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Home , Giant cell arteritis, Knee arthritis, Polymyositis, Rheumatoid arthritis, Systemic vasculitis

Polymyalgia Rheumatica and BRIAN UNWIN, COL, MC, USA, CYNTHIA M. WILLIAMS, CAPT (R), MC, USN, and WILLIAM GILLILAND, COL, MC, USA, Uniformed Services University of the Health Sciences, Bethesda, Maryland

Polymyalgia rheumatica and are common, closely related vasculitic conditions that almost exclusively occur in patients older than 50 years. They may be manifestations of the same underlying disease and often coexist. Patients with polymyalgia rheumatica usually present with onset of stiffness and in the and pelvic musculature, which may be accompanied by , , and . If untreated, polymyalgia rheumatica may result in significant disability. Giant cell arteritis may manifest as visual loss or , abnormalities of the temporal artery such as tenderness or decreased pulsation, jaw , and new-onset . Erythrocyte sedimenta- tion rate and temporal artery help make the diagnosis. Giant cell arteritis requires urgent diagnosis because without treatment it may lead to irreversible blindness. Patients with either condition also may have nonspecific symptoms. are the mainstay of therapy for both conditions, with higher doses required for treatment of giant cell arteritis. Duration of therapy can be five years or longer before complete clinical remission is achieved. Monitoring for corticosteroid-associated side effects such as and , as well as for relapses and flare-ups, is key to chronic management. The prognosis for either condition, if treated, is good. (Am Fam Physician 2006;74:1547-54, 1557-8. Copyright © 2006 American Academy of Family Physicians.) ▲ Patient information: olymyalgia rheumatica (PMR) and GCA is less common, with an annual inci- A handout on polymyalgia giant cell arteritis (GCA; also known dence in persons older than 50 of approxi- rheumatica and giant cell arteritis, written by Jill as temporal arteritis) are common, mately 18 per 100,000. In both conditions the Giordano, MSIV, University interrelated inflammatory disorders incidence peaks in those between 70 and 80 of Medicine and Dentistry Pthat occur predominantly in persons older years of age, and diagnosis is more common of New Jersey School of than 50 years. GCA most commonly involves in northern latitudes.6 Osteopathic Medicine, is provided on page 1557. the temporal artery, but arteries in other parts of the body also can be inflamed. It is Pathogenesis the most common primary among Although the pathogeneses of GCA and older persons and can lead to blindness if not PMR are uncertain, similar cellular immune diagnosed and treated in a timely manner.1 responses involving T cells, -present- About 50 percent of persons with GCA also ing cells, -derived inflammatory have PMR, and about 10 percent of those , genetic with PMR also have GCA.2 PMR manifests as molecules, and are found in severe stiffness and pain in the girdle muscles both conditions.7 Because there is so much (i.e., neck, , buttocks, and thighs); clinical and pathophysiologic overlap, the the forearms, , calves, and feet usually conditions are thought to be manifestations are not affected.3 Without treatment, PMR of the same disease. can cause significant disability. In GCA, a syndrome of systemic inflam- mation accompanies the vascular mani- Epidemiology festations. Arterial often reveal The most important risk factor for both inflammatory changes to the tunica media conditions is older age, and the number of vasorum and tunica adventitia, which cause persons at risk in developed countries is narrowing or occlusion of the vessel lead- expected to double in the next 25 years as ing to distal to the lesion. GCA the average age of the population increases.4 most commonly affects the branches of PMR has a prevalence of one in 133 among the internal and external carotid arteries. persons older than 50, with women two The involvement of these branches leads times more likely to be affected than men.5 to the clinical findings of , jaw

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SORT: Key Recommendations for Practice

Evidence Clinical recommendation rating References

If the erythrocyte sedimentation rate is normal, then GCA is unlikely. C 11 Patients older than 50 years with ; diplopia; and C 11, 14 temporal artery beading, prominence, and tenderness should have a temporal artery biopsy to diagnose GCA. should be given as first-line therapy for treatment of B 11, 14 PMR and GCA. Treatment of GCA should not be delayed while awaiting biopsy. C 14 Ultrasonography and positron emission tomography are not B 18-20 replacements for temporal artery biopsy.

