US Pharm. 2012;37(6):HS-14-HS-16.

Polymyalgia rheumatica (PMR) is an inflammatory condition of the muscles and joints and is characterized by stiffness and pain in the neck, shoulders, hips, and buttocks. Morning stiffness that lasts several hours is common. The onset of pain can be sudden or gradual and affects both sides of the body. Approximately 15% of patients with PMR develop giant cell arteritis (GCA), and nearly 50% of patients with GCA will develop PMR over time.1  

PMR is a complicated disease with many complex symptoms. An accurate diagnosis must exclude many other potential diseases. Corticosteroids (e.g., prednisone) are considered the treatment of choice. Patients have an excellent prognosis, although exacerbations may occur if steroids are tapered too rapidly, and relapse is common.1  

While there have been no major studies on the relationship between inflammatory foods (e.g., wheat products) and PMR, many patients have reported that by following a paleo or gluten-free diet and exercising, they have been able to control their symptoms and taper off the steroids in a period of up to 1 year. In general, avoiding foods that cause inflammation and gastrointestinal problems can sometimes alleviate fibromyalgia. Fibromyalgia affects about 2% of the U.S. population, with women older than 50 years being more susceptible to the disorder than men.2


The cause of PMR is unknown. PMR is closely linked to GCA, although the two are believed to be separate disease processes. Patients with PMR often have elevated levels of interleukin-2 and interleukin-6. The pattern of T cell–derived cytokines distinguishes these patient populations.

One hypothesis is that in a genetically predisposed patient, an environmental factor, possibly a virus, causes monocyte activation, which helps the production of the cytokines that induce PMR and GCA. The prevalence of antibodies to adenovirus and respiratory syncytial virus is reportedly higher in patients with PMR. Increased occurrence in siblings suggests a genetic role in the pathophysiology of the disease.3

Although PMR causes severe pain in the proximal muscle groups, no evidence of disease is present on muscle biopsy. Muscle strength and electromyographic findings are normal. Some evidence suggests the presence of cell-mediated injury to the elastic lamina in the blood vessels of the affected muscle groups.

The disease is more common among northern Europeans, which may indicate a genetic predisposition. As mentioned earlier, other risk factors for PMR are age of 50 years or older and the presence of GCA. An autoimmune process may play a role in PMR development.3


In the U.S., the average annual incidence of PMR is 52.5 cases per 100,000 persons aged 50 years and older. The prevalence was nearly 0.5% to 0.7%, but it is now up to 2%.

In Europe, the frequency decreases from north to south, with a high incidence in Scandinavian countries and low incidences in Mediterranean countries. In Italy, for example, the incidence is 13 cases per 100,000 persons.

Whites are affected with PMR more than other ethnic groups. PMR is twice as common in females, and the incidence increases with advancing age.4

Signs and Symptoms

The signs and symptoms of PMR are variable and nonspecific. The general symptoms are fatigue, low-grade temperature, and limb swelling with pitting edema. The main symptoms are musculoskeletal; however, there is normal muscle strength and no muscle atrophy.

The majority of patients have pain in the shoulder and hip without significant clinical swelling that reduces mobility. Tenderness, palpations, and decreased active range of motion in the musculature of the proximal hip, leg, shoulder, and arm cause patients to do less exercise and therefore gain weight.

Over time, disuse of muscle causes atrophy with proximal muscle weakness. In addition, contractures of the shoulder capsule may lead to limitations of passive and active movement.5

Laboratory Diagnosis

Laboratory tests and studies in PMR include the following:  

• The erythrocyte sedimentation rate (ESR) is the most sensitive diagnostic study for PMR, although it is not specific. The ESR is frequently elevated and greater than 40 mm/h, but it 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 prednisone (10-15 mg/day).  

• The C-reactive protein level is often elevated and may parallel the ESR. Studies suggest that high-sensitive CRP may be a more specific test than the ESR for the diagnosis of PMR.

• The complete blood cell test reveals mild normocytic, normochromic anemia in 50% of cases. The white blood cell count may be normal or mildly elevated. Platelet counts are often increased.

• Liver function tests reveal normal transaminase enzyme levels. Alkaline phosphatase may be mildly increased. Serum albumin levels may be slightly decreased.

• The creatine kinase level is normal; this finding helps differentiate PMR from polymyositis and other primary myopathic disorders.6

Finally, antinuclear antibodies and rheumatoid factor levels are usually normal, and serum interleukin-6 levels are elevated and often closely parallel the inflammatory activity of the disease.6

Radiographic Diagnosis

Radiography of painful joints may rarely show abnormalities such as osteopenia, joint space narrowing, or erosions. Magnetic resonance imaging (MRI) is not necessary for diagnosis, but MRI of the shoulder reveals subacromial and subdeltoid bursitis and glenohumeral joint synovitis in the vast majority of patients. MRI of the hands and feet demonstrates inflammation of the tendon sheaths in many patients.

Ultrasonography is very operator dependent but may be useful when the diagnosis is uncertain. Bursa ultrasonography may reveal an effusion within the shoulder bursae. The ultrasonography findings and those of MRI usually correlate well.7  

Temporal Artery Biopsy (TAB)

Why is this test important? Patients should be monitored for symptoms or signs of arteritis after treatment initiation, because low-dose corticosteroids such as prednisone do not prevent progression of PMR to GCA. If clinical signs of vasculitis develop, TAB should be performed.

