Journal of Autoimmunity xxx (2014) 1e3
Contents lists available at ScienceDirect
Journal of Autoimmunity journal homepage: www.elsevier.com/locate/jautimm
Polymyalgia rheumatica e Diagnosis and classification Gideon Nesher a, b, c, * a
Department of Internal Medicine A and the Rheumatology Service, Shaare-Zedek Medical Center, Jerusalem, Israel The Hebrew University, Jerusalem, Israel c St. Louis University School of Medicine, St. Louis, MO, USA b
a r t i c l e i n f o
a b s t r a c t
Article history: Received 7 October 2013 Accepted 13 November 2013
Polymyalgia rheumatica is the most common inflammatory rheumatic disease of the elderly, and shares many pathogenetic and epidemiological features with giant cell arteritis. The typical symptoms are bilateral aching of the shoulder girdle, associated with morning stiffness. The neck and hip girdle may also be involved. The diagnosis of polymyalgia rheumatica is made primarily on clinical grounds. There is no single diagnostic test, but sets of diagnostic or classification criteria have been suggested by several groups of investigators, based on the typical clinical presentation and laboratory evidence of acute-phase reaction. Other conditions that may mimic polymyalgia rheumatic, such as elderly-onset rheumatoid arthritis, must be excluded by appropriate testing and close monitoring of the disease course. Glucocorticoids at low doses (15e20 mg prednisone per day initially) are the mainstay of treatment. Ó 2014 Elsevier Ltd. All rights reserved.
Keywords: Giant cell arteritis Morning stiffness Sedimentation rate Glucocorticoids
1. Disease manifestations Polymyalgia rheumatica (PMR) is the most common inflammatory rheumatic disease of the elderly. PMR patients share many pathogenetic features with giant cell arteritis (GCA) [1]. There is evidence for vascular inflammation with increased expression of inflammatory cytokines in the temporal arteries of PMR patients, without overt histological evidence of arteritis. Using fluorodeoxyglucose positron emission tomography, increased uptake was documented in thoracic blood vessels in PMR patients, suggestive of inflammation in these vessels [2]. Similar to GCA the highest annual incidence rates were observed in Northern Europe, 50e100 per 100,000 population older than 50 years. The estimated prevalence was 1:200 persons older than 50 years [3]. The typical symptoms of polymyalgia rheumatica (PMR) are bilateral aching of the shoulder girdle [1]. The neck and hip girdle may also be involved. Morning stiffness, lasting 30 min or more, is a prominent feature (Table 1). These symptoms are probably related to inflammation of the subacromial, subdeltoid and trochanteric bursae, and the glenohumeral or hip joints [4,5]. Onset of PMR symptoms may be acute or gradual. One-third of PMR patients have systemic manifestations such as low-grade fever, malaise and
* Department of Internal Medicine A, Shaare-Zedek Medical Center, P.O. Box 3235, Jerusalem 91031, Israel. Tel.: þ972 2 6666372; fax: þ972 2 6666049. E-mail address: [email protected].
