Polymyalgia rheumatica overview
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Cafer Zorkun, M.D., Ph.D. [2]; Ujjwal Rastogi, MBBS [3]; Rim Halaby, M.D. [4]
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Overview
Polymyalgia rheumatica (PMR) is a chronic inflammatory disease that involves the articular and periarticular parts of the cervical region, shoulder girdle and pelvic girdle. PMR affects subjects over the age of 50 years and it is characterized by pain and stiffness in the neck, shoulders, upper arms, hip and thighs. Although myalgia is one of the symptoms of PMR, there is no inflammation of the muscles; instead, PMR is a disease of the joint that causes synovitis. The diagnosis of PMR relies on the clinical findings and laboratory evidence of systemic inflammation. PMR is associated with giant cell arteritis. The cause of PMR is unknown but it has been suggested that both genetic and environmental factors are implicated.[1] The mainstay of treatment of PMR is steroid therapy.[1]
Historical Perspective
Polymyalgia rheumatica was first described in 1888 by Bruce William as "senile rheumatic gout".[2] The disease was referred to as "polymyalgia rheumatica" by Stuart Barber in 1957 in his article entitled "mylagic syndrome with constitutional effects; polymyalgia rheumatica".[3]
Classification
Pathophysiology
PMR is a chronic inflammatory disease of the articular and periarticular structures of the cervical region, shoulder girdle and hip girdle. The underlying pathophysiology of PMR remains unknown.[1] It has been hypothesized that genetic and environmental factors are implicated, particularly due to the seasonal and geographical differences in the prevalence of this disease.[4][5][6] It has also been hypothesized that PMR is associated with infections such as parainfluenza virus type 1,[7] mycoplasma pneumoniae, chlamydia pneumoniae, and parvovirus B19.[8] In addition, histological examinations of synovial biopsies of affected individuals reveal mild synovitis with predominance of CD4 T cells and macrophages.[9] Although myalgia is a symptom of PMR, there is no inflammation of the muscles.
Causes
Differentiating Polymyalgia Rheumatica from other Diseases
PMR must be differentiated from other conditions such as late onset rheumatoid arthritis, polymyositis, dermatomyositis, fibromyalgia, and remitting seronegative symmetrical synovitis with pitting edema.
Epidemiology and Demographics
PMR affects mostly subjects who are more than 50 years of age.[10] The prevalence of PMR is highest among subjects from Scandanavian countries and those from northern European origin.[11]
Risk Factors
Age, female sex, Scandanavian and northern Europe origin are risk factors for polymyalgia rheumatica. Smoking, sun exposure, infections, nulliparity have also been considered risk factors.[12]
Natural History, Complications and Prognosis
PMR affects the quality of life of the patients. The pain and stiffness in the proximal joints might lead to sleep disturbance as well as inability to do regular daily activities such as getting dressed and getting out of a chair. The symptoms begin rapidly and last for weeks. Once the steroid treatment is initiated, the symptoms resolve rapidly within few days. In fact, the rapid resolution of symptoms with the steroid therapy reinforces the diagnosis of PMR. The steroid treatment can be associated with complications such as weight gain and bone fracture.[1] Approximately 40 to 50% of subjects experience relapse of the symptoms. PMR is associated with giant cell arteritis.
