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Tan et al recently described a case of “resistant giant cell arteritis” successfully treated with etanercept.1 Their patient, who had classical symptoms of polymyalgia rheumatica (PMR), developed headaches while receiving low dose steroids. Biopsy of a temporal artery showed no arteritis. Because giant cell arteritis (GCA) was suspected on clinical grounds, high dose steroids were instituted. Six months later, despite continued steroid treatment, a transient ischaemic attack (TIA) involving right arm weakness occurred, which was ascribed to “arteritis (sic)”. An insufficiency fracture ensued. As the erythrocyte sedimentation rate and C reactive protein were persistently raised, a diagnosis of GCA resistant to treatment was made, and etanercept was given. The acute phase reactants normalised, and the symptoms referable to PMR resolved completely.
I am not persuaded that the patient in question had GCA.
Firstly, the temporal artery biopsy was negative. Definitive criteria for the entity of so-called biopsy negative GCA are lacking, and, in my opinion, this concept remains a problematic one. Negative temporal artery (TA) biopsies do occur in certain subsets of GCA—for example, upwards of 50% of …