anorexia, but these are often milder than systemic symptoms in GCA patients. PMR may be associated with other GCA clinical manifestations, but may be an “isolated” phenomenon. Like GCA, PMR develops in patients older than 50 years, and is more common in women. 2. PMR diagnosis The diagnosis of PMR is made primarily on clinical grounds and is bolstered by laboratory evidence of an acute phase reaction (Table 2). There is no single diagnostic test for PMR, but sets of diagnostic and classification criteria have been suggested by several groups of investigators (Table 3) [3,6e9]. Other conditions that may mimic PMR, such as inflammatory myopathies, elderly-onset rheumatoid arthritis (EORA), fibromyalgia, osteoarthritis, rotatorcuff tendinitis, subacute infections, thyroid diseases and occult malignancies, must be excluded by appropriate testing [10]. These sets of criteria used for diagnostic purposes are empirical. They have been defined by clinical experts who had studied the disease extensively. Each set of criteria has its own advantages and disadvantages. Recently, provisional classification criteria (Table 4) were published by a collaborative initiative of the European League Against Rheumatism and the American College of Rheumatology [11]. These classification criteria are helpful in distinguishing PMR from other disorders such as EORA, but they need further validation. Imaging studies such as magnetic resonance imaging (MRI) or ultrasonography typically show a predominantly periarticular
0896-8411/$ e see front matter Ó 2014 Elsevier Ltd. All rights reserved. http://dx.doi.org/10.1016/j.jaut.2014.01.016
Please cite this article in press as: Nesher G, Polymyalgia rheumatica e Diagnosis and classification, Journal of Autoimmunity (2014), http:// dx.doi.org/10.1016/j.jaut.2014.01.016
2
G. Nesher / Journal of Autoimmunity xxx (2014) 1e3 Table 1 Clinical features of polymyalgia rheumatica (PMR). Clinical feature
Frequency
Pain in shoulder girdle Morning stiffness (>30 min) Bilateral upper arm tenderness Neck pain Pain in hip girdle Distal musculoskeletal manifestationsa Fever, malaise, anorexia
90e100% 90e100% 50e75% 30e60% 30e75% 20e40% 20e50%
a
Arthritis/arthralgia of the hands, pitting edema of the hands (RS3PE syndrome), carpal tunnel syndrome.
Table 2 Abnormalities in laboratory tests in polymyalgia rheumatica. Test
Frequency
Elevated erythrocyte sedimentation rate (ESR) Elevated C-reactive protein and/or ESR Anemia (normocytic) Thrombocytosis Elevated alkaline phosphatase
80e95% >90% 20e50% 50 years
>50
neck, shoulder, or pelvic girdle
>1 month 1. neck or torso, 2. shoulders or arms, 3. hips or thighs
Morning stiffness Tenderness Systemic symptoms
>1 h
Erythrocyte sedimentation rate (ESR) Response to glucocorticoids
elevated
Requirements for diagnosis
rapid, to 20 mg or less age must be > 50, plus 3 of the other criteria
(at least 2 of 3) >30 min.
Jones and Hazleman 1981
>2 months shoulder and pelvic girdle
present
>40 mm/ha
>30 mm/h, or C-reactive protein >6 mg/l prompt and dramatic
all criteria
all criteria
Bird et al. 1979
Hamrin 1972
>65 years 50 years
bilateral shoulder pain and stiffness
>1 h upper arms depression, weight loss >40 mm/h
if any 3 criteria present e sensitivity 92% specificity 80%
>2 months neck, shoulder or pelvic girdle (at least 2 of 3)
present >50 mm/h
criteria of age, pain, and ESR are obligatory
a If ESR is borderline, look instead for other evidence to support the diagnosis: change in ESR compared to pre-illness period, rapid response to low-dose steroids, history of GCA, fever, weight loss or anemia.
Please cite this article in press as: Nesher G, Polymyalgia rheumatica e Diagnosis and classification, Journal of Autoimmunity (2014), http:// dx.doi.org/10.1016/j.jaut.2014.01.016
G. Nesher / Journal of Autoimmunity xxx (2014) 1e3
