Temporal Arteritis in Polymyalgia Rheumatica
February 28, 1997 2 minutes read
Temporal Arteritis in Polymyalgia Rheumatica
ABSTRACT & COMMENTARY
Synopsis: A seven-year prospective study of residents of one county in Norway found a very low coincidence of biopsy-proven temporal arteritis in patients with polymyalgia rheumatica who had no headache or visual symptoms.
Source: Myklebust G, Gran JT. Br J Rheumatol 1996;35: 1161-1168.
Treatment for temporal arteritis in general is more aggressive, in terms of corticosteroid dose, than treatment for uncomplicated polymyalgia rheumatica (PMR). Reports of biopsy-proven temporal arteritis in patients who have none of the classic symptoms of temporal arteritis (TA) have led to concern about the most appropriate management of patients with PMR. Myklebust and Gran have shed some light on this otherwise murky area by performing a prospective study of cases of PMR and TA which were seen in the one hospital serving a single county in Norway. Over the course of seven years, 287 patients were enrolled when PMR or TA were diagnosed. Another 31 patients were identified by retrospective record review for the same period. Of the 335 total patients, 80% had PMR only, 15% had TA only, and 5% had both PMR and TA. All patients classified as having TA had positive temporal artery biopsies. Of the 233 patients with "pure" PMR, a random sample of 68 underwent temporal artery biopsy. Only three of the 68 had positive biopsies (4.4%). One interesting finding was the presence of arthritis in 24% of the PMR cases but in none of the TA cases. Another reassuring finding was that the ESR was elevated in all cases of TA and the C-reactive protein (CRP) was elevated in 97.1% of the TA cases.
COMMENT BY JERRY M. GREENE, MD
Much higher rates of TA in patients with PMR have been previously reported, mainly from Scandinavian countries. The much lower coincidence of TA in patients with PMR and without headache, visual loss, or jaw claudication in this study is reassuring, since it makes the use of low-dose corticosteroids as a diagnostic trial seem much less hazardous than it would if rates of TA in PMR were in the 40-50% range. Although the minimum dose of prednisone required to prevent blindness in TA is not known, it seems likely to me that it is more than the 7.5-10 mg of prednisone that may dramatically improve PMR symptoms.
The prospect of performing unilateral or bilateral temporal artery biopsies on every patient with suspected PMR or, alternatively, treating everyone with PMR as though TA were present, are about equally repellent. This population-based study provides support for a more conservative management approach and the time-honored use of low-dose prednisone or equivalent corticosteroid in a trial that may be both therapeutic and diagnostic.
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