elastin and Polymyalgia-Rheumatica

There is much evidence to suggest that temporal arteritis and rhizomelic polymyalgia are both immunological diseases. The classic results of experimental pathology are discussed, together with the relations between rhizomelic polymyalgia and both virus hepatitis B and the HLA system. From the clinical standpoint, it is now agreed that differences in individual response may lead to either a synovial or an arteritic response in both forms. Their association in what Hamrin has called "polymyalgia arteritica" is also common.

Topics: Antigen-Antibody Complex; Antigens, Viral; Elastin; Giant Cell Arteritis; Hepatitis B; Hepatitis B virus; HLA Antigens; Humans; Hypersensitivity, Delayed; Polymyalgia Rheumatica

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.

Topics: Blood Protein Electrophoresis; Elastic Tissue; Elastin; Female; Fluorescence; Giant Cell Arteritis; Haptoglobins; Humans; Male; Polymyalgia Rheumatica; Skin; Ultraviolet Rays

Actinic damage (actinic elastosis) affecting the internal elastic lamina appears to be the prime cause of 'age change' and arteritis of the temporal artery. Resorption and removal of altered elastin (elastolysis) is an integral part of the pathology of actinic damage. Actinic irradiation is probably responsible for the destruction and disappearance of a vast number of arterioles in elastotic skin. The intimate connection between temporal arteritis and polymyalgia rheumatica prompts the belief that the vascular and other internal malign components of the temporal arteritis/polymyalgia rheumatica syndrome might likewise be due, albeit indirectly, to the same actinic cause. Actinic elastotic damage at the body surface could have this effect by provoking a state of systemic elastolysis. Although ultraviolet (uv) light is often regarded as the sole cause of actinic elastosis, penetrating infrared (heat) irradiation may deserve a large or even a dominant share of the blame.

Topics: Adult; Aged; Arterioles; Elastic Tissue; Elastin; Female; Giant Cell Arteritis; Humans; Male; Middle Aged; Polymyalgia Rheumatica; Skin; Sunlight; Temporal Arteries