will eventually develop the characteristic features of RA [19e21]. The lack of antibodies to citrullinated peptide (ACPA) in PMR patients may help to distinguish them in early stages from patients with EORA [22]. A follow-up of several months may be required to make a definite distinction between PMR and EORA. 3. Therapy and disease course Glucocorticoids are the mainstay of treatment for PMR. The starting dose is 15e20 mg/day [23]. Symptoms typically begin to abate within 1e3 days of commencing therapy. Prompt response to low-dose glucocorticoid therapy is characteristic [8,9], but patients may still have some pain and stiffness 3e4 weeks after initiation of treatment [23]. After 2e4 weeks, following improvement of the clinical features of the disease together with normalization of the acute phase reactants, the dose of glucocorticoids can be tapered while monitoring for possible recurrence of symptoms. Relapses occur in about one-half of the patients, with response to increasing the dose to the previous level. Symptoms of GCA may develop while the glucocorticoid dose is being tapered. These patients, initially diagnosed as PMR, will require a diagnostic and therapeutic approach appropriate for GCA. The duration of treatment for PMR varies from one to several years, and the majority of patients develop steroid-related side effects. Methotrexate was assessed as a steroid-sparing agent with mixed results [23e25]. Addition of methotrexate can be considered in relapsing disease, in patients who are regarded at high risk for developing adverse events or in patients experiencing steroidrelated adverse effects. Overall, the prognosis is favorable and survival is similar to that of the general population. References [1] Nesher G, Nesher R. Giant cell arteritis and polymyalgia rheumatica. In: Ball GV, Bridges Jr SL, editors. Vasculitis. 2nd ed. Oxford University Press; 2008. [2] Moosig F, Czech N, Mehl C, Henze E, Zeuner RA, Kneba M, et al. Correlation between 18-fluorodeoxyglucose accumulation in large vessels and serological markers of inflammation in polymyalgia rheumatica: a quantitative PET study. Ann Rheum Dis 2004;63:870e3. [3] Chuang TY, Hunder GG, Ilstrup DM, Kurland LT. Polymyalgia rheumatica: a 10year epidemiologic and clinical study. Ann Intern Med 1982;97:672e80. [4] Salvarani C, Cantini F, Olivieri I, Barozzi L, Macchioni L, Niccoli L, et al. Proximal bursitis in active polymyalgia rheumatica. Ann Intern Med 1997;127:27e31. [5] Cantini F, Nicoli L, Mannini C, Padula A, Olivieri I, Boiardi L, et al. Inflammatory changes of the hip synovial structures in polymyalgia rheumatica. Clin Exp Rheumatol 2005;23:462e8.
3
[6] Hamrin B. Polymyalgia arteritica. Acta Med Scand 1972;533(Suppl.):1e131. [7] Bird HA, Esselinckx W, Dison ASJ, Mowat AG, Wood PHN. An evaluation of criteria for polymyalgia rheumatica. Ann Rheum Dis 1979;38:434e9. [8] Jones JG, Hazleman BL. Prognosis and management of polymyalgia rheumatica. Ann Rheum Dis 1981;40:1e5. [9] Healey LA. Long-term follow-up of polymyalgia rheumatica: evidence for synovitis. Semin Arthritis Rheum 1984;13:322e8. [10] González-Gay MA, García-Porrua C, Salvarani C, Olivieri I, Hunder GG. Polymyalgia manifestations in different conditions mimicking polymyalgia rheumatica. Clin Exp Rheumatol 2000;18:755e9. [11] Dasgupta B, Cimmino MA, Maradit-Kremers H, Schmidt WA, Schirmer M, Salvarani C, et al. 2012 Provisional classification criteria for polymyalgia rheumatica: a European League against Rheumatism/American College of Rheumatology collaborative initiative. Ann Rheum Dis 2012;71:484e92. [12] Breuer GS, Nesher G. What does imaging tell us about polymyalgia rheumatica? Rheumatol (Oxford) 2012;51:5e6. [13] Lange U, Teichmann J, Stracke H, Bretzel RG, Neeck G. Elderly onset rheumatoid arthritis and polymyalgia rheumatica: ultrasonographic study of the glenohumeral joints. Rheumatol Int 1998;17:229e32. [14] Blockmans D, De Ceuninck I, Vanderschueren S, Knockaert D, Mortelmans L, Bobbaers H. Repetitive 18-fluorodeoxyglucose positron emission tomography in isolated polymyalgia rheumatic: a prospective study in 35 patients. Rheumatol (Oxford) 2007;46:672e7. [15] Healey LA. Relation of giant cell arteritis to polymyalgia rheumatica. Bailliere’s Clin Rheumatol 1991;5:371e8. [16] Schmidt WA, Gromnica-Ihle EJ. Incidence of temporal arteritis in patients with polymyalgia rheumatica: a prospective study using color Doppler ultrasonography of the temporal arteries. Rheumatology 2002;20:309e18. [17] Hunder GG. Giant cell arteritis in polymyalgia rheumatica. Am J Med 1997;102:514e6. [18] Arida A, Kyprianou M, Kanakis M, Sfikakis PP. The diagnostic value of ultrasonography-derived edema of the temporal artery wall in giant cell arteritis: a second meta-analysis. BMC Muscukoskeletal Disord 2010;11:44. [19] Caporali R, Montecucco C, Epis O, Bobbio-Pallavicini F, Maio T, Cimmino MA. Presenting features of polymyalgia rheumatica (PMR) and rheumatoid arthritis with PMR-like onset: a prospective study. Ann Rheum Dis 2001;60: 1021e4. [20] Gran JT, Myklebust G. The incidence and clinical characteristics of peripheral arthritis in polymyalgia rheumatica and temporal arteritis: a prospective study of 231 cases. Rheumatology 2000;39:283e7. [21] Pease CT, Haugeberg G, Morgan AW, Montague B, Hensor EM, Bhakta BB. Diagnosing late-onset rheumatoid arthritis, polymyalgia rheumatica, and temporal arteritis in patients presenting with polymyalgic symptoms. A prospective longterm study. J Rheumatol 2005;32:1043e6. [22] Lopez-Hoyos M, Ruis de Alegria C, Blanco R, Crespo J, Pena M, RodriguezValverde V, et al. Clinical utility of anti-CCP antibodies in the differential diagtnosis of elderly-onset rheumatoid arthritis and polymyalgia rheumatica. Rheumatology 2004;43:655e7. [23] Kermani TA, Warrington KJ. Polymyalgia rheumatica. Lancet 2013;381:63e72. [24] Caporali R, Cimmino MA, Ferraccioli G, Gerli R, Klersy C, Salvarani C, et al. Prednisone plus methotrexate for polymyalgia rheumatica: a randomized, double-blind, placebo-controlled trial. Ann Intern Med 2004;141:493e500. [25] Cimmino MA, Salvarani C, Macchioni P, Gerli R, Bartoloni Bocci E, Montecucco C, et al. Long-term follow-up of polymyalgia rheumatica patients treated with methotrexate and steroids. Clin Exp Rheumatol 2008;26:395e400.
Please cite this article in press as: Nesher G, Polymyalgia rheumatica e Diagnosis and classification, Journal of Autoimmunity (2014), http:// dx.doi.org/10.1016/j.jaut.2014.01.016
Contents lists available at ScienceDirect
Journal of Autoimmunity journal homepage: www.elsevier.com/locate/jautimm
Polymyalgia rheumatica e Diagnosis and classification Gideon Nesher a, b, c, * a
Department of Internal Medicine A and the Rheumatology Service, Shaare-Zedek Medical Center, Jerusalem, Israel The Hebrew University, Jerusalem, Israel c St. Louis University School of Medicine, St. Louis, MO, USA b
a r t i c l e i n f o
a b s t r a c t
Article history: Received 7 October 2013 Accepted 13 November 2013
Polymyalgia rheumatica is the most common inflammatory rheumatic disease of the elderly, and shares many pathogenetic and epidemiological features with giant cell arteritis. The typical symptoms are bilateral aching of the shoulder girdle, associated with morning stiffness. The neck and hip girdle may also be involved. The diagnosis of polymyalgia rheumatica is made primarily on clinical grounds. There is no single diagnostic test, but sets of diagnostic or classification criteria have been suggested by several groups of investigators, based on the typical clinical presentation and laboratory evidence of acute-phase reaction. Other conditions that may mimic polymyalgia rheumatic, such as elderly-onset rheumatoid arthritis, must be excluded by appropriate testing and close monitoring of the disease course. Glucocorticoids at low doses (15e20 mg prednisone per day initially) are the mainstay of treatment. Ó 2014 Elsevier Ltd. All rights reserved.