GCA = giant cell arteritis; PMR = polymyalgia rheumatica. A = consistent, good-quality patient-oriented evidence; B = inconsistent or limited-quality patient-oriented evi- dence; C = consensus, disease-oriented evidence, usual practice, expert opinion, or case series. For information about the SORT evidence rating system, see page 1463 or http://www.aafp.org/afpsort.xml.

claudication, tenderness, and blind- thighs; low-grade temperature elevation; ness.7 However, GCA can affect vessels any- evidence of weight loss; and . Distal where in the body.4,8,9 extremity manifestations are more promi- In PMR, the systemic inflammatory nent in PMR than in GCA. These findings response is the most prominent feature, but may include asymmetrical peripheral of the blood vessels remains and , syndrome, clinically undetectable. and swelling of the hands and feet.10

Diagnosis GIANT CELL ARTERITIS Distinguishing between GCA and PMR is GCA often manifests as a new-onset headache important because GCA can lead to blindness or a headache that is different from previous and requires higher doses of . headaches. The headache usually is ongo- ing for two to three months before patients POLYMYALGIA RHEUMATICA seek medical attention. Other common The onset of PMR usually is acute. However, symptoms generally are present for longer than one month before patients seek an eval- table 1 uation. Table 14,6 summarizes the findings Findings Associated with associated with a diagnosis of PMR. This dis- Polymyalgia Rheumatica ease can be functionally devastating to older adults. Shoulder pain is the most common Age 50 years or older symptom,6 and the pain and stiffness experi- Erythrocyte sedimentation rate greater than enced in the shoulders and upper arms may 50 mm per hour make hygiene and self-care tasks difficult. Mild, normochromic, normocytic The physical examination of a patient Aching, pain, and morning stiffness in the with PMR often is less striking than the shoulders and upper arms, and thighs, history would suggest; however, findings or neck and torso may include limited range of motion in the Symptoms of (e.g., , depression, fever, malaise, night neck, shoulders, and hips secondary to pain sweats, weight loss) in the associated proximal muscles; inflam- mation of the bursae in the shoulder and Information from references 4 and 6. regions; tenderness of the upper arms and

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reveal reduced range of motion in the shoul- table 2 der and hip because of pain, or a more distal Findings Associated with synovitis, usually of the .11 Giant Cell Arteritis Temporal artery biopsy should be per- formed when clinical and laboratory evi- Age 50 years or older dence suggests GCA.14 One meta-analysis Erythrocyte sedimentation rate greater than found only a few features were predictive 50 mm per hour of a positive temporal artery biopsy.11 Find- Anemia ings in GCA that increase the likelihood of Headache: temporal with temporal artery a positive temporal artery biopsy result are involvement, or occipital with occipital artery 11 involvement listed in Table 3. A normal erythrocyte Jaw claudication with variant presentation: sedimentation rate generally excludes the usually occurs when chewing tough foods; diagnoses of GCA and PMR. vague discomfort around the jaw; diffuse mandibular discomfort; dental discomfort; sinus pain and pressure; pain The differential diagnosis for GCA and PMR Abnormal temporal artery includes diseases and conditions that may Constitutional symptoms: fever, weight loss, present with pain, , weight loss, and depression, malaise fever. The most common conditions that Polymyalgia rheumatica should be considered are listed in Table 4.15 Visual symptoms: partially obscured vision, blindness from occlusion of posterior ciliary In a review, about 16 percent of patients with artery, , diplopia, visual were diagnosed with field cuts GCA.16 Infectious diseases, such as viral infec- tions, , (A, B, and C), and human immu- Information from references 4, 6, 11, and 12. nodeficiency virus or acquired The erythrocyte sedimen- immunodeficiency syndrome, tation rate is the most also should be considered.3 useful laboratory test for symptoms and findings in patients with GCA Other diseases and conditions diagnosing polymyalgia are outlined in Table 2.4,6,11,12 About 40 per- that may mimic GCA and PMR rheumatica and giant cell cent of patients with GCA present with atypi- or have similar findings include arteritis. cal symptoms. These can include dry cough, cancer, systemic erythe- choking sensation, fever of unknown origin, matosus, and seronegative rheu- and upper- and lower-extremity claudica- matoid arthritis. GCA and PMR are rare in tion. Neurologic manifestations may include patients younger than 50 years and therefore mononeuropathies, peripheral polyneuropa- should be considered only in those older than thies, and, rarely, transient ischemic attacks 50 years with suggestive symptoms. or .1,6 As with PMR, physical examination in LABORATORY EVALUATION a patient with GCA may be unremarkable. The most useful laboratory test for diag- Patients with gradual-onset GCA may pres- nosing GCA and PMR is the erythrocyte ent with a low-grade fever and abnormali- sedimentation rate. Patients with GCA gen- ties of the temporal artery (e.g., thickened, erally have an erythrocyte sedimentation rate lacking pulsation, tender, erythematous, greater than 40 to 50 mm per hour, and rates nodular). Eye examination is important to greater than 100 mm per hour are common. evaluate for other possible causes of vision It is unusual for a patient with GCA or PMR loss. Examination should include visual acu- to have a normal rate unless there has been ity, assessment of pupils for an afferent preceding corticosteroid use, and therefore pupillary defect, ocular motility, and an this test has a strong negative predictive ophthalmoscopic examination of the retina value for positive temporal artery biopsy. and optic disc.13 examination may The upper limit of a normal erythrocyte

