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A Polymyalgia Rheumatica
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Patients with isolated polymyalgia rheumatica (ie, those not having above the neck symptoms of headache, jaw claudication, scalp tenderness, or visual symptoms) are treated with prednisone, 10 20 mg/d orally If the patient does not experience a dramatic improvement within 72 hours, the diagnosis should be revisited Usually after 2 4 weeks of treatment, slow tapering of the prednisone can be attempted Most patients require some dose of prednisone for a minimum of approximately 1 year; 6 months is too short in most cases Disease flares are common (50% or more) as prednisone is tapered The addition of weekly methotrexate may increase the chance of successfully tapering prednisone in some patients
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B Giant Cell Arteritis
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The urgency of early diagnosis and treatment in giant cell arteritis relates to the prevention of blindness Once blindness develops, it is usually permanent Therefore, when a patient has symptoms and findings suggestive of temporal arteritis, therapy with prednisone (60 mg/d orally) should be initiated immediately and a temporal artery biopsy performed promptly For patients who seek medical attention for visual loss, intravenous pulse methylprednisolone (eg, 1 g daily for 3 days) has been advocated; unfortunately, few patients recover vision no matter what the initial treatment One study too small and too preliminary to change the standard therapy recommendations mentioned above suggested that initiating treatment with intravenous pulse methylprednisolone may increase the chance of a patient with giant cell arteritis will achieve remission and be able to taper off of prednisone Retrospective studies suggest that low-dose aspirin ( 81 mg orally daily) may reduce the chance of visual loss or stroke in patients with giant cell arteritis and should be added to prednisone in the initial treatment Although it is prudent to obtain a temporal artery biopsy as soon as possible after instituting treatment, diagnostic findings of giant cell arteritis may still be present 2 weeks (or even considerably longer) after starting corticosteroids Typically, a positive biopsy shows inflammatory infiltrate in the media and adventitia with lymphocytes, histiocytes, plasma cells, and giant cells An adequate biopsy specimen is essential (at least 2 cm in length is ideal), because the disease may be segmental Unilateral temporal artery biopsies are positive in approximately 80 85% of patients, but bilateral biopsies add incrementally to the yield (10 15% in some studies, less in others) Prednisone should be continued in a dosage of 60 mg/d for about 1 month before tapering When only the symptoms of polymyalgia rheumatica are present, temporal artery biopsy is not necessary In adjusting the dosage of corticosteroid, the ESR (or Creactive protein) is a useful but not absolute guide to disease activity A common error is treating the ESR rather than the patient The ESR often rises slightly as the prednisone is
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C Laboratory Findings
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Nearly 90% of patients with giant cell arteritis have ESRs > 50 mm/h The ESR in this disorder is often > 100 mm/h, but cases in which the ESR is low or even normal do occur In one series, 5% of patients with biopsy-proven giant cell arteritis had ESRs < 40 mm/h Although the C-reactive protein is slightly more sensitive, patients with biopsyproven giant cell arteritis with normal C-reactive proteins have also been described Most patients also have a mild normochromic, normocytic anemia and thrombocytosis
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tapered, even as the disease remains quiescent Because elderly individuals often have baseline ESRs that are above the normal range, mild ESR elevations should not be an occasion for renewed treatment with prednisone in patients who are asymptomatic Unfortunately, no highly effective prednisonesparing therapy has been identified Methotrexate was modestly effective in one double-blind, placebo-controlled treatment trial but ineffective in another Anti-TNF therapies have produced disappointing results in giant cell arteritis Thoracic aortic aneurysms occur 17 times more frequently in patients with giant cell arteritis than in normal individuals and can result in aortic regurgitation, dissection, or rupture The aneurysms can develop at any time but typically occur 7 years after the diagnosis of giant cell arteritis is made
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Blockmans D et al Repetitive 18F-fluorodeoxyglucose positron emission tomography in giant cell arteritis: a prospective study of 35 patients Arthritis Rheum 2006 Feb 15;55(1): 131 7 [PMID: 16463425] Gonzalez-Gay MA et al Giant cell arteritis: disease patterns of clinical presentation in a series of 240 patients Medicine (Baltimore) 2005 Sep;84(5):269 76 [PMID: 16148727] Lee MS et al Antiplatelet and anticoagulant therapy in patients with giant cell arteritis Arthritis Rheum 2006 Oct;54(10): 3306 9 [PMID: 17009265] Mazlumzadeh M et al Treatment of giant cell arteritis using induction therapy with high-dose glucocorticoids: a double-blind, placebo-controlled, randomized prospective clinical trial Arthritis Rheum 2006 Oct;54(10):3310 8 [PMID: 17009270] Nesher G et al Low-dose aspirin and prevention of cranial ischemic complications in giant cell arteritis Arthritis Rheum 2004 Apr;50(4):1332 7 [PMID: 15077317] Parikh M et al Prevalence of a normal C-reactive protein with an elevated erythrocyte sedimentation rate in biopsy-proven giant cell arteritis Ophthalmology 2006 Oct;113(10):1842 5 [PMID: 16884778]
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