Background Southern Norway has been shown to have the highest incidence of TA worldwide.¹ Extended histopathological findings from TABs performed in this area have previously not been presented.

Objectives To examine the frequency and pattern of histopathological findings in TABs performed in patients recruited from a high endemic area for TA.

Methods All registered TABs in the biopsy database at the Department of Pathology at Vest-Agder Central Hospital (Southern Norway) from the 5-year period 1992–96 were examined. All biopsies were re-examined by one experienced pathologist. All slides were stained with HE stain. In addition, positive biopsies were stained with Giemsa and Lendrum stain.

Results TABs were performed in 275 patients of which 271 were regarded as representative (180 women and 91 men; mean age 70.9 ± 11.4 yrs). Vasculitis was found in 59 cases (18 men and 41 women; mean age 71.4 ± 8.2 yrs). Arteries with vasculitis had significantly larger diameters than those without inflammation (1.6 ± 0.7 mm vs. 1.2 ± 0.8 mm, P = 0.001), whereas no difference of artery length was found (7.5 ± 3.2 mm vs. 7.6 ± 3.5 mm, P = 0.77). Extension of the inflammation throughout the vessel wall was as follows: transmural 55.2%, media and adventitia 22.4%, adventitia 19.0% and media 3.4%. Reparative fibrosis was found in 52.5%, thrombosis in 3.4% and fibrinoid necrosis in 3.4% of the TABs. The following frequencies of different inflammatory cell types in the TABs were found: giant cells 37.3%, macrophages 45.8%, lymfocytes 100%, plasma cells 37.3%, mast cells 54.3%, neutrophilic granulocytes 88.2% and eosinophilic granulocytes 25.4%.

Conclusion Histopathologic findings consistent with vasculitis were detected in approx. 1 out of 5 TABs examined in our high endemic area of TA. No difference in biopsy length was found between positive and negative TABs, questioning the importance of recommended large biopsies of 20 mm examining TABs for vasculitis. The types of inflammatory cells were found to be in accordance with previous reports.

Reference

1. Haugeberg, et al. J Rheumatol. 2000;27:2624–7