November 1, 2006 ◆ Volume 74, Number 9 www.aafp.org/afp American Family Physician 1549 table 3 Findings Most Closely Correlated with Giant Cell Arteritis

Positive LR* Negative LR† Sensitivity‡ Finding (95% CI) (95% CI) (95% CI)

Beaded temporal artery 4.6 (1.1 to 18.4) 0.93 (0.88 to 0.99) 0.16 (0.07 to 0.28) Prominent or enlarged 4.3 (2.1 to 8.9) 0.67 (0.50 to 0.89) 0.47 (0.40 to 0.54) temporal artery Jaw claudication 4.2 (2.8 to 6.2) 0.72 (0.65 to 0.81) 0.34 (0.29 to 0.41) Diplopia 3.4 (1.3 to 8.6) 0.95 (0.91 to 0.99) 0.09 (0.07 to 0.13) Absent temporal artery 2.7 (0.55 to 13.4) 0.71 (0.38 to 1.3) 0.45 (0.26 to 0.66) pulse Tender temporal artery 2.6 (1.9 to 3.7) 0.82 (0.74 to 0.92) 0.41 (0.30 to 0.52) Any temporal artery 2.0 (1.4 to 3.0) 0.53 (0.38 to 0.75) 0.65 (0.54 to 0.74) abnormality ESR > 50 mm per hour 1.2 (1.0 to 1.4) 0.35 (0.18 to 0.67) 0.83 (0.75 to 0.90) ESR abnormal 1.1 (1.0 to 1.2) 0.2 (0.08 to 0.51) 0.96 (0.93 to 0.97) White race 1.1 (0.99 to 1.2) 0.86 (0.62 to 0.97) Male sex 0.83 (0.72 to 0.96) 0.32 (0.29 to 0.35)

LR = likelihood ratio; CI = confidence interval; ESR = erythrocyte sedimentation rate. *—Increased likelihood of giant cell arteritis if the finding is present. †—Decreased likelihood of giant cell arteritis if the finding is absent. ‡—Proportion of patients with biopsy-confirmed giant cell arteritis in whom the finding is present. Adapted with permission from Smetana GW, Shmerling RH. Does this patient have temporal arteritis? JAMA 2002;287:97-8.

sedimentation rate is estimated using the fol- temporal arteritis. A contralateral biopsy lowing formulas: could be considered if clinical suspicion is for men: age ÷ 2 high and an initial temporal artery biopsy result is negative.13,17 for women: (age + 10) ÷ 2 A negative temporal artery biopsy result One meta-analysis showed the mean does not rule out GCA because other arteries erythrocyte sedimentation rate for patients can be involved, or the artery with inflamma- with GCA to be 88 mm per hour.11 tion may not be biopsied. However, it should Most patients with PMR or GCA have prompt reassessment of the differential an elevated C-reactive protein level.11 Nor- mochromic, normocytic anemia; reactive thrombocytopenia; microscopic hematu- table 4 ria; and mild elevation of liver-associated Differential Diagnosis of PMR enzymes also may be found. and GCA Biopsy of the temporal artery has a piv- otal role in the diagnosis and subsequent management of GCA. Because treatment involves prolonged courses of corticosteroid from statin therapy therapy, it is important to confirm the diag- nosis with a biopsy even when the clinical Polymyositis probability is high. Long biopsy specimens (i.e., greater than 2 cm) of the temporal artery, serial sectioning, and experienced PMR = polymyalgia rheumatica; GCA = giant cell pathologic assessment improve diagnostic arteritis. yield. Frozen sections demonstrate higher Adapted with permission from Woolley DC. Polymyal- gia rheumatica. In: Ham RJ, Sloane PD, Warshaw GA, rates of false-negative biopsies. Empiric eds. Primary Care : A Case-Based Approach. bilateral temporal artery biopsies offer no 4th ed. St. Louis, Mo.: Mosby, 2002:646. significant benefit in diagnostic yield for

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diagnosis. Of 68 patients who had suspected temporal arteritis with negative biopsies, table 5 21 percent had PMR, 22 percent had a Polymyalgia Rheumatica neurologic disorder, and 15 percent had Activity Scale another disorder.11 Malig- nancy, arteriosclerotic peripheral vascular Total disease activity score = CRP (mg per dL) disease of the carotids, diabetes, ischemic + VASp + VASph + (MST x 0.1) + EUL optic , sinusitis, endocarditis, and Score less than 7 suggests low activity also were found in this group Score of 7 through 17 suggests medium disease activity of patients.11 Score greater than 17 suggests high disease activity IMAGING The use of ultrasonography and positron CRP = C-reactive protein; VASp = visual analog emission tomography in the diagnosis and scale–patient derived (0-10); VASph = visual analog scale–physician derived (0-10); MST = morning stiff- management of GCA and PMR still is experi- ness time (measured in minutes); EUL = elevation of mental. Color-coded duplex ultrasonography upper limbs (3 = none, 2 = below shoulder girdle, 1 = sometimes is performed by trained technicians up to shoulder girdle, 0 = above shoulder girdle). to assess GCA using specific protocols. Sensi- Information from reference 23. tivity and specificity for histologically con- firmed GCA have been reported as 95 percent and 76 percent, respectively, when hypoechoic weeks. Tapering of the corticosteroid dosage halo, stenosis, or occlusion were evident on should be individualized and should begin examination.16 One third of patients with after the patient has been stabilized for two acute GCA in one study had sonographi- to four weeks. A general suggestion is to cally detectable occlusions.16 However, other decrease the prednisone dosage by 1 mg per studies indicate that color-coded duplex day each week until most symptoms have ultrasonography cannot distinguish precisely resolved. Duration of therapy commonly is between inflammatory and degenerative arte- two to three years.14,22 Patients with a clini- rial disease.18,19 Ultrasonography may be help- cal diagnosis of PMR whose symptoms do ful in selecting ideal temporal artery segments not respond to low-dosage corticosteroid for biopsy.18,19 A negative result on ultraso- therapy should be evaluated for an alterna- nography of the temporal arteries should not tive diagnosis such as GCA. be used to exclude GCA.20 A disease activity score for PMR, termed Positron emission tomography has been the Polymyalgia Rheumatica Activity Scale studied in several small trials involving (PMR-AS), has been developed (Table 5).23 patients with GCA and PMR, and its use This score is derived from five variables: a with radioactively labeled fludeoxyglucose visual analog scale for pain from the patient, F 18 has demonstrated large-vessel inflam- a visual analog scale for the physician’s mation in these patients.21 Positron emission assessment, C-reactive protein level, morn- tomography is not suitable for use in evalua- ing stiffness time (measured in minutes), and tion of the temporal arteries because of their assessment of the ability to elevate the upper small size, but it may be useful in patients limbs. PMR-AS scores less than 7 suggest with unexplained inflammation or fever of low disease activity, scores of 7 through 17 unknown origin with unexplained somatic suggest medium disease activity, and scores symptoms.21 greater than 17 suggest high disease activity. This scale is used to help monitor and adjust Treatment therapy based on the patient’s response. Low-dosage prednisone (10 to 20 mg per Prednisone also is first-line therapy for day) usually improves symptoms of PMR GCA, but much higher dosages (usually within days. Optimal response to cortico- 40 to 60 mg per day) typically are required steroid therapy usually develops over two for suppression of disease activity. In patients

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with visual symptoms, treatment often is ini- hypertension, diabetes, elevated , tiated with intravenous formulations, such and fluid retention. as (Medrol). Treatment Baseline ophthalmologic evaluation is should not be delayed while awaiting tem- essential to assess any development of isch- poral artery biopsy. Corticosteroid therapy emic optic atrophy from GCA. Most visual has no effect on biopsy results for up to four loss occurs early in the disease. Late visual weeks after initiation.22 loss while receiving therapy is uncommon.13 Symptoms should resolve within days, and , D, and calcium high-dosage therapy should be continued have been found to be effective for pre- for two to four weeks before a slow taper venting loss in patients treated with is initiated. Alternate-day therapy has not corticosteroids.28,29 The American College been shown to be effective and may increase of recommends calcium sup- symptoms. Corticosteroid doses should be plementation (1,200 mg per day), vitamin D maintained at a sufficient level to reduce supplementation (800 U per day), lifestyle visual complaints, fever, headache, and myal- modification, regular weight-bearing exer- gia complaints. High-dosage corticosteroid cise, and therapy for preven- therapy to normalize sedimentation rates is tion of -induced osteoporosis, unnecessary. Typically, corticosteroids can and suggests bone-density assessment for be tapered to a low dosage (7.5 to 10 mg patients receiving long-term glucocorticoid per day) after six months, with complete therapy.30 Hormone replacement and calci- tapering to discontinuation within two to tonin should be considered as second-line three years. Flare-ups and relapses usually therapies when there are contraindications respond to corticosteroid increases to the to or intolerance of bisphosphonates.31 level at which symptoms previously were Hypertension can precede or develop controlled. Protracted courses of therapy from corticosteroid therapy. Assessment of often are necessary.22 bilateral upper- and lower-extremity blood Use of adjuvant to treat pressures is particularly relevant in patients GCA is not routinely recommended. Stud- with subclinical vasculitis. Hypertension, ies using methotrexate as an adjunct to diabetes, and should be treated as therapy in GCA are inconclusive. In one usual to prevent complications. study, methotrexate therapy combined with Corticosteroid can cause falls daily prednisone therapy was more effective or weakness associated with rising from a than prednisone alone in preserving remis- chair. It is improved only on reduction in sion and reducing overall corticosteroid corticosteroid dose. Interventions include exposure.24 However, another study using fall precautions, home safety assessment, alternate-day prednisone with methotrexate , and assistive devices. showed no benefit.25 Use of methotrexate These interventions also are helpful in for PMR demonstrated little additional ben- managing the bruising and tissue-heal- efit over prednisone alone.26,27 Subspecialty ing difficulties encountered with long-term consultation may be considered for patients corticosteroid use. who want methotrexate therapy, those who Depression, sleep disturbance, and emo- are intolerant of glucocorticoid therapy, and tional lability typically respond to appro- those with significant comorbidities that priate reductions in corticosteroid dosing. may complicate therapy. However, treatment with may be required to reduce symptoms. Seda- Monitoring Complications tive hypnotics and should Complications related to GCA and PMR be avoided because they increase the risk for and to therapy for these conditions include falls and confusional states. osteoporosis, corticosteroid myopathy, Any limitation of strength, range of motion, bruising, emotional symptoms (e.g., insom- cognition, or vision should prompt consider- nia, restlessness, hypomania, depression), ation of assessment for driving fitness.

