AUTHOR AND EDITOR INFORMATION

Section 1 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

INTRODUCTION

Section 2 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Background

Polymyalgia rheumatica (PMR) is a relatively common clinical syndrome of unknown etiology. It is characterized by proximal myalgia of the hip and shoulder girdles with accompanying morning stiffness that lasts for more than 1 hour. Approximately 15% of patients with polymyalgia rheumatica develop giant cell arteritis (GCA), and approximately 50% of patients with giant cell arteritis have associated polymyalgia rheumatica.

Pathophysiology

The cause of polymyalgia rheumatica is unknown. HLA-DR4 is found with increased frequency in persons with polymyalgia rheumatica and in those with giant cell arteritis, and systemic monocyte activation is characteristic of both conditions. Both diseases show a sequence polymorphism encoded within the second hypervariable region of the HLA-DRB1 gene.

The pattern of T-cell–derived cytokines distinguishes the two patient populations. Patients with polymyalgia rheumatica often have elevated interleukin-2 (IL-2) and interleukin-6 (IL-6) levels. One hypothesis holds that, in a genetically predisposed patient, an environmental factor, possibly a virus, causes monocyte activation, which helps determine the production of cytokines that induce manifestations characteristic of polymyalgia rheumatica and giant cell arteritis.¹ The prevalence of antibodies to adenovirus and respiratory syncytial virus was reportedly higher in patients with polymyalgia rheumatica.² Occurrence in siblings suggests a genetic role in the pathophysiology of the disease.

Frequency

United States

The average annual incidence is 52.5 cases per 100,000 persons aged 50 years and older. The prevalence is approximately 0.5-0.7%.

International

The frequency varies by country; highest rates occur in northern Europe. For example, in Italy, the incidence is 12.7 cases per 100,000 persons.

Mortality/Morbidity

• With appropriate treatment, the survival rate is similar to that of unaffected persons of the same age; however, some reports document increased mortality from vascular disease among men with polymyalgia rheumatica after the initial 2 years following diagnosis.
• Polymyalgia rheumatica is self-limited and often remits in 1-3 years. Untreated patients, however, often feel unwell and have an impaired quality of life.

Race

Polymyalgia rheumatica almost always affects whites but is also occasionally reported in African American persons.

Sex

Polymyalgia rheumatica is twice as common in females.

Age

The incidence increases with advancing age. Polymyalgia rheumatica rarely affects persons younger than 50 years. The median age at diagnosis is 72 years.

CLINICAL

Section 3 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

History

Patients are often in good health prior to disease onset, which is abrupt in about 50% of patients. In most patients, the shoulder girdle is first to become symptomatic. In the remainder, the hip or neck is involved at onset. At presentation, symptoms may be unilateral but usually become bilateral within a few weeks.

• Criteria for diagnosis
• • Age 50 years or older at onset
  • Bilateral aching and morning stiffness for at least 1 month and involving at least 2 of 3 areas: neck or torso, shoulders or arms, hips or thighs
  • Westergren erythrocyte sedimentation rate (ESR) 40 mm/h or greater
  • Prompt response of symptoms to corticosteroids (15 mg/d)
• Systemic
• • Low-grade fever and weight loss
  • Malaise, fatigue, and depression
  • Difficulty rising from bed in the morning
  • Difficulty getting up from the toilet
  • Difficulty completing daily life activities
  • High, spiking fevers (rare)
• Musculoskeletal
• • Morning stiffness for more than 1 hour, often more prolonged
  • Muscle stiffness after prolonged inactivity
  • Carpal tunnel syndrome (in about 15% of patients)
  • Distal extremity swelling (uncommon)
  • Possible development of arthralgia and myalgia up to 6 months after onset of systemic symptoms

Physical

Polymyalgia rheumatica is a clinical diagnosis based on the complex of presenting symptoms and exclusion of the other potential diseases.

• General
• • Fatigued appearance
  • Low-grade temperature
  • Distal extremity swelling with pitting edema, which should be distinguished from remitting seronegative symmetrical synovitis with pitting edema (RS3PE)³
• Musculoskeletal
• • Normal muscle strength
  • Pain in the shoulder and hip with movement without significant clinical swelling
  • Transient synovitis of the knee, wrist, and sternoclavicular joints
  • Tenderness to palpation with decreased active range of motion in the proximal hip/leg and/or shoulder/arm girdle musculature
  • In later stages: Disuse muscle atrophy with proximal muscle weakness and even contractures of the shoulder capsule may lead to limitation of passive and active movement.

Causes

• Exact causes are unknown. The disease is more common among northern Europeans, which may indicate a genetic predisposition.
• An autoimmune process may play a role in polymyalgia rheumatica development. Polymyalgia rheumatica is associated with the HLA-DR4 haplotype. High levels of IL-2 are associated with polymyalgia rheumatica, and high serum levels of IL-6 correlate with increased disease activity.
• T2-weighted MRI of the shoulders may reveal subdeltoid, subacromial, and bicipital tenosynovitis. These findings have led many investigators to believe that nonerosive synovitis and tenosynovitis are responsible for many symptoms of polymyalgia rheumatica.

DIFFERENTIALS

Section 4 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Other Problems to be Considered

Acute or chronic infection
Endocarditis
Malignancy
Parkinson disease
RS3PE
Shoulder disorders, including shoulder synovitis, rotator cuff tendinitis, and subdeltoid bursitis
Cervical spondylosis

WORKUP

Section 5 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Lab Studies

• Erythrocyte sedimentation rate
• • ESR is the most sensitive diagnostic study for polymyalgia rheumatica, although it is not specific.
  • The ESR is frequently elevated and greater than 40 mm/h, but the rate can exceed 100 mm/h.
  • In 20% of patients, the ESR is mildly elevated or, occasionally, normal, which may occur in patients with limited disease activity. In these cases, diagnosis is based on rapid positive response to low-dose oral corticosteroids (10-15 mg/d).
• C-reactive protein
• • The C-reactive protein level is often elevated and may parallel the ESR.
  • Longitudinal studies suggest that it may be a more sensitive test than ESR for the diagnosis of polymyalgia rheumatica.⁴
• CBC count with differential
• • CBC count reveals mild normocytic, normochromic anemia.
  • The WBC count may be normal or mildly elevated. Platelet counts are often increased.
• Other laboratory tests
• • Liver function tests reveal normal transaminase enzyme levels, the alkaline phosphatase may be mildly increased. Serum albumin levels may be slightly decreased.
  • The creatine kinase level is normal and helps differentiate the disease from polymyositis and other primary myopathic disorders.
  • Antinuclear antibodies and rheumatoid factor levels are usually normal.
  • Serum IL-6 levels are elevated and often closely parallel inflammatory activity of the disease.

Imaging Studies

• Radiography: Radiographs of the painful joints rarely show abnormalities such as osteopenia, joint space narrowing, or erosions.
• MRI
• • MRI is not necessary for diagnosis.
  • MRI of the shoulder reveals subacromial and subdeltoid bursitis and glenohumeral joint synovitis in the vast majority of patients.⁵
  • MRI of the hands and feet demonstrates inflammation of the tendon sheaths in many patients.
  • T2-weighted MRI of the shoulders may reveal subdeltoid, subacromial, ad bicipital tenosynovitis. These findings have led many investigators to believe that nonerosive synovitis and tenosynovitis are responsible for many symptoms of polymyalgia rheumatica.
• Bursa ultrasonography⁶
• • This study may reveal an effusion within the shoulder bursae.
  • The ultrasonography findings and those of MRI usually correlate well.
  • Ultrasonography is very operator-dependent and may be useful when the diagnosis is uncertain.

Procedures

• Occasionally, synovitis with effusions may be observed. In these cases, synovial fluid analysis reveals signs of mild inflammation, including poor mucin clotting. WBC counts are usually 1000-20,000 cells/µL, with 40-50% polymorphonuclear leukocytes.
• Temporal artery biopsy
• • Temporal artery biopsy (TAB) has a very low yield in patients with isolated polymyalgia rheumatica and is therefore usually unnecessary in patients with polymyalgia rheumatica without symptoms of giant cell arteritis.
  • TAB is not indicated in patients with mild symptoms of polymyalgia rheumatica that is of recent onset or in patients who have remained stable over a long period (1 y or longer without current or previous clinical evidence of arteritis).
  • Patients should be monitored for symptoms or signs of arteritis after treatment initiation because low-dose corticosteroids do not prevent progression of polymyalgia rheumatica to giant cell arteritis. If clinical signs of vasculitis develop, TAB should be performed.
  • TAB may also be warranted in patients with polymyalgia rheumatica who are receiving low-dose corticosteroids if the clinical response is incomplete or if the ESR remains elevated or rises despite symptom resolution on corticosteroid therapy. Low-dose corticosteroids do not appear to affect biopsy yield.

Histologic Findings

• Synovitis is histologically mild and is characterized by a predominance of macrophages and CD4+ helper cells.

TREATMENT

Section 6 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Medical Care

• Polymyalgia rheumatica is a chronic, self-limited disorder. Therapy is based on empiric experiences because few randomized clinical trials are available to guide treatment decisions.
• The therapeutic goals are to control painful myalgia, to improve muscle stiffness, and to resolve constitutional features of the disease.
• Corticosteroids are considered the treatment of choice because they often cause complete or near-complete symptom resolution and reduction of the ESR to normal. However, no definite evidence demonstrates that corticosteroids (or any other therapy) alter the natural history of polymyalgia rheumatica. The low-dose corticosteroids used in polymyalgia rheumatica are almost certainly ineffective in the prevention of vasculitis progression.
• Nonsteroidal anti-inflammatory drugs (NSAIDs) can be administered to some patients with mild symptoms; however, most patients require corticosteroids for total control of symptoms. NSAIDs may be helpful in later stages of corticosteroid dosage tapering. NSAIDs generally have no effect on ESR.
• Methotrexate, azathioprine, and other immunosuppressive drugs have been used in some centers in an effort to limit dosage and duration of corticosteroid therapy. At present, no clear-cut data suggest that any of these drugs is superior to corticosteroid therapy. They are seldom indicated for the vast majority of patients with polymyalgia rheumatica who do not have giant cell arteritis because these patients generally respond to low doses of corticosteroids. In fact, symptomatic palliation of pain with analgesic therapy alone may be preferable in situations of corticosteroid intolerance (eg, uncontrolled diabetes mellitus, severe symptomatic osteoporosis, psychosis).

