The role of imaging in polymyalgia rheumatica/giant cell arteritis
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PERSPECTIVE
The role of imaging in polymyalgia rheumatica/giant cell arteritis William S. Wilke
Published online: 2 July 2008 # ISS 2008
Introduction Polymyalgia rheumatica (PMR) has a venerable hypothetical pathophysiologic history. Some thought it was primarily vasculitis, and others thought it was arthritis. The term was inaugurated in 1957 by the British physician Barber who treated patients at a spa in Buxton [1]. Prior to that time, series of patients with diagnoses such as senile rheumatic gout, periarticular fibrositis, and, importantly, anarthritic rheumatoid disease were published and probably represent the earliest clinical descriptions of PMR [2–4]. Articular and periarticular signs and symptoms were well-recognized by these observers. Yet, another literature set evolved in parallel which emphasized the vasculitic nature of PMR. In 1968, Hamrin and colleagues presented six cases of “polymyalgia arteritica” in which clinically unsuspected characteristic histopathology in the superficial temporal arteries was discovered in three patients and, at autopsy, three further patients showed histopathologic signs of giant cell arteritis in the aorta or its branches [5]. They also reviewed similar cases from even earlier literature. Healey and others presented a strong argument that PMR and giant cell arteritis (GCA) were part of the same disease spectrum in 1971 [6]. Alestig and Barr in 1963 and later confirmed by Fauchald et al. in 1972 both published strong evidence that this was so [7, 8]. They showed that superficial temporal biopsies were positive for GCA in up to 40% patients who had only symptoms of PMR.
W. S. Wilke (*) Department Rheum/ORI, Cleveland Clinic Foundation, 9500 Euclid Avenue/A50, Cleveland, OH 44195, USA e-mail: [email protected]
The modern literature supports this interpretation. Clinical PMR occurs initially in at least 30% of new GCA patients and may occur for the first time later in the course with disease flare as corticosteroids are tapered [9]. In addition, PMR and GCA share human leukocyte antigenDRB1–04 alleles in the second hypervariable region [10]. In addition, both diseases respond more or less to the same treatment. All of this information suggests shared identity. So, what is the place for imaging in PMR? A recent GCA “management guideline” concluded that “…no imaging tests are established in the routine evaluation of patients with giant cell arteritis” [11]. A closer look is in order. Let us artificially separate the two diseases and begin with PMR. The most commonly used criteria are interchangeable. Criteria for classification of PMR—Bird et al. [12]: 1. 2. 3. 4. 5. 6. 7.
Bilateral shoulder pain /stiffness Duration of onset of 2 weeks or less Initial Westergren sedimentation rate (WSR) >40 mm/h Duration of morning stiffness >1 h Age=/>65 years Depression/weight loss Bilateral upper arm tenderness
Definite PMR is defined as the presence of three or more criteria or, if less than three criteria, clinical abnormality of the temporal artery and positive response to corticoster
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