Are we losing focus on the internal elastic lamina in giant cell arteritis?

✍ Scribed by John P. O'Brien; William Regan

• Book ID: 102751890
• Publisher: John Wiley and Sons
• Year: 1992
• Tongue: English
• Weight: 517 KB
• Volume: 35
• Category: Article
• ISSN: 0004-3591
• DOI: 10.1002/art.1780350713

✦ Synopsis

I t thus seems likely that elastin evolved us an adaptive response to the stresses imposed on arteries by the eficient high pressure circulatory system achieved etirly in vertebrate evolution. ''

Sage and Gray (I )

Approaches to the etiology of giant cell (temporal) arteritis

In researching the etiology and pathogenesis of a disease, it is often helpful to start by defining its locus or site. Until recently, it has been almost universally agreed that the locus of giant cell arteritis (GCA) is the supporting internal elastic lamina of the temporal and other superficial arteries. This was first clearly demonstrated by Kimmelstiel and coworkers in 1952 (2). Those authors also emphasized that a peculiar degeneration, with rigid changes, swelling, and fragmentation of the lamina, elicited the granulomatous giant cell reaction. Many studies and accounts of the disease accept this view of the initiating role of the lamina. Thus, after likewise noting the "peculiar destructive alterations in the internal elastic lamina," and the possibility of "some insult," Healey and Wilske (3) conclude their chapter on the etiology of GCA by saying: