Correspondence
Polymyalgia Rheumatica and Giant-Cell Arteritis
N Engl J Med 2002; 347:2083-2085December 19, 2002
- Article
To the Editor:
The prognosis for patients with polymyalgia rheumatica and temporal arteritis may not be as benign as intimated by Salvarani et al. (July 25 issue).1 Despite the rapid initial response to corticosteroids, treatment is usually required for at least two years in the majority of patients. Studies in the United States suggest a shorter duration of therapy, in contrast to the European experience; this difference may be a manifestation of variations in demographic characteristics, the selection of patients, or the study design. In a study in Sweden, only 24 percent of patients with polymyalgia rheumatica, 16 percent of patients with polymyalgia rheumatica and temporal arteritis, and 5 percent of patients with temporal arteritis were able to discontinue prednisolone after two years of treatment.2 In another study, less than 50 percent of patients with polymyalgia rheumatica had discontinued treatment after a mean of 23 months, and among those with both polymyalgia rheumatica and temporal arteritis, only 28 percent had stopped treatment after a mean of 31 months.3 We have previously reported that only 24 percent of patients with polymyalgia rheumatica were able to discontinue corticosteroids successfully after two years.4
The results of a preliminary study suggest that severe polymyalgia rheumatica may be identified on the basis of a combination of the erythrocyte sedimentation rate and the interleukin-6 level.5 If this finding is confirmed, prognostication may improve, leading to clearer guidelines on the length of treatment required. We currently tell patients that treatment is usually required for at least two years and may be required for a longer period. Furthermore, a small proportion of patients require treatment indefinitely, and such patients have a greatly increased incidence of corticosteroid complications.
5 ReferencesAndrew J.K. Ostor, M.B., B.S.
Brian L. Hazleman, M.B.
Addenbrooke's Hospital, Cambridge CB2 2QQ, United Kingdom
brian.hazleman@addenbrookes. nhs. uk 1
Salvarani C ,Cantini F ,Boiardi L ,Hunder GG . Polymyalgia rheumatica and giant-cell arteritis. N Engl J Med 2002;347:261-271
Full Text | Web of Science | Medline2
Myklebust G ,Gran JT . Prednisolone maintenance dose in relation to starting dose in the treatment of polymyalgia rheumatica and temporal arteritis: a prospective two-year study in 273 patients. Scand J Rheumatol 2001;30:260-267
CrossRef | Web of Science | Medline3
Narvaez J ,Nolla-Sole JM ,Clavaguera MT ,Valverde-Garcia J ,Roig-Escofet D . Longterm therapy in polymyalgia rheumatica: effect of coexistent temporal arteritis. J Rheumatol 1999;26:1945-1952
Web of Science | Medline4
Kyle V ,Hazleman BL . The clinical and laboratory course of polymyalgia rheumatica/giant cell arteritis after the first two months of treatment. Ann Rheum Dis 1993;52:847-850
CrossRef | Web of Science | Medline5
Hunder GG. Polymyalgia rheumatica new treatment (new steroid sparing agents). Presented at the Second Annual European League Against Rheumatism Congress, Prague, Czech Republic, June 13–16, 2001. abstract.
To the Editor:
Salvarani et al. report that giant-cell arteritis causes visual loss from “ischemic optic neuritis.” No such disease exists. They have conflated optic neuritis and ischemic optic neuropathy. The former is an inflammatory disease often associated with multiple sclerosis; the latter is an ischemic disease that can occur in patients with giant-cell arteritis.1 The authors also recommend that, when possible, a temporal-artery biopsy be performed before treatment is initiated. In patients with visual symptoms, corticosteroids should be administered immediately, not withheld until a biopsy has been performed. There is no evidence that a few days of corticosteroid treatment will mask the histopathological features of giant-cell arteritis. However, this delay is plenty of time for a patient to go blind.