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Prognosis Author disclosure: Nothing to disclose. The prognosis for patients with GCA or PMR is dependent on the underlying condition and REFERENCES control of corticosteroid-associated complica- 1. Hellman DB. Temporal arteritis: a cough, toothache, tions. GCA and PMR are not associated with and tongue . JAMA 2002;287:2996-3000. increased mortality. When treated, patients 2. Cantini F, Niccoli L, Storri L, Nannini C, Olivieri I, Padula with PMR experience relief of pain and other A, et al. Are polymyalgia rheumatica and giant cell symptoms and a return to previous func- arteritis the same disease? Semin Arthritis Rheum 2004;33:294-301. tion. Patients with GCA also experience relief 3. Spiera R, Spiera H. Inflammatory diseases in older with treatment, but spontaneous relapses are adults: polymyalgia rheumatica. Geriatrics 2004;59: common and unpredictable within the first 39-43. years of the disease. Partial or complete loss 4. Weyand CM, Goronzy JJ. Giant-cell arteritis and polymyalgia rheumatica. Ann Intern Med 2003;139: of vision occurs in about 15 to 20 percent of 505-15. 11 patients. Blindness in both eyes is rare. 5. Labbe P, Hardouin P. Epidemiology and optimal man- agement of polymyalgia rheumatica. Drugs Aging The opinions and assertions contained herein are the 1998;13:109-18. private views of the authors and are not to be construed 6. Salvarani C, Cantini F, Boiardi L, Hunder GG. Polymy- as official or as reflecting the views of the U.S. Army and algia rheumatica and giant-cell arteritis. N Engl J Med Navy Medical Departments or the U.S. Department of 2002;347:261-71. Defense. 7. Weyand CM, Goronzy JJ. Medium- and large-vessel vasculitis. N Engl J Med 2003;349:160-9. The Authors 8. Loddenkemper T. Temporal arteritis. Arch Neurol 2004;61:1620-2. BRIAN UNWIN, COL, MC, USA, is assistant professor of 9. Gran JT. Some thoughts about the etiopathogenesis family medicine and geriatrics at the Uniformed Services of temporal arteritis—a review. Scand J Rheumatol University of the Health Sciences, Bethesda, Md., where he 2002;31:1-5. also received his medical degree. He completed his residency 10. Narvaez J, Nolla-Sole JM, Narvaez JA, Clavaguera MT, training in family medicine at Martin Army Community Valverde-Garcia J, Roig-Escofet D. Musculoskeletal Hospital, Fort Benning, Ga. He holds a certificate of added manifestations in polymyalgia rheumatica and temporal qualifications in geriatrics, and completed a clinical geriat- arteritis. Ann Rheum Dis 2001;60:1960-3. rics fellowship at Madigan Army Medical Center–VA Puget 11. Smetana GW, Shmerling RH. Does this patient have Sound Health Care System, Tacoma, Wash. temporal arteritis? JAMA 2002;287:92-101. CYNTHIA M. WILLIAMS, CAPT (R), MC, USN, was an 12. Gonzalez-Gay MA, Lopez-Diaz MJ, Barros S, Garcia- assistant professor of family medicine and geriatrics at the Porrua C, Sanchez-Andrade A, Paz-Carreira J, et al. Uniformed Services University of the Health Sciences at Giant cell arteritis: laboratory tests at the time of diag- the time this article was written. Currently, she is a fellow nosis in a series of 240 patients. Medicine (Baltimore) in pain and palliative medicine at the National Institutes of 2005;84:277-90. Health, Bethesda, Md. She graduated from the Philadelphia 13. Spiera R, Spiera H. Inflammatory disease in older adults. (Pa.) College of Osteopathic Medicine, and completed her Cranial arteritis. Geriatrics 2004;59:25-9. residency training in family medicine at Naval Hospital 14. Frearson R, Cassidy T, Newton J. Polymyalgia rheu- Camp Pendleton, Camp Pendleton, Calif. She holds a cer- matica and temporal arteritis: evidence and guidelines tificate of added qualification in geriatrics and completed for diagnosis and management in older people. Age a geriatrics fellowship at Pitt Memorial Hospital–East Ageing 2003;32:370-4. Carolina School of Medicine, Greenville, N.C. 15. Woolley DC. Polymyalgia rheumatica. In: Ham RJ, Sloane PD, Warshaw GA, eds. Primary Care Geriatrics: WILLIAM GILLILAND, COL, MC, USA, is director of the A Case-Based Approach. 4th ed. St. Louis, Mo.: Mosby, Rheumatology Program at Walter Reed Army Medical 2002:647. Center (WRAMC), Washington, D.C., and associate pro- fessor of internal medicine at the Uniformed Services 16. Schmidt W. Doppler sonography in rheumatology. Best Pract Res Clin Rheumatol 2004;18:827-46. University of the Health Sciences, where he completed his medical degree. He completed an internal medicine 17. Danesh-Meyer H, Savino PJ, Eagle RC Jr, Kubis KC, residency at Fitzsimons Army Medical Center in Aurora, Sergott RC. Low diagnostic yield with second biopsies Colo., and a rheumatology fellowship at WRAMC. He has in suspected giant cell arteritis. J Neuroophthalmol 2000;20:213-5. a master’s degree in health professional education from the University of Illinois–Chicago. 18. Pfadenhauer K, Weber H. Duplex sonography of the temporal and occipital artery in the diagnosis of Address correspondence to Brian Unwin, M.D., temporal arteritis. A prospective study. J Rheumatol Uniformed Services University of the Health Sciences, 2003;30:2177-81. 4301 Jones Bridge Road, Bethesda, MD 20814 (e-mail: 19. Karassa FB, Matsagas MI, Schmidt WA, Ioannidis JP. [email protected]). Reprints are not available from Meta-analysis: test performance of ultrasonography for the authors. giant-cell arteritis. Ann Intern Med 2005;142:359-69.

