PubMed · 15401417
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R LOPEZ ZAMORA, G PARISI. 1949-12-19. [Aortitis].. https://pubmed.ncbi.nlm.nih.gov/15401417/
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PURPOSE OF REVIEW: Ultrasonography and positron emission tomography have been increasingly studied and, in part, introduced in clinical practice to diagnose large-vessel vasculitides, such as temporal arteritis, Takayasu arteritis, large-vessel giant cell arteritis, and isolated aortitis. RECENT FINDINGS: Ultrasonography reveals characteristic homogenous, concentric wall thickening in vasculitis, often combined with stenoses and, less frequently, with acute occlusions. Thirteen studies describe sensitivities of 40 to 100% (median, 86%) for temporal artery vessel wall edema compared with histology, and of 35 to 86% (median, 70%) compared with clinical diagnosis. If wall edema, stenoses, and occlusions are included, sensitivities increase to 91 to 100% (median, 95%) compared with histology, and to 83 to 100% (median, 88%) compared with clinical diagnosis. Specificities for wall edema are 68 to 100% (median, 93%) compared with histology, and 78 to 100% (median, 97%) compared with clinical diagnosis. One should be aware of large-vessel giant cell arteritis in all patients with temporal arteritis and polymyalgia rheumatica. Ultrasonography reveals characteristic wall thickening, particularly of the distal subclavian, axillary, and proximal brachial arteries. Findings in Takayasu arteritis are similar, but the vessel wall swelling is usually brighter. Positron emission tomography reveals vasculitis in arteries with a diameter of more than 4 mm. Ultrasonography and positron emission tomography agreed completely in the anatomic distribution of changes in patients with large-vessel giant cell arteritis. It reveals asymptomatic large-vessel vasculitis in giant cell arteritis and Takayasu arteritis. Positron emission tomography is not suitable for the assessment of temporal arteries. SUMMARY: Ultrasonography and positron emission tomography are new, promising techniques to assess large-vessel vasculitides.
PRINCIPLE AND OTHER CAUSES: Takayasu's arteritis, giant cell arteritis and Behçet's disease are the three main causes of inflammatory aortitis. More rarely, aortitis can be observed in Cogan's syndrome, atrophic polychondritis, sarcoidosis, ankylosing spondylitis and in rheumatoid arthritis. RISKS OF PROGRESSION: Takayasu's arteritis is distinct with the development of stenotic lesions of the aorta. With the other causes, aortitis can be complicated by ectasia or even aneurysm, with the risk of rupture. Indeed, during giant cell arteritis, patients are 17 times more likely to develop thoracic aortic aneurysm. Aortic regurgitation is a frequent complication of inflammatory aortitis. Sometimes, aortitis is only manifested by general signs such as fever or an inflammatory syndrome. SUPPLEMENTARY EXPLORATIONS: Recent advances in diagnosis and follow-up of patients with inflammatory aortitis concern the use of non-invasive imaging techniques: Doppler ultrasonography, computed tomography with injection of a contrast product and magnetic resonance imaging, which currently replace the aortography. DIAGNOSTIC PROBLEMS: Infectious aortitis, inflammatory atheromatous aneurysm and retroperitoneal fibrosis are sometimes misleading differential diagnoses.