The role of actinically provoked systemic elastolysis in polymyalgic vascular disease. A study based on serum fluorescence and haptoglobin.
This study of cutaneous elastic tissue and serum fluorescence supports the hypothesis that widespread destruction and resorption of elastic tissue (elastolysis) occurs in the temporal arteritis/polymyalgia rheumatica syndrome. A systemic elastolysis of this nature may be provoked by actinic (radiant) damage to the "exposed" elastic tissues in the skin and superficial arteries, the archetype of such injury being seen in temporal arteritis. Scattered giant cells are the usual agents of elastolysis but tuberculoid ("sarcoid") infiltrates often take over in the later stages. In acute polymyalgia, the phenomenon probably becomes diffuse and humoral. Elastolysis may be a direct pathogenetic link between polymyalgia and other vascular diseases such as idiopathic aneurysm and atherosclerosis.
D001797:Blood Protein Electrophoresis; D004547:Elastic Tissue / Q000378:metabolism* / Q000473:pathology / Q000528:radiation effects; D004549:Elastin / Q000097:blood; D005260:Female; D005453:Fluorescence; D013700:Giant Cell Arteritis / Q000097:blood*; D006242:Haptoglobins / Q000032:analysis; D006801:Humans; D008297:Male; D011111:Polymyalgia Rheumatica / Q000097:blood*; D012867:Skin / Q000473:pathology / Q000528:radiation effects; D014466:Ultraviolet Rays
D006242:Haptoglobins; D004549:Elastin