Either of the alternative names of temporal arteritis or giant cell arteritis is unfortunate, because this common serious condition in the elderly also affects other arteries, and giant cells are not always present. Blindness and stroke are the most significant threats, and the preceding clinical manifestations, including headache and those related to the often-associated polymyalgia rheumatica (morning stiffness in shoulders or neck), are relatively nonspecific. Treatment with steroids is highly effective, but given that glucocorticoid toxicity develops in 35%–65% of patients, it is best restricted to patients who actually have the condition. A temporal artery biopsy, a comparatively benign procedure, can provide a definitive diagnosis by demonstrating a chronic lymphohistiocytic inflammatory cell infiltrate centered upon the internal elastic lamina, although it may involve other arterial layers. The infiltrate, which may or may not contain multinucleated giant cells, typically shows a patchy sectorial (across the arterial circumference) and segmental (along its length) distribution, requiring careful examination of multiple sections. Cases with no inflammatory cell infiltrate at all, often showing medial calcification or atherosclerosis, representing pitfalls on palpation, receive a negative pathological diagnosis, which does not exclude the possibility of the inflammation being present in other segments or arteries. The problem lies with those cases where inflammation is limited to small blood vessels, either restricted to the adventitia of the large artery (vasa vasorum) or even further afield. A diagnosis of temporal arteritis is not possible, but do these findings have any significance? Pejhan et al have examined this question. First, they found that vasculitis involving small blood vessels was always an additional finding in temporal arteritis. Second, temporal arteritis and isolated small vessel vasculitis constituted each approximately one-quarter of the biopsies. Third, biopsies showing isolated small vessel vasculitis are much more frequently associated with high clinical probability of temporal arteritis prior to the biopsy, and are twice as likely to receive the clinical diagnosis of temporal arteritis within a year of the biopsy than inflammation-negative cases. The finding that small vessel vasculitis markedly increases the risk of harboring or developing temporal arteritis would help clinicians reach decisions regarding treatment of these high-risk patients.
Either of the alternative names of temporal arteritis or giant cell arteritis is unfortunate, because this common serious condition in the elderly also affects other arteries, and giant cells are not always present. Blindness and stroke are the most significant threats, and the preceding clinical manifestations, including headache and those related to the often-associated polymyalgia rheumatica (morning stiffness in shoulders or neck), are relatively nonspecific. Treatment with steroids is highly effective, but given that glucocorticoid toxicity develops in 35%–65% of patients, it is best restricted to patients who actually have the condition. A temporal artery biopsy, a comparatively benign procedure, can provide a definitive diagnosis by demonstrating a chronic lymphohistiocytic inflammatory cell infiltrate centered upon the internal elastic lamina, although it may involve other arterial layers. The infiltrate, which may or may not contain multinucleated giant cells, typically shows a patchy sectorial (across the arterial circumference) and segmental (along its length) distribution, requiring careful examination of multiple sections. Cases with no inflammatory cell infiltrate at all, often showing medial calcification or atherosclerosis, representing pitfalls on palpation, receive a negative pathological diagnosis, which does not exclude the possibility of the inflammation being present in other segments or arteries. The problem lies with those cases where inflammation is limited to small blood vessels, either restricted to the adventitia of the large artery (vasa vasorum) or even further afield. A diagnosis of temporal arteritis is not possible, but do these findings have any significance? Pejhan et al have examined this question. First, they found that vasculitis involving small blood vessels was always an additional finding in temporal arteritis. Second, temporal arteritis and isolated small vessel vasculitis constituted each approximately one-quarter of the biopsies. Third, biopsies showing isolated small vessel vasculitis are much more frequently associated with high clinical probability of temporal arteritis prior to the biopsy, and are twice as likely to receive the clinical diagnosis of temporal arteritis within a year of the biopsy than inflammation-negative cases. The finding that small vessel vasculitis markedly increases the risk of harboring or developing temporal arteritis would help clinicians reach decisions regarding treatment of these high-risk patients.
Competing interests
None.