Keywords: Giant cell arteritis Morning stiffness Sedimentation rate Glucocorticoids
1. Disease manifestations Polymyalgia rheumatica (PMR) is the most common inflammatory rheumatic disease of the elderly. PMR patients share many pathogenetic features with giant cell arteritis (GCA) [1]. There is evidence for vascular inflammation with increased expression of inflammatory cytokines in the temporal arteries of PMR patients, without overt histological evidence of arteritis. Using fluorodeoxyglucose positron emission tomography, increased uptake was documented in thoracic blood vessels in PMR patients, suggestive of inflammation in these vessels [2]. Similar to GCA the highest annual incidence rates were observed in Northern Europe, 50e100 per 100,000 population older than 50 years. The estimated prevalence was 1:200 persons older than 50 years [3]. The typical symptoms of polymyalgia rheumatica (PMR) are bilateral aching of the shoulder girdle [1]. The neck and hip girdle may also be involved. Morning stiffness, lasting 30 min or more, is a prominent feature (Table 1). These symptoms are probably related to inflammation of the subacromial, subdeltoid and trochanteric bursae, and the glenohumeral or hip joints [4,5]. Onset of PMR symptoms may be acute or gradual. One-third of PMR patients have systemic manifestations such as low-grade fever, malaise and
* Department of Internal Medicine A, Shaare-Zedek Medical Center, P.O. Box 3235, Jerusalem 91031, Israel. Tel.: þ972 2 6666372; fax: þ972 2 6666049. E-mail address: [email protected].
anorexia, but these are often milder than systemic symptoms in GCA patients. PMR may be associated with other GCA clinical manifestations, but may be an “isolated” phenomenon. Like GCA, PMR develops in patients older than 50 years, and is more common in women. 2. PMR diagnosis The diagnosis of PMR is made primarily on clinical grounds and is bolstered by laboratory evidence of an acute phase reaction (Table 2). There is no single diagnostic test for PMR, but sets of diagnostic and classification criteria have been suggested by several groups of investigators (Table 3) [3,6e9]. Other conditions that may mimic PMR, such as inflammatory myopathies, elderly-onset rheumatoid arthritis (EORA), fibromyalgia, osteoarthritis, rotatorcuff tendinitis, subacute infections, thyroid diseases and occult malignancies, must be excluded by appropriate testing [10]. These sets of criteria used for diagnostic purposes are empirical. They have been defined by clinical experts who had studied the disease extensively. Each set of criteria has its own advantages and disadvantages. Recently, provisional classification criteria (Table 4) were published by a collaborative initiative of the European League Against Rheumatism and the American College of Rheumatology [11]. These classification criteria are helpful in distinguishing PMR from other disorders such as EORA, but they need further validation. Imaging studies such as magnetic resonance imaging (MRI) or ultrasonography typically show a predominantly periarticular
0896-8411/$ e see front matter Ó 2014 Elsevier Ltd. All rights reserved. http://dx.doi.org/10.1016/j.jaut.2014.01.016
Please cite this article in press as: Nesher G, Polymyalgia rheumatica e Diagnosis and classification, Journal of Autoimmunity (2014), http:// dx.doi.org/10.1016/j.jaut.2014.01.016
2
G. Nesher / Journal of Autoimmunity xxx (2014) 1e3 Table 1 Clinical features of polymyalgia rheumatica (PMR). Clinical feature
Frequency
Pain in shoulder girdle Morning stiffness (>30 min) Bilateral upper arm tenderness Neck pain Pain in hip girdle Distal musculoskeletal manifestationsa Fever, malaise, anorexia
90e100% 90e100% 50e75% 30e60% 30e75% 20e40% 20e50%
a
Arthritis/arthralgia of the hands, pitting edema of the hands (RS3PE syndrome), carpal tunnel syndrome.
Table 2 Abnormalities in laboratory tests in polymyalgia rheumatica. Test
Frequency
Elevated erythrocyte sedimentation rate (ESR) Elevated C-reactive protein and/or ESR Anemia (normocytic) Thrombocytosis Elevated alkaline phosphatase
80e95% >90% 20e50% 50 years
>50
neck, shoulder, or pelvic girdle
>1 month 1. neck or torso, 2. shoulders or arms, 3. hips or thighs
Morning stiffness Tenderness Systemic symptoms
>1 h
Erythrocyte sedimentation rate (ESR) Response to glucocorticoids
elevated
Requirements for diagnosis
rapid, to 20 mg or less age must be > 50, plus 3 of the other criteria
(at least 2 of 3) >30 min.
