Giant cell arteritis: a systemic vascular disease

Abstract

Giant cell arterits (GCA) is increasingly being recognized as a systemic vascular disease, not confined to the cranial arteries. Epidemiological studies have shown that almost one-third of the patients with GCA develop serious peripheral vascular complications during long-term follow up, and there is growing evidence that unrecognized extracranial involvement may be even more common. GCA of largeand medium-sized peripheral arteries typically leads to long tapering and occlusion of the arterial lumen due to concentric intimal thickening, sometimes accompanied by spontaneous dissection. Depending on the extent of the arterial obliteration and on the anatomy of the involved arterial segment, this may result in severe ischemia of the limbs during the acute phase of the disease. GCA of the aorta usually remains asymptomatic for many years, and leads to a markedly increased risk of aneurysms and dissections, particularly of the thoracic aorta. Evolving vascular imaging techniques such as duplex ultrasound, computer tomography (CT), magnetic resonance imaging (MRI), and fluorine-18-desoxyglucose positron emission tomography (18F-FDG-PET) have greatly improved our ability to detect and study arterial changes in large-artery vasculitis. Boosted by these advances in vascular imaging, vascular specialists are increasingly involved in the early diagnosis, follow-up and treatment of patients with large-vessel vasculitis.

Dr. Czihal replies: Figure 1.

“…However, we agree with Milchert and colleagues that the accuracy of this method in evaluating the carotid and lower extremity arteries may be hampered in patients exhibiting concomitant, calcified arteriosclerotic lesions 4,5,6 . It is of interest in this context that, as a result of the high prevalence of arteriosclerosis of lower extremity arteries in the elderly population with GCA, 18F fluorodeoxyglucose-positron emission tomography (FDG-PET) imaging has a low specificity for diagnosis of vasculitis of the lower extremity arteries 7 .…”

“…It is of interest in this context that, as a result of the high prevalence of arteriosclerosis of lower extremity arteries in the elderly population with GCA, 18F fluorodeoxyglucose-positron emission tomography (FDG-PET) imaging has a low specificity for diagnosis of vasculitis of the lower extremity arteries 7 . It is our hypothesis that concomitant arteriosclerosis of the lower extremity arteries results in the sonographic "beaded tube" appearance of the innermost layer of the thickened vessel wall in vasculitis of the femoropopliteal arteries (Figure 1) 2,6 .…”

Translational Mini-Review Series on Immunology of Vascular Disease: Mechanisms of vascular inflammation and remodelling in systemic vasculitis

“…Gelatinase activation and proteolytic activity favour leucocyte infiltration and vessel injury. Nevertheless, enzyme action is critical for artery repair [27,28], and macrophages produce trophic and angiogenic factors, such as vascular endothelial growth factor and platelet-derived growth factor which recruit neovessels [7,29] and provide an additional port of entrance, besides the vasa vasorum capillary network of the adventitia for leucocytes.…”

“…2 NO-drawn survival of activated immune cells, including DCs and lymphocytes, and of vessel stem cells in inflamed tissues [29,31], prolongs inflammation and possibly enhance maladptive remodelling.…”

Ultrasonography in Diagnosis and Follow-Up of Temporal Arteritis: An Update

“…During follow-up, the halo thickness in all the 25 patients disappeared 2-weeks after starting corticosteroids ( Obviously, this observation needs further confirmations in larger series since the role of CDUS in follow-up of TA is still currently considered rather doubtful and less useful for monitoring disease activity than the patient's history and/or ESR (Schmidt, 2004). Furthermore, in extracranial GCA the sonographic appearance of the arterial wall has not been validated yet as a reliable parameter for the assessment of disease activity (Tato & Hoffmann, 2008). Although the halo decreases during treatment, some degree of thickening of the arterial wall and stenosis can persist even in patients in complete remission, and complete recanalization of occluded arterial segments does not always occur (Schmidt & Blockmans, 2005;Tato e& Hoffmann, 2008).…”