The Aetiology, Pathology and Course of Giant-Cell Arteritis.*.

Kinmont, P.D.C.; McCallum, Dugald

doi:10.1111/j.1365-2133.1965.tb14630.x

Cited by 53 publications

(15 citation statements)

References 7 publications

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“…Clustering of diagnoses in the early summer months similar to that seen in our study has been reported, [24][25][26] while other studies have reported peaks in the winter months. 27 28 Other studies have reported no seasonal effect.…”

Section: Discussionsupporting

confidence: 90%

Incidence of diagnosed polymyalgia rheumatica and temporal arteritis in the United Kingdom, 1990-2001

Smeeth

Cook²,

Hall³

2006

Annals of the Rheumatic Diseases

266

163

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Section: Discussionsupporting

confidence: 90%

Incidence of diagnosed polymyalgia rheumatica and temporal arteritis in the United Kingdom, 1990-2001

Smeeth

Cook²,

Hall³

2006

Annals of the Rheumatic Diseases

266

163

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“…The effects of radiation on blood vessels have been studied, but vasculitis was not a reported outcome (22). Other than anecdotal cases (16,23), there has been little clinical evidence of a relationship between GCA and the degree of sun exposure. Reported incidence rates of GCA in Europe and the United States have shown an opposite relationship: higher rates in northern latitudes, where the intensity of sun exposure tends to be less (24)(25)(26)(27), and lower in southern latitudes (28)(29)(30).…”

Section: Alternative and New Evidence Against The Actinic Hypothesismentioning

confidence: 99%

Pathogenesis of giant cell arteritis

Hunder

Lie

Goronzy

et al. 1993

Arthritis & Rheumatism

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The actinic hypothesis generates more heat than lightIn a recent Current Comment published in Arthritis and Rheumatism (l), O'Brien and Regan review their concept of the pathogenesis of giant cell arteritis (GCA) and emphasize their commitment to the ''actinic hypothesis." This hypothesis proposes that the primary causative lesion in GCA is an alteration or degeneration of the elastic lamina of the temporal artery caused by solar radiation. O'Brien and Regan believe the degenerated elastin then triggers the development of the arteritis, and cannot understand why others do not share their enthusiasm for this idea.For many years elastic tissues of the aorta and its proximal branches have been thought to be somehow involved in the development of GCA (2). Various investigators have noted that the inflammatory reactions in positive biopsy specimens often appear more intense around the internal elastic lamina of the temporal artery (2-4). Multinucleated giant cells, which are characteristic of the disease, are often in direct

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“…Other environmental factors have been implicated; a role for sunshine has been suggested by Kinmont et al [33], but was not found by Barrier et al [28].…”

Section: Discussionmentioning

confidence: 96%