TAB may also be warranted in patients with PMR 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.7,8


The goals of therapy in PMR are to control painful myalgia, to improve muscle stiffness, and to resolve constitutional features of the disease. Oral corticosteroids such as prednisone (see sidebar) are the first line of treatment. Nonsteroidal anti-inflammatory drugs (NSAIDs) may be helpful as adjuncts to corticosteroids during tapering, or alone in mild cases.9

PMR is usually a self-limiting disease. If untreated, patients will have an impaired quality of life. With early diagnosis and correct therapy, patients have an excellent prognosis. The average length of disease is 3 years. However, exacerbations may occur if steroids are tapered too rapidly, and relapse is common, affecting up to 25% of all treated patients.

Generally, PMR is not associated with serious complications; however, patients treated with corticosteroids are at risk for long-term complications of corticosteroid therapy. Every patient should be considered at risk for GCA.

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, they do not cure the disease. The low-dose corticosteroids used in PMR are almost certainly ineffective in the prevention of vasculitis progression.

It has been found that remission of PMR seemed to be achieved with a 15-mg/d dose of prednisone for most patients. A slow tapering of the prednisone, less than 1 mg/mo, was associated with fewer relapses.

Nevertheless, controversy remains regarding the dose and duration of treatment. The dose depends on the patient’s weight and the severity of symptoms. The dose should be increased if symptoms are not well controlled within 1 week, and a diagnosis of GCA may need to be pursued. In contrast to results with other rheumatic diseases, alternate-day administration of corticosteroids in PMR has been largely unsuccessful.9

NSAIDs may provide supplemental pain relief. They may be used alone in the treatment of 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 and generally have no effect on the ESR.

Methotrexate, azathioprine, and other immunosuppressive therapies are seldom used in PMR treatment. Occasionally, they may be considered in patients with corticosteroid intolerance or as corticosteroid-sparing agents.

In fact, symptomatic palliation of pain with analgesic therapy alone may be preferable in patients with intolerable adverse effects from corticosteroids (e.g., uncontrolled diabetes mellitus, severe symptomatic osteoporosis, psychosis).8

Long-Term Monitoring

PMR requires a primary care physician, rheumatologist, ophthalmologist, pathologist, and surgeon on an as-needed basis. Both the primary care physician and the rheumatologist play an important role in diagnosis, treatment, and follow-up care. Consultation with an ophthalmologist is important if concomitant GCA causes decreased vision. Consultation with a surgeon for performance of TAB is essential if the presence of GCA is in doubt.

PMR is typically treated in an outpatient setting. Patients receiving steroids should have monthly follow-up, with regular monitoring of the ESR. An isolated increase of the ESR without symptoms during the course of treatment is not a valid reason to increase the corticosteroid dose; however, a temporary delay in dose reduction may be necessary. After steroid tapering, follow-ups can be performed quarterly.

To prevent osteopenia or osteoporosis during the treatment, supplementation with calcium (1,000-1,200 mg/day) and vitamin D (up to 1,000 IU/day) should be initiated in all patients with PMR who are starting corticosteroid therapy.11

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% to 75% of patients can discontinue corticosteroid therapy after 2 years of treatment, and patients with PMR should be monitored regularly and carefully for symptoms and signs suggestive of GCA development.11


1. Salvarani C, Cantini F, Hunder GG. Polymyalgia rheumatica and giant-cell arteritis. Lancet. 2008;372(9634):234-245.
2. Michet CJ, Matteson EL. Polymyalgia rheumatica. BMJ. 2008;336(7647):765-769.
3. Dasgupta B, Salvarani C, Schirmer M, et al. Developing classification criteria for polymyalgia rheumatica: comparison of views from an expert panel and wider survey. J Rheumatol. 2008;35(2):270-277.
4. Dasgupta B, Hassan N. Giant cell arteritis: recent advances and guidelines for management. Clin Exp Rheumatol. 2007;25(1 suppl 44):S62-S65.
5. Dasgupta B, Matteson EL, Maradit-Kremers H. Management guidelines and outcome measures in polymyalgia rheumatica (PMR). Clin Exp Rheumatol. 2007;25(6 suppl 47):130-136.
6. MayoClinic. May 17, 2008. Accessed January 19, 2012.
7. Hellmann DB, Imboden JB Jr. Polymyalgia rheumatica and giant cell arteritis section of musculoskeletal and immunologic disorders. In: SJ McPhee, MA Papadakis, eds. Current Medical Diagnosis and Treatment. 49th ed. New York, NY: McGraw-Hill; 2010:766-767.
8. Both M, Aries PM, Muller-Hulsbeck S, et al. Balloon angioplasty of arteries of the upper extremities in patients with extracranial giant-cell arteritis. Ann Rheum Dis. 2006;65(9):1124-1130.
9. Hellmann DB. Giant cell arteritis, polymyalgia rheumatica, and Takayasu’s arteritis. In: GS Firestein GS, Budd RC, Harris ED Jr, et al, eds. Kelley’s Textbook of Rheumatology. Vol 2. 8th ed. Philadelphia, PA: Saunders Elsevier; 2008:1409-1428.
10. MayoClinic. December 4, 2010. Accessed January 19, 2012.
11. MayoClinic. May 17, 2008. Accessed January 19, 2012.

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