Jones and Hazleman 1981
>2 months shoulder and pelvic girdle
present
>40 mm/ha
>30 mm/h, or C-reactive protein >6 mg/l prompt and dramatic
all criteria
all criteria
Bird et al. 1979
Hamrin 1972
>65 years 50 years
bilateral shoulder pain and stiffness
>1 h upper arms depression, weight loss >40 mm/h
if any 3 criteria present e sensitivity 92% specificity 80%
>2 months neck, shoulder or pelvic girdle (at least 2 of 3)
present >50 mm/h
criteria of age, pain, and ESR are obligatory
a If ESR is borderline, look instead for other evidence to support the diagnosis: change in ESR compared to pre-illness period, rapid response to low-dose steroids, history of GCA, fever, weight loss or anemia.
Please cite this article in press as: Nesher G, Polymyalgia rheumatica e Diagnosis and classification, Journal of Autoimmunity (2014), http:// dx.doi.org/10.1016/j.jaut.2014.01.016
G. Nesher / Journal of Autoimmunity xxx (2014) 1e3
will eventually develop the characteristic features of RA [19e21]. The lack of antibodies to citrullinated peptide (ACPA) in PMR patients may help to distinguish them in early stages from patients with EORA [22]. A follow-up of several months may be required to make a definite distinction between PMR and EORA. 3. Therapy and disease course Glucocorticoids are the mainstay of treatment for PMR. The starting dose is 15e20 mg/day [23]. Symptoms typically begin to abate within 1e3 days of commencing therapy. Prompt response to low-dose glucocorticoid therapy is characteristic [8,9], but patients may still have some pain and stiffness 3e4 weeks after initiation of treatment [23]. After 2e4 weeks, following improvement of the clinical features of the disease together with normalization of the acute phase reactants, the dose of glucocorticoids can be tapered while monitoring for possible recurrence of symptoms. Relapses occur in about one-half of the patients, with response to increasing the dose to the previous level. Symptoms of GCA may develop while the glucocorticoid dose is being tapered. These patients, initially diagnosed as PMR, will require a diagnostic and therapeutic approach appropriate for GCA. The duration of treatment for PMR varies from one to several years, and the majority of patients develop steroid-related side effects. Methotrexate was assessed as a steroid-sparing agent with mixed results [23e25]. Addition of methotrexate can be considered in relapsing disease, in patients who are regarded at high risk for developing adverse events or in patients experiencing steroidrelated adverse effects. Overall, the prognosis is favorable and survival is similar to that of the general population. References [1] Nesher G, Nesher R. Giant cell arteritis and polymyalgia rheumatica. In: Ball GV, Bridges Jr SL, editors. Vasculitis. 2nd ed. Oxford University Press; 2008. [2] Moosig F, Czech N, Mehl C, Henze E, Zeuner RA, Kneba M, et al. Correlation between 18-fluorodeoxyglucose accumulation in large vessels and serological markers of inflammation in polymyalgia rheumatica: a quantitative PET study. Ann Rheum Dis 2004;63:870e3. [3] Chuang TY, Hunder GG, Ilstrup DM, Kurland LT. Polymyalgia rheumatica: a 10year epidemiologic and clinical study. Ann Intern Med 1982;97:672e80. [4] Salvarani C, Cantini F, Olivieri I, Barozzi L, Macchioni L, Niccoli L, et al. Proximal bursitis in active polymyalgia rheumatica. Ann Intern Med 1997;127:27e31. [5] Cantini F, Nicoli L, Mannini C, Padula A, Olivieri I, Boiardi L, et al. Inflammatory changes of the hip synovial structures in polymyalgia rheumatica. Clin Exp Rheumatol 2005;23:462e8.