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20. Reinhard M, Schmidt D, Hetzel A. Color-coded sonog- Group of the Italian Society for Rheumatology. Pred- raphy in suspected temporal arteritis—experiences nisone plus methotrexate for polymyalgia rheumatica: after 83 cases. Rheumatol Int 2004;24:340-6. a randomized, double-blind, placebo-controlled trial. 21. Schmidt WA, Blockmans D. Use of ultrasonography Ann Intern Med 2004;141:493-500. and positron emission tomography in the diagnosis 27. Stone JH. Methotrexate in polymyalgia rheumatica: ker- and assessment of large-vessel vasculitis. Curr Opin nel of truth or curse of Tantalus? [Editorial]. Ann Intern Rheumatol 2005;17:9-15. Med 2004;141:568-9. 22. Nordborg E, Nordborg C. Giant cell arteritis: strate- 28. Homik JJ, Adachi JD, Cranney A, Shea BJ, Suarez-Alm- gies in diagnosis and treatment. Curr Opin Rheumatol azor ME, Tugwell P, et al. Bisphosphonates for steroid 2004;16:25-30. induced osteoporosis. Database Syst Rev 23. Leeb BF, Bird HA. A disease activity score for polymyal- 1999;(1):CD001347. gia rheumatica. Ann Rheum Dis 2004;63:1279-83. 29. Homik JJ, Cranney A, Shea BJ, Suarez-Almazor ME, 24. Jover JA, Hernandez-Garcia C, Morado IC, Vargas E, Tugwell P, Wells G. Calcium and vitamin D for cortico- Banares A, Fernandez-Gutierrez B. Combined treat- steroid-induced osteoporosis. Cochrane Database Syst ment of giant-cell arteritis with methotrexate and Rev 1998;(2):CD000952. prednisone. A randomized, double-blind, placebo-con- 30. Recommendations for the prevention and treatment trolled trial. Ann Intern Med 2001;134:106-14. of glucocorticoid-induced osteoporosis: 2001 update. 25. Hoffman GS, Cid MC, Hellmann DB, Guillevin L, Stone American College of Rheumatology Ad Hoc Commit- JH, Schousboe J, et al., for the International Network tee on Glucocorticoid-Induced Osteoporosis. Arthritis for the Study of Systematic Vasculitides. A multicenter, Rheum 2001;44:1496-503. randomized, double-blind, placebo-controlled trial of 31. Cranney A, Adachi JD, Homik JJ, Robinson VA, Shea BJ, adjuvant methotrexate treatment for giant cell arteritis. Suarez-Almazor ME, et al. Calcitonin for preventing and Arthritis Rheum 2002;46:1309-18. treating corticosteroid-induced osteoporosis. Cochrane 26. Caporali R, Cimmino MA, Ferraccioli G, Gerli R, Klersy Database Syst Rev 2000;(1):CD001983. C, Salvarani C, et al., for the Study

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