Background Temporal artery biopsy (TAB) showing transmural inflammation is considered the gold standard for the diagnosis of giant cell arteritis (GCA). A negative TAB does not rule out GCA, and a diagnosis of biopsy-negative GCA was reported in 5-25% of patients. In the absence of active inflammation (negative TAB), other structural changes in the wall of TA are often present and some of those have been described as “healed” or quiescent arteritis, but if these histological changes are expression of GCA is still debated.
Objectives To evaluate if there are histopathological features of negative TAB that allow to differentiate patients with GCA from those without.
Methods 42 consecutive patients with negative TAB were retrospectively selected. All patients underwent TAB for suspected GCA between January 2009 and December 2012. Demographic, clinical and laboratory data at presentation and at each follow up visit were collected. A pathologist with expertise in vasculitis blinded to clinical data and final diagnosis reviewed all 42 negative TABs. Histopathologic features evaluated were: the presence of a focal medio-intimal scar with medial attenuation, intimal hyperplasia, fragmentation of inner elastic lamina (IEL), calcification, adventitial fibrosis and neoangiogenesis.
Results After a median follow-up period of 177 days (interquartile range 38, 508), 20 of the 42 patients had a final diagnosis of GCA, while in the remaining 22 patients GCA was excluded (9 had polymyalgia rheumatica, 4 non arteritic anterior ischemic optic neuropathy, 3 fibromyalgia, 2 non-specific elevation of inflammatory markers, 1 fever of unknown origin, 1 rheumatoid arthritis, 1 ANCA associated vasculitis, 1 osteoarthitis). 1990 ACR classification criteria for GCA were satisfied in 13 of the 20 patients with GCA (65%) and in none of the 22 non-GCA patients. 12 patients (60%) with GCA and 14 patients (64%) with non-GCA were on steroid therapy when TAB was performed (p>0.05). The mean prednisone dose was (mg± SD) 23.75 ±12.95 for GCA patients and 13.57 ±11.67 for non-GCA patients (p=0.05). Mean duration of prednisone treatment was (days±SD) 30.58±44.23 for GCA patients and 144.36±162.24 for non GCA patients (p<0.05). A focal medio-intimal scar with medial attenuation was found in 15% of GCA vs 14% of non-GCA patients (p>0.05). Intimal hyperplasia was present in 45% vs 59%, fragmentation of IEL in 80% vs 91%, calcification in 30% vs 18%, adventitial fibrosis in 10% vs 5% and neoangiogenesis in 10% vs 9% of GCA vs non-GCA patients respectively (all p NS). 4 patients with GCA had visual loss. A focal medio-intimal scar with medial attenuation was not observed in these 4 patients, intimal hyperplasia was observed in 2, fragmentation of IEL in all 4, calcification in 2, adventitial fibrosis in 1 and neoangiogenesis in 1. Histological findings of GCA patients with visual loss were similar to those of patients with non-GCA.
Conclusions The histological features of negative TAB evaluated in this study do not allow to differentiate between GCA and non-GCA patients. These data suggest that in the absence of mural active inflammation, other histological changes of the TA wall are not specific for GCA.
Disclosure of Interest None declared