Fenofibrate and losartan.

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 rheu-matica (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 patients with so-called large artery involvement have such negative biopsies 2 —but the extent to which TA biopsies are negative in bona fide cases of cranial arteritis in GCA is unclear. Two recent papers have suggested that in fact a unilateral TA biopsy negative for arteritis markedly reduces the probability of the diagnosis of GCA, because the yield of a positive contralateral biopsy is no more than 1–3%. 3 4 The issue of what constitutes a flare in GCA (and PMR) is also problematic. It has been my experience over the years that many cases of alleged flares of both conditions involve little more than asymptomatic rises in the acute phase reactants, and that the pursuit of such rises with increased doses of steroids not uncommonly results in sundry untoward complications—notably, steroid induced osteoporosis and associated fractures. The patient under discussion is a case in point. The acute phase reactants were raised coincident with the occurrence of a TIA, but it is unlikely that this latter episode was caused by GCA. Though GCA is occasionally complicated by stroke, such an event nearly always involves the territory of the vertebral-basilar circulation, and rarely occurs in the distribution of the internal carotid artery. The explanation for this fact may result from the specific exclusion of the intracranial arteries from involvement by GCA, possibly …