1 ReferencesJonathan C. Horton, M.D., Ph.D.
University of California, San Francisco, San Francisco, CA 94143To the Editor:
Salvarani et al. suggest the use of calcium and vitamin D supplementation to prevent glucocorticoid-induced osteoporosis. In its 1996 recommendations for the prevention and treatment of glucocorticoid-induced osteoporosis,1 the American College of Rheumatology suggests the use of bisphosphonates only in patients with reduced bone mineral density.
Salvarani et al. did not consider that the American College of Rheumatology Ad Hoc Committee on Glucocorticoid-Induced Osteoporosis updated those recommendations in 2001,2 suggesting that for patients who are beginning therapy with glucocorticoids (a prednisone equivalent of 5 mg per day), with plans for three months or more of treatment, bisphosphonates should always be prescribed, irrespective of the bone mineral density. As the authors say, in these patients serious corticosteroid-related complications are very frequent; thus, we think it is important to stress their correct prevention.
2 ReferencesLuisa Praderio, M.D.
Gabriele Di Comite, M.D.
Nicoletta Saporiti, M.D.
IRCCS Hospital San Raffaele, 20132 Milan, Italy
praderio.luisa@hsr. it 1
American College of Rheumatology Task Force on Osteoporosis Guidelines
CrossRef | Web of Science | Medline2
American College of Rheumatology Ad Hoc Committee on Glucocorticoid-Induced Osteoporosis
CrossRef | Web of Science | Medline
To the Editor:
Salvarani et al. do not mention positron-emission tomography (PET) with the use of 18F-fluorodeoxyglucose (FDG) as an imaging tool. My colleagues and I and other groups have shown that this scintigraphic technique can be used to visualize thoracic large-vessel inflammation in polymyalgia rheumatica and giant-cell arteritis.1,2 In patients with mainly systemic symptoms (e.g., fever, weight loss, and malaise), its sensitivity reaches 75 percent (Figure 1Figure 1
PET Scan Showing Increased Uptake of 18F-Fluorodeoxyglucose in the Subclavian and Carotid Arteries and Thoracic Aorta (Arrows) in a 59-Year-Old Woman with Weight Loss and Fatigue Due to Giant-Cell Arteritis.), with a specificity exceeding 95 percent.1 Our results also demonstrate that in the majority of cases, giant-cell arteritis involves not only the temporal arteries but also the aorta and its proximal branches. One examination can demonstrate vasculitic involvement in the whole body. Therefore, I suggest that FDG PET scintigraphy be performed, in addition to arteriography, computed tomography, and magnetic resonance angiography, as Salvarani et al. suggest, whenever extracranial giant-cell arteritis is suspected. FDG PET scintigraphy is of great value for the diagnosis of giant-cell arteritis and of polymyalgia rheumatica when typical clinical signs are absent, when systemic symptoms predominate, or when temporal-artery biopsies are negative.2 ReferencesDaniël E. Blockmans, M.D., Ph.D.
University Hospital Gasthuisberg, B-3000 Leuven, Belgium
daniel.blockmans@uz. kuleuven. ac. be 1
Blockmans D ,Stroobants S ,Maes A ,Mortelmans L . Positron emission tomography in giant cell arteritis and polymyalgia rheumatica: evidence for inflammation of the aortic arch. Am J Med 2000;108:246-249
CrossRef | Web of Science | Medline2
Turlakow A ,Yeung HW ,Pui J , et al. Fludeoxyglucose positron emission tomography in the diagnosis of giant cell arteritis. Arch Intern Med 2001;161:1003-1007
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Author/Editor Response
The authors reply:
To the Editor: We did not mean to imply that polymyalgia rheumatica and giant-cell arteritis are benign conditions. Some cases of giant-cell arteritis are fatal, and with both syndromes, the majority of patients have important adverse effects of treatment. However, overall, we have found no significant reduction in life span. Drs. Ostor and Hazleman raise an important question about reported prognostic differences in northern European and U.S. studies of polymyalgia rheumatica and giant-cell arteritis. The reports suggest the presence of two subgroups of patients. One subgroup presents with mild, self-limiting disease requiring short-term treatment; the other subgroup has persistent disease requiring long-term treatment.1,2 The conflicting data on the duration of corticosteroid therapy in polymyalgia rheumatica and giant-cell arteritis may be related to differences in the study setting. Studies in the United Kingdom and Scandinavian countries, which report a longer duration of corticosteroid therapy, enrolled patients with more severe disease who were recruited at secondary or tertiary referral centers. Our studies were population-based and included all diagnosed cases, without selection bias.
