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WHERE DOES POLYMYALGIA RHEUMATICA END AND GIANT CELL ARTERITIS BEGIN? LESSONS FROM POSITRON EMISSION TOMOGRAPHY STUDIES

The relationship between giant cell arteritis (GCA) and polymyalgia rheumatica (PMR) has been recognised since more than forty years, since it became clear that both disorders frequently occurred in the same patient, whether simultaneously or at different time points (1, 2). Patients with GCA may relapse under the form of PMR, or vice versa. Several investigators have discussed the relationship between both conditions (3, 4), but a definite conclusion has not been reached. Others have argued that PMR and late onset seronegative rheumatoid arthritis (RA) may be the same entity (5). GCA and PMR are almost never encountered before the age of 50 (although PMR patients tend to be somewhat younger than GCA patients), and peak between 70 and 80 years of age. Women are more frequently involved than men, and the highest incidences of both GCA and PMR are found in northern European countries and Minnesota (USA), which share a similar ethnic background. The HLA-DRB1*04 allele (most frequently DRB1*0401, but also *0404) has been mapped to increased suspectibility to GCA and also in some populations to PMR (6). Rheumatoid arthritis is also associated with the HLA-DRB1*04 haplotype (7). PMR is overall three times more frequent than GCA. GCA as well as PMR are accompanied by a marked elevation of inflammatory parameters, both respond promptly to steroid therapy, and occur together: 40-50% of biopsy-proven GCA patients have PMR complaints, 10% of ‘isolated PMR patients’ have a positive temporal artery biopsy. Glucocorticoids remain the cornerstone of treatment of both PMR and GCA, but patients with GCA require higher starting doses (40 mg prednisolone daily in uncomplicated cases of GCA versus 15 mg daily in PMR). Both conditions tend to recur in about half of patients, at the time when steroids are tapered down to very low daily doses or in the first months after the cessation of steroid therapy. Based on my experience with fluorodeoxyglucose (FDG) – positron emission tomography (PET) and taking into account the literature on other investigational methods, I hypothesise that PMR is not a distinct disorder but only a manifestation of an underlying systemic vasculitis (GCA), as weight loss, jaw claudication or fever are. Other PMR patients with inflammation of distal joints meet the American College of Rheumatology criteria for RA. So probably, we should quit the term ‘isolated polymyalgia rheumatica’.