Consultations

• Diagnosis and treatment involve the primary care physician and rheumatologist. Ophthalmologists, pathologists, and surgeons may be consulted on an as-needed basis.
• In coordination with the primary care physician, the rheumatologist plays an important role in diagnosis, treatment, and follow-up care.
• Consult with an ophthalmologist if concomitant giant cell arteritis may be causing decreased vision.
• In order to perform TAB, a consultation with a surgeon is essential if the presence of giant cell arteritis is in doubt.

Diet

Ensure adequate calcium and vitamin D intake with corticosteroid use.

Activity

Generally, activity restriction is unnecessary.

MEDICATION

Section 7 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

The goals of pharmacotherapy are to reduce morbidity and to prevent complications.

Drug Category: Corticosteroids

Oral corticosteroids are the first line of treatment. These agents cause profound and varied metabolic effects. The exact mechanism of action in polymyalgia rheumatica is not well-known, although the disease may be caused by general anti-inflammatory and immunomodulatory effects. In addition, corticosteroids down-regulate cytokine production.

Drug Category: Nonsteroidal anti-inflammatory drugs

These agents can be administered to some patients with mild symptoms; however, most patients require corticosteroids for total control of symptoms. NSAIDs may be helpful in later stages of corticosteroid dosage tapering. NSAIDs generally have no effect on ESR.

FOLLOW-UP

Section 8 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Further Outpatient Care

• Polymyalgia rheumatica is typically treated in an outpatient setting. Objective means of determining prognosis and decisions concerning duration of treatment remain empiric and often need careful supervision.
• Calcium and vitamin D supplementation should be initiated in all patients with polymyalgia rheumatica who are starting corticosteroid therapy. Osteopenia or osteoporosis discovered with a bone mineral density study (eg, dual-energy x-ray absorptiometry [DEXA] scan) is an indication to start antiresorptive therapy.
• An isolated increase of ESR without symptoms during the course of treatment is not a valid reason to increase corticosteroid dose; however, a temporary delay in dosage reduction may be necessary.
• Because relapses are more likely to occur during the initial 18 months of therapy and within 1 year of corticosteroid withdrawal, all patients should be monitored for symptom recurrence throughout corticosteroid tapering and until 12 months after cessation of therapy.
• Approximately 50-75% of patients can discontinue corticosteroid therapy after 2 years of treatment.

In/Out Patient Meds

• If not contraindicated, NSAIDs may provide supplemental pain relief. They may be used alone in the treatment of patients with mild symptoms.
• Methotrexate and other immunosuppressive therapies are seldom used in polymyalgia rheumatica treatment. Occasionally, they may be considered in patients with corticosteroid intolerance or as corticosteroid-sparing agents.

Deterrence/Prevention

• No method or strategy is known to be effective in preventing polymyalgia rheumatica.

Complications

• Polymyalgia rheumatica usually has a limited course of several months to 5 years. Untreated patients often feel unwell and have an impaired quality of life.
• Generally, polymyalgia rheumatica is not associated with serious complications.
• Patients treated with corticosteroids are at risk for long-term complications of corticosteroid therapy.
• Relapses are common and may occur in up to 25% of all treated patients. Arteritic relapse in a patient who presented exclusively with polymyalgia rheumatica is unusual.
• Every patient should be considered at risk for giant cell arteritis.
• Several cases of systemic amyloidosis-associated polymyalgia rheumatica have been reported.⁷

Prognosis

• Polymyalgia rheumatica is usually self-limited. With prompt diagnosis and adequate therapy, the condition has an excellent prognosis.

Patient Education

• Inform the patient about the potential benefits and risks of corticosteroid treatment and encourage the patient to participate in choosing the treatment plan.
• Emphasize the importance of healthy dietary habits and ensure adequate calcium and vitamin D supplementation.
• Emphasize compliance with long-term treatment plans and follow-up care in order to prevent relapses, flares, and subsequent morbidity secondary to corticosteroid therapy.
• Advise patients to immediately seek medical care if symptoms recur.
• For excellent patient education resources, visit eMedicine's Muscle Disorders Center. Also, see eMedicine's patient education article Chronic Fatigue Syndrome.

MISCELLANEOUS

Section 9 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Medical/Legal Pitfalls

• Failure to consider giant cell arteritis in atypical cases of polymyalgia rheumatica
• Failure to consider alternative causes of systemic illness with an elevated ESR
• Failure to fully inform the patient about potential risks secondary to prolonged corticosteroid therapy
• Failure to arrange timely follow-up care

Special Concerns

• Patients with polymyalgia rheumatica should be monitored regularly and carefully for symptoms and signs suggestive of giant cell arteritis development.

REFERENCES

Section 10 of 10

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

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Article Last Updated: Nov 26, 2007