We are also convinced that some cases of polymyalgia rheumatica and giant-cell arteritis are overtreated. Corticosteroid therapy is sometimes continued late in the course of the disease for indeterminate musculoskeletal symptoms and normal or slightly elevated values for the erythrocyte sedimentation rate, C-reactive protein, or both. Such atypical symptoms are more likely due to noninflammatory causes such as corticosteroid withdrawal than to active polymyalgia rheumatica. Aside from the erythrocyte sedimentation rate and C-reactive protein level, interleukin-6 appears to be a promising marker but is not routinely used in clinical practice.
We thank Dr. Horton for his clarification. We agree that ischemic optic neuropathy is the more correct term for the visual lesion in giant-cell arteritis. We agree that in the presence of visual symptoms, corticosteroids should be administered immediately rather than withheld until a biopsy has been performed. Temporal-artery biopsy specimens may show arteritis after more than two weeks of corticosteroid therapy.3
In the American College of Rheumatology's recommendations for the prevention and treatment of corticosteroid-induced osteoporosis, men and postmenopausal women who are beginning corticosteroid therapy, with a planned treatment duration of at least three months, are differentiated from those already receiving long-term corticosteroid therapy.4 Bisphosphonate therapy is recommended only in the first group, whereas in the second group, it is recommended when the T score for bone mineral density at either the lumbar spine or the hip is below normal. Apart from these recommendations, in our clinical practice, we initiate bisphosphonate therapy only in patients with a reduced T score for bone mineral density. However, we always measure bone mineral density when initiating corticosteroid therapy for polymyalgia rheumatica and giant-cell arteritis, and we repeat the measurements annually in patients receiving long-term treatment.
We discussed FDG PET in our review. Although promising, it is an experimental technique for the diagnosis of giant-cell arteritis and is not routinely used in clinical practice.
4 ReferencesCarlo Salvarani, M.D.
Arcispedale S. Maria Nuova, 42100 Reggio Emilia, ItalyFabrizio Cantini, M.D.
Ospedale di Prato, 59100 Prato, ItalyGene G. Hunder, M.D.
Mayo Clinic, Rochester, MN 559051
Salvarani C ,Macchioni PL ,Tartoni PL , et al. Polymyalgia rheumatica and giant-cell arteritis: a 5-year epidemiologic and clinical study in Reggio Emilia, Italy. Clin Exp Rheumatol 1987;5:205-215
Web of Science | Medline2
Ayoub WT ,Franklin CM ,Torretti D . Polymyalgia rheumatica: duration of therapy and long-term outcome. Am J Med 1985;79:309-315
CrossRef | Web of Science | Medline3
Achkar AA ,Lie JT ,Hunder GG ,O'Fallon WM ,Gabriel SE . How does previous corticosteroid treatment affect the biopsy findings in giant cell (temporal) arteritis? Ann Intern Med 1994;120:987-992
Web of Science | Medline4
American College of Rheumatology Ad Hoc Committee on Glucocorticoid-Induced Osteoporosis
CrossRef | Web of Science | Medline
- Citing Articles (1)
Citing Articles
1
Nicolò Pipitone, Luigi Boiardi, Carlo Salvarani. (2005) Are steroids alone sufficient for the treatment of giant cell arteritis?. Best Practice & Research Clinical Rheumatology 19:2, 277-292
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