Destruction of elastic tissue (elastolysis) as a link between atherosclerosis and the temporal arteritis/polymyalgia rheumatica syndrome. Observations on an actinic factor in vascular disease.
Destruction (elastolysis) of the internal elastic lamina is frequently observed near early atherosclerotic plaques. Elastolysis and plaque formation are also found together in the temporal arteritis/polymyalgia rheumatica syndrome. Could it be that atherosclerosis and the syndrome are more closely akin than usually thought, with elastolysis acting as the pathogenetic link between them? A kinship of this nature is in accord with the growing recognition that elastin-related autoimmunity prevails in both these forms of vascular disease. A case can also be made out for the belief that the autoimmune reactions in internal vessels may be provoked by events in the integument where a slow but ultimately massive turnover of dermal and vascular elastic tissue takes place under the harmful influence of solar and other forms of actinic radiation.
D001161:Arteriosclerosis / Q000276:immunology / Q000378:metabolism* / Q000473:pathology; D004547:Elastic Tissue / Q000276:immunology / Q000378:metabolism* / Q000473:pathology; D013700:Giant Cell Arteritis / Q000276:immunology / Q000378:metabolism* / Q000473:pathology; D006801:Humans; D008027:Light; D011111:Polymyalgia Rheumatica / Q000276:immunology / Q000378:metabolism* / Q000473:pathology