Diagnosis
Diagnostic Criteria
The diagnosis of PMR is mostly clinical and it is supported with specific findings on laboratory tests and ultrasound of the affected joints. The European League Against Rheumatism/American College of Rheumatology collaborative initiative developed a provisional classification criteria for PMR. The following criteria are required for the diagnosis of PMR: age more than 50 years, bilateral shoulder pain, and elevated C-reactive protein (CRP) and/or erythrocyte sedimentation rate (ESR).[13]
History and Symptoms
PMR is typically characterized by symmetrical pain and morning stiffness in the proximal joints and limbs, including the neck, the shoulder girdle, the pelvic girdle, the lower back, and the thighs. In some patients, there is involvement of the distal parts of the body such as peripheral synovitis or arthritis. Constitutional symptoms can also be present, and they include fever, fatigue, loss of appetite, and weight loss.[13] There is an association between PMR and giant cell arteritis which can present with one or more of the following symptoms that include headaches, scalp tenderness, jaw claudication, fever, or distorted vision.[14][15][16]
Physical Examination
Physical examination of patients with PMR reveals limitation of the active and passive range of motion of the affected joint. There is no true muscle weakness.[17]
Laboratory Findings
PMR is a clinical diagnosis that is supported by laboratory tests. Elevation in C-reactive protein (CRP) and/or erythrocyte sedimentation rate (ESR) is essential for the diagnosis of PMR.[13]
Electrocardiography
Chest X Ray
CT
MRI
MRI is used for the assessment of bursitis, synovitis, and tenosynovitis among patients with PMR. MRI is more sensitive than ultrasonography for the evaluation of iliopsoas bursitis and hip synovitis.[18] A study has demonstrated that MRI of the shoulders facilitates the proper diagnosis in patients with the typical proximal symptoms of PMR with normal ESR values.[19]
Echocardiography or Ultrasound
Ultrasound exam is important for the diagnosis of PMR. It can reveal evidence of bursitis, synovitis or tenosynovitis in the affected areas.[13]
Other Imaging Findings
Other Diagnostic Studies
A muscle biopsy might be performed to differentiate PMR from other diseases. In addition, temporal artery biopsy is required when a subject with PMR have symptoms suggestive of giant cell arteritis.
Treatment
Medical Therapy
The mainstay of treatment of PMR is low dose glucocorticoids, typically prednisone or prednisolone. The starting dose of the glucocorticoid treatment is 15-20 mg daily for 2 to 4 weeks after which the treatment should be slowly tapered. The average duration of the treatment with glucocorticoids is 1 to 2 years; nevertheless, longer corticosteroids regimens might be necessary among patients who experience relapse of the symptoms. Prophylaxis for osteoporosis with calcium and vitamin D should be started with the steroid therapy.[1]
Surgery
Primary Prevention
Secondary Prevention
Cost-Effectiveness of Therapy
Future or Investigational Therapies
Case Studies
References
- ↑ 1.0 1.1 1.2 1.3 1.4 Kermani TA, Warrington KJ (2013). "Polymyalgia rheumatica". Lancet. 381 (9860): 63–72. doi:10.1016/S0140-6736(12)60680-1. PMID 23051717.
- ↑ Bruce W (1888). "Senile Rheumatic Gout". Br Med J. 2 (1450): 811–3. PMC 2198572. PMID 20752457.
- ↑ BARBER HS (1957). "Myalgic syndrome with constitutional effects; polymyalgia rheumatica". Ann Rheum Dis. 16 (2): 230–7. PMC 1006948. PMID 13445065.
- ↑ Smeeth L, Cook C, Hall AJ (2006). "Incidence of diagnosed polymyalgia rheumatica and temporal arteritis in the United Kingdom, 1990-2001". Ann Rheum Dis. 65 (8): 1093–8. doi:10.1136/ard.2005.046912. PMC 1798240. PMID 16414971.
- ↑ Alvarez-Rodriguez L, Carrasco-Marin E, Lopez-Hoyos M, Mata C, Fernandez-Prieto L, Ruiz-Soto M; et al. (2009). "Interleukin-1RN gene polymorphisms in elderly patients with rheumatic inflammatory chronic conditions: Association of IL-1RN*2/2 genotype with polymyalgia rheumatica". Hum Immunol. 70 (1): 49–54. doi:10.1016/j.humimm.2008.10.011. PMID 19026700.
- ↑ Cimmino MA, Caporali R, Montecucco CM, Rovida S, Baratelli E, Broggini M (1990). "A seasonal pattern in the onset of polymyalgia rheumatica". Ann Rheum Dis. 49 (7): 521–3. PMC 1004141. PMID 2383076.
- ↑ Duhaut P, Bosshard S, Calvet A, Pinede L, Demolombe-Rague S, Dumontet C; et al. (1999). "Giant cell arteritis, polymyalgia rheumatica, and viral hypotheses: a multicenter, prospective case-control study. Groupe de Recherche sur l'Artérite à Cellules Géantes". J Rheumatol. 26 (2): 361–9. PMID 9972970.
