Polymyalgia Rheumatica Workup

Updated: Nov 10, 2020
  • Author: Ehab R Saad, MD, MA, FACP, FASN; Chief Editor: Herbert S Diamond, MD  more...
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Approach Considerations

Joint guidelines from the European League Against Rheumatism (EULAR) and the American College of Rheumatology (ACR) recommend performing the following laboratory studies in all patients with polymyalgia rheumatica (PMR), both to help to exclude mimicking conditions and to establish a baseline for monitoring therapy [23] :

  • Rheumatoid factor and/or anti-cyclic citrullinated peptide antibodies (anti-CCP)
  • C-reactive protein (CRP) and/or erythrocyte sedimentation rate (ESR)
  • Complete blood cell count (CBC) with differential
  • Blood glucose
  • Serum creatinine
  • Liver function tests
  • Bone profile (including calcium and alkaline phosphatase)
  • Dipstick urinalysis

Additional studies to consider are as follows [23] :

  • Protein electrophoresis
  • Thyroid-stimulating hormone (TSH)
  • Creatine kinase
  • Vitamin D

If clinically indicated, tests such as the following may be considered to exclude alternative diagnoses [23] :

  • Antinuclear antibodies (ANA)
  • Anti–cytoplasmic neutrophil antibodies (ANCA)
  • Tuberculosis tests
  • Chest radiographs

The ESR is a sensitive diagnostic study for PMR, but it is not specific. The ESR is frequently greater than 40 mm/hr, but it can exceed 100 mm/hr. The ESR is mildly elevated in 7-20% of patients. Occasionally, the ESR is normal; this may occur in patients with limited disease activity. [24] In these cases, the diagnosis is based on rapid positive response to low-dose oral corticosteroids (10-15 mg/day).

The CRP level is often elevated and may parallel the ESR. Longitudinal studies suggest that CRP may be a more sensitive test than ESR for the diagnosis of PMR

The CBC reveals mild normocytic, normochromic anemia in most patients. The white blood cell count may be normal or mildly elevated. Platelet counts are often increased, reflecting systemic inflammation.

Liver function tests reveal normal transaminase enzyme levels. Alkaline phosphatase may be mildly increased in approximately one third of patients. The serum albumin level may be slightly decreased.

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

Antinuclear antibodies, complement, rheumatoid factor, and anti-CCP levels are usually normal. The serum interleukin-6 (IL-6) level is elevated and often closely parallels the inflammatory activity of the disease; however, this test is not readily available in most laboratories. Plasma fibrinogen assays are widely available, and elevation in the plasma fibrinogen level has been recommended for the diagnosis of active PMR, with subsequent decreases used for confirmation of response to treatment. [25]

In a study of serum markers related to immune cells that may be involved in PMR and giant cell arteritis (GCA), serum B-cell activating factor (BAFF) and IL-6 were most strongly associated with disease activity in both GCA and PMR patients. Serum CCL2, CCL11, IL-10, and sIL-2R were modulated in GCA patients only, while CXCL10 was modulated in PMR patients only. The study population comprised 24 newly diagnosed, untreated GCA/PMR patients; 14 corticosteroid-treated GCA/PMR patients in remission; and 13 controls. [26]

In patients who have synovitis with effusions, synovial fluid analysis reveals signs of mild inflammation, including poor mucin clotting. Synovial fluid WBC counts range between 1,300-11,000 cells/µL (median 6,000 cells/µL), with 34% polymorphonuclear leukocytes (range 12-78%).

Imaging studies

Radiographs reveal either normal joints or evidence of osteoarthritis. Evidence of erosive arthritis should prompt evaluation for other disorders such as rheumatoid arthritis or crystalline arthritis. Magnetic resonance imaging (MRI) is not necessary for diagnosis, but MRI of the shoulder reveals subacromial, 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.

In a Japanese study, MRI of the shoulder showed a significantly thicker supraspinatus tendon and more frequent severe rotator cuff tendinopathy in patients with PMR than in patients with rheumatoid arthritis or controls. In both shoulder and hip joint MRIs, effusion around the joints was greater in PMR patients, and periarticular soft tissue edema was significantly more frequent. [27]

Ultrasonography is 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. [28]

Symptomatic vasculitis in cranial and extracranial vessels is rare in PMR, but a study by Kermani et al demonstrated subclinical involvement in about one third of patients using ultrasonography and positron emission tomography (PET) scanning. [29] In a study of 18F-fluorodeoxyglucose (FDG)-PET/CT, Wakura et al reported abnormal FDG accumulation at the entheses, suggesting that enthesitis may be a feature of PMR and that its presence can help differentiate.PMR from elderly-onset rheumatoid arthritis. [30]   

A joint international guideline on functional FDG-PET combined with anatomical CT angiography concluded that FDG-PET imaging has high diagnostic value for the detection of large-vessel vasculitis (ie, Takayasu arteritis and GCA) or PMR and has an important role in the diagnosis of extracranial vascular involvement in these patients, although there are no definitive consensus criteria for the presence of vascular inflammation with FDG-PET in these disorders. [31]


Temporal Artery Biopsy

Temporal artery biopsy (TAB) has a very low yield in patients with isolated polymyalgia rheumatica (PMR) and is therefore usually unnecessary in patients with PMR who do not have symptoms of giant cell arteritis (GCA). TAB is not indicated in patients with mild symptoms of PMR that is of recent onset or in patients who have remained stable over a long period (1 year or longer without current or previous clinical evidence of arteritis).

Patients should be monitored for symptoms or signs of GCA after treatment initiation because low-dose corticosteroids do not prevent progression of PMR to GCA. TAB should be considered if clinical signs of vasculitis develop, if clinical response is incomplete with low doses of prednisone (≤20 mg/d), and/or if the ESR or CRP remains elevated or rises despite symptom resolution on corticosteroid therapy. Low-dose corticosteroids do not appear to affect biopsy yield.