3
[6] Hamrin B. Polymyalgia arteritica. Acta Med Scand 1972;533(Suppl.):1e131. [7] Bird HA, Esselinckx W, Dison ASJ, Mowat AG, Wood PHN. An evaluation of criteria for polymyalgia rheumatica. Ann Rheum Dis 1979;38:434e9. [8] Jones JG, Hazleman BL. Prognosis and management of polymyalgia rheumatica. Ann Rheum Dis 1981;40:1e5. [9] Healey LA. Long-term follow-up of polymyalgia rheumatica: evidence for synovitis. Semin Arthritis Rheum 1984;13:322e8. [10] González-Gay MA, García-Porrua C, Salvarani C, Olivieri I, Hunder GG. Polymyalgia manifestations in different conditions mimicking polymyalgia rheumatica. Clin Exp Rheumatol 2000;18:755e9. [11] Dasgupta B, Cimmino MA, Maradit-Kremers H, Schmidt WA, Schirmer M, Salvarani C, et al. 2012 Provisional classification criteria for polymyalgia rheumatica: a European League against Rheumatism/American College of Rheumatology collaborative initiative. Ann Rheum Dis 2012;71:484e92. [12] Breuer GS, Nesher G. What does imaging tell us about polymyalgia rheumatica? Rheumatol (Oxford) 2012;51:5e6. [13] Lange U, Teichmann J, Stracke H, Bretzel RG, Neeck G. Elderly onset rheumatoid arthritis and polymyalgia rheumatica: ultrasonographic study of the glenohumeral joints. Rheumatol Int 1998;17:229e32. [14] Blockmans D, De Ceuninck I, Vanderschueren S, Knockaert D, Mortelmans L, Bobbaers H. Repetitive 18-fluorodeoxyglucose positron emission tomography in isolated polymyalgia rheumatic: a prospective study in 35 patients. Rheumatol (Oxford) 2007;46:672e7. [15] Healey LA. Relation of giant cell arteritis to polymyalgia rheumatica. Bailliere’s Clin Rheumatol 1991;5:371e8. [16] Schmidt WA, Gromnica-Ihle EJ. Incidence of temporal arteritis in patients with polymyalgia rheumatica: a prospective study using color Doppler ultrasonography of the temporal arteries. Rheumatology 2002;20:309e18. [17] Hunder GG. Giant cell arteritis in polymyalgia rheumatica. Am J Med 1997;102:514e6. [18] Arida A, Kyprianou M, Kanakis M, Sfikakis PP. The diagnostic value of ultrasonography-derived edema of the temporal artery wall in giant cell arteritis: a second meta-analysis. BMC Muscukoskeletal Disord 2010;11:44. [19] Caporali R, Montecucco C, Epis O, Bobbio-Pallavicini F, Maio T, Cimmino MA. Presenting features of polymyalgia rheumatica (PMR) and rheumatoid arthritis with PMR-like onset: a prospective study. Ann Rheum Dis 2001;60: 1021e4. [20] Gran JT, Myklebust G. The incidence and clinical characteristics of peripheral arthritis in polymyalgia rheumatica and temporal arteritis: a prospective study of 231 cases. Rheumatology 2000;39:283e7. [21] Pease CT, Haugeberg G, Morgan AW, Montague B, Hensor EM, Bhakta BB. Diagnosing late-onset rheumatoid arthritis, polymyalgia rheumatica, and temporal arteritis in patients presenting with polymyalgic symptoms. A prospective longterm study. J Rheumatol 2005;32:1043e6. [22] Lopez-Hoyos M, Ruis de Alegria C, Blanco R, Crespo J, Pena M, RodriguezValverde V, et al. Clinical utility of anti-CCP antibodies in the differential diagtnosis of elderly-onset rheumatoid arthritis and polymyalgia rheumatica. Rheumatology 2004;43:655e7. [23] Kermani TA, Warrington KJ. Polymyalgia rheumatica. Lancet 2013;381:63e72. [24] Caporali R, Cimmino MA, Ferraccioli G, Gerli R, Klersy C, Salvarani C, et al. Prednisone plus methotrexate for polymyalgia rheumatica: a randomized, double-blind, placebo-controlled trial. Ann Intern Med 2004;141:493e500. [25] Cimmino MA, Salvarani C, Macchioni P, Gerli R, Bartoloni Bocci E, Montecucco C, et al. Long-term follow-up of polymyalgia rheumatica patients treated with methotrexate and steroids. Clin Exp Rheumatol 2008;26:395e400.
Please cite this article in press as: Nesher G, Polymyalgia rheumatica e Diagnosis and classification, Journal of Autoimmunity (2014), http:// dx.doi.org/10.1016/j.jaut.2014.01.016
