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Angeline Wang, Krishna Surapaneni, Daniel M Albert; The Site of Inflammation in the Artery Wall in Temporal Arteritis. Invest. Ophthalmol. Vis. Sci. 2015;56(7 ):5556.
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Temporal arteritis is an ophthalmic emergency and requires prompt treatment to prevent vision loss. The gold standard for diagnosis is the temporal artery biopsy. Current literature describes a positive biopsy as revealing chronic granulomatous inflammation at the level of the internal elastic lamina. The purpose of this study was to verify the location of most severe inflammation within a positive temporal artery and study other characteristics of our series in comparison to previous reports.
The list of patients with biopsy-proven temporal arteritis was generated by searching the University of Wisconsin Eye Pathology Laboratory database for the terms “giant cell arteritis” and “temporal arteritis.” Charts and pathology slides for patients from the last 15 years (1999 to present) were reviewed (n = 32). Cases with indeterminate diagnoses were excluded, as were cases where clinical information was unavailable.
The average age of onset was 76.2 years, with 81% (26/32) of positive cases diagnosed in women. Patients were treated with oral steroids for an average of 4.25 days prior to biopsy. Unilateral temporal artery biopsies were submitted in 91% of cases (29/32); the remaining biopsies were bilateral. Both arteries were positive in two of the bilateral cases; one was positive and the other negative in the third case. The average artery sample length was 20 mm. Histopathologic features of the positive biopsies included intimal hyperplasia (32/32), lymphocytes (32/32), epithelioid cells (32/32), giant cells (29/32), fragmented internal elastic lamina (29/32), lumen narrowing (18/32), and concomitant Monckeberg’s arteriosclerosis (15/32). Skip areas were noted in 9% (3/32) of cases. The most severe inflammation was at the level of the media and adventitia in 37% of biopsies (12/32); the remaining had full thickness inflammation. No biopsies had inflammation isolated at or centered on the internal elastic lamina.
In contrast to the current literature, biopsies of patients with temporal arteritis reveal the principal focus of chronic granulomatous inflammation to be at the level of the media and adventitia or throughout the layers of the artery, not at the level of the internal elastic lamina. Other findings are generally consistent with previous reported series. Our findings lead us to hypothesize that the muscularis and adventitia may play an inciting role in the pathogenesis of temporal arteritis.
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