- ↑ Elling P, Olsson AT, Elling H (1996). "Synchronous variations of the incidence of temporal arteritis and polymyalgia rheumatica in different regions of Denmark; association with epidemics of Mycoplasma pneumoniae infection". J Rheumatol. 23 (1): 112–9. PMID 8838518.
- ↑ Meliconi R, Pulsatelli L, Uguccioni M, Salvarani C, Macchioni P, Melchiorri C; et al. (1996). "Leukocyte infiltration in synovial tissue from the shoulder of patients with polymyalgia rheumatica. Quantitative analysis and influence of corticosteroid treatment". Arthritis Rheum. 39 (7): 1199–207. PMID 8670331.
- ↑ Doran MF, Crowson CS, O'Fallon WM, Hunder GG, Gabriel SE (2002). "Trends in the incidence of polymyalgia rheumatica over a 30 year period in Olmsted County, Minnesota, USA". J Rheumatol. 29 (8): 1694–7. PMID 12180732.
- ↑ Pamuk ON, Dönmez S, Karahan B, Pamuk GE, Cakir N (2009). "Giant cell arteritis and polymyalgia rheumatica in northwestern Turkey: Clinical features and epidemiological data". Clin Exp Rheumatol. 27 (5): 830–3. PMID 19917168.
- ↑ Cimmino MA, Zaccaria A (2000). "Epidemiology of polymyalgia rheumatica". Clin. Exp. Rheumatol. 18 (4 Suppl 20): S9–11. PMID 10948749.
- ↑ 13.0 13.1 13.2 13.3 Dasgupta B, Cimmino MA, Maradit-Kremers H, Schmidt WA, Schirmer M, Salvarani C; et al. (2012). "2012 provisional classification criteria for polymyalgia rheumatica: a European League Against Rheumatism/American College of Rheumatology collaborative initiative". Ann Rheum Dis. 71 (4): 484–92. doi:10.1136/annrheumdis-2011-200329. PMC 3298664. PMID 22388996.
- ↑ Salvarani C, Gabriel SE, O'Fallon WM, Hunder GG (1995). "The incidence of giant cell arteritis in Olmsted County, Minnesota: apparent fluctuations in a cyclic pattern". Ann Intern Med. 123 (3): 192–4. PMID 7598301.
- ↑ Salvarani C, Gabriel SE, O'Fallon WM, Hunder GG (1995). "Epidemiology of polymyalgia rheumatica in Olmsted County, Minnesota, 1970-1991". Arthritis Rheum. 38 (3): 369–73. PMID 7880191.
- ↑ Franzén P, Sutinen S, von Knorring J (1992). "Giant cell arteritis and polymyalgia rheumatica in a region of Finland: an epidemiologic, clinical and pathologic study, 1984-1988". J Rheumatol. 19 (2): 273–6. PMID 1629827.
- ↑ Salvarani C, Cantini F, Hunder GG (2008). "Polymyalgia rheumatica and giant-cell arteritis". Lancet. 372 (9634): 234–45. doi:10.1016/S0140-6736(08)61077-6. PMID 18640460.
- ↑ Cantini F, Niccoli L, Nannini C; et al. (2005). "Inflammatory changes of hip synovial structures in polymyalgia rheumatica". Clin. Exp. Rheumatol. 23 (4): 462–8. PMID 16095113.
- ↑ Cantini F, Salvarani C, Olivieri I, Niccoli L, Macchioni P, Boiardi L; et al. (2001). "Inflamed shoulder structures in polymyalgia rheumatica with normal erythrocyte sedimentation rate". Arthritis Rheum. 44 (5): 1155–9. doi:10.1002/1529-0131(200105)44:5<1155::AID-ANR198>3.0.CO;2-N. PMID 11352249.
External links
- Polymyalgia Rheumatica - The Arthritis Society
- Patient Education - Polymyalgia Rheumatica - American College of Rheumatology
Template:Diseases of the musculoskeletal system and connective tissue