1. Angiogenesis and Giant Cell Arteritis.
- Author
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Mackie, Sarah L., Morgan, Ann W., and Jones, Pamela F.
- Abstract
Giant cell arteritis (GCA) is an autoimmune/inflammatory disease affecting older people. In GCA, inflammation of the wall of large or medium-sized arteries can cause stenosis (narrowing), or complete occlusion, of the lumen. The effects of the resulting end-organ ischaemia can include jaw claudication, transient visual loss, irreversible blindness, and stroke. The only established treatment at present is corticosteroids, which have significant adverse effects, particularly in the elderly. The diagnosis may be confirmed by biopsy of the temporal artery, which classically shows an inflammatory infiltrate in all layers of the vessel wall, with multinucleated giant cells and intimal hyperplasia. In such classical cases, angiogenesis is often observed on standard haematoxylin and eosin staining, but immunohistochemistry has demonstrated increased microvessel density even in lesions with limited intimal hyperplasia. Vascular endothelial growth factor production by the giant cells is reported to correlate with the number of microvessels present. Many other mediators known to be present in GCA also have an angiogenic effect, including platelet-derived growth factor, matrix metalloproteinases, interleukin-6 (IL-6), tissue growth factor beta and nitric oxide. In GCA temporal artery biopsies, angiogenesis often accompanies the most severe, stenosing lesions, but it is not clear whether the newly-formed microvessels promote further intimal hyperplasia, or whether they represent a compensatory response, acting to limit the hyperplasia. In patients with GCA, IL-6-induced angiogenesis has been postulated to improve perfusion of the ischaemic end-organs, perhaps reducing the frequency of ischaemic events. An improved understanding of the role of angiogenesis in GCA could suggest novel treatments that might reduce the burden of corticosteroid treatment for these patients. [ABSTRACT FROM AUTHOR]
- Published
- 2011
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