in the adventitia. 23 At the media-intima junction the macrophages produce matrix metalloproteinase-2, which contribute to the arterial wall destruction. 13 These metalloproteinase release proteolytic enzymes that oxidize macromolecules and lipids in addition to fragmenting the internal elastic lamina.…”

Giant Cell Arteritis Causing Retinal and Posterior Carotid Circulation Strokes

“…Classical symptoms of giant cell arteritis [3][4][5] include age over 50, new onset headache, temporal tenderness, jaw claudication, visual disturbance, general malaise, and polymyalgia. However, GCA patients may experience none of these symptoms and still present with ischemic complications such AION, CRAO, cranial nerve palsies, brain stem syndromes, scalp necrosis or tongue infarction [3][4][5][6][7][8]. A high index of suspicion is therefore necessary and patients should be fully investigated and urgent inflammatory markers requested.…”

“…The second episode of ischemic complications was seen in the anterior circulation. Thromboembolism observed in the retina by the examining ophthalmologist may have resulted from arteritis affecting atheromatous vessels such as the internal carotid artery or its branches [1][2][3]. This is particularly significant when considering literature claiming up to fivefold risk reduction in cranial ischaemic complications in patients taking low dose aspirin at presentation, who were treated with high dose steroids compared to patients not taking aspirin.…”

“…Although adding aspirin to high-dose steroid treatment regimens has been proposed, sufficient data does not exist to support the notion that adding aspirin after the diagnosis of GCA prevents ischaemic complications. Urgent administration of high dose systemic steroids is strongly advocated in patients diagnosed with GCA [3,4,9]. There remains controversy over the ideal route of administration [3,4].…”