Polymyalgia Rheumatica Workup

Author: Patricia J Papadopoulos, MD; Chief Editor: Herbert S Diamond, MD more...

Updated: Apr 4, 2012

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Approach Considerations
Temporal Artery Biopsy
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Approach Considerations

Laboratory studies in polymyalgia rheumatica include the following^[13]:

Erythrocyte sedimentation rate (ESR)
C-reactive protein (CRP)
Complete blood count (CBC) with differential
Liver function studies
Creatine kinase level
Serum creatinine and urinalysis
Thyroid function test
Calcium measurements
Blood glucose measurement

Antinuclear antibodies, complement levels, rheumatoid factor, and anticyclic citrullinated peptide (anti-CCP) levels are usually normal. Serum interleukin-6 (IL-6) levels are elevated and often closely parallel the inflammatory activity of the disease; however, the test is not readily available in most laboratories.

In the occasional patient who has synovitis with effusions, synovial fluid analysis reveals signs of mild inflammation, including poor mucin clotting. Synovial fluid WBC counts are usually 1,300-11,000 cells/µL (median 6,000 cells/µL), with 34% polymorphonuclear leukocytes (range 12-78%).^[12]

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 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 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. A study by Matteson et al revealed that ultrasound findings at diagnosis correlate well with corticosteroid response at 4 weeks.^[14]

Symptomatic vasculitis in cranial and extracranial vessels is rare in polymyalgia rheumatica, but a study by Kermani et al demonstrated subclinical involvement in about one third of patients using ultrasonography and positron emission tomography (PET) scanning.^{[8, 15]}Symptoms of claudication should be sought in patients presenting with polymyalgia rheumatic and should prompt evaluation of large-vessel vasculitis such as giant cell arteritis. Routine screening with imaging needs further study.

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, particularly in those with giant cell arteritis that is biopsy proven. Serum albumin levels may be slightly decreased.

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

The 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 it can exceed 100 mm/hr.

In 7-20% of patients, the ESR is mildly elevated or, occasionally, normal, which may occur in patients with limited disease activity.^[16]In these cases, diagnosis is based on rapid positive response to low-dose oral corticosteroids (10-15 mg/day). CRP may be a more sensitive indicator of disease activity in these cases as well.

The CRP 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 PMR.

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 who do not have 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 giant cell 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, if clinical response is incomplete with low doses of prednisone (≤20 mg/d), or if the ESR or CRP remains elevated or rises despite symptom resolution on corticosteroid therapy, TAB should be considered. Low-dose corticosteroids do not appear to affect biopsy yield.

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Contributor Information and Disclosures

Author

Patricia J Papadopoulos, MD Key Clinical Faculty, Rheumatology Service, Department of Medicine, Walter Reed National Military Medical Center; Assistant Professor of Medicine, Uniformed Services University of the Health Sciences

Patricia J Papadopoulos, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians-American Society of Internal Medicine, and American College of Rheumatology

Disclosure: Merck Ownership interest Own stock

Coauthor(s)

Ehab R Saad, MD, MA, FACP, FASN Assistant Professor, Department of Medicine, Medical College of Wisconsin

Ehab R Saad, MD, MA, FACP, FASN is a member of the following medical societies: American College of Physicians-American Society of Internal Medicine, American Geriatrics Society, American Society of Nephrology, and National Kidney Foundation

Disclosure: Nothing to disclose.

Gloria Fioravanti, DO Clinical Assistant Professor, Program Director, Department of Internal Medicine, St Luke's Hospital of Bethlehem, Temple University School of Medicine

Gloria Fioravanti, DO is a member of the following medical societies: American College of Physicians-American Society of Internal Medicine and American Osteopathic Association

Disclosure: Nothing to disclose.

Allen Samuels, MD Consulting Staff, Department of Internal Medicine, Division of Rheumatology, St Luke's Hospital, Lehigh Valley Hospital, Pocono Medical Center

Allen Samuels, MD is a member of the following medical societies: American College of Rheumatology

Disclosure: Nothing to disclose.

Chief Editor

Herbert S Diamond, MD Adjunct Professor of Medicine, Division of Rheumatology, University of Pittsburgh School of Medicine; Chairman Emeritus, Department of Internal Medicine, Western Pennsylvania Hospital

Herbert S Diamond, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians, American College of Rheumatology, American Medical Association, and Phi Beta Kappa

Disclosure: Merck Ownership interest Other; Smith Kline Ownership interest Other; Zimmer Ownership interest Other

Additional Contributors

The views expressed in this article are those of the authors and do not reflect the official policy of the Department of the Army, Department of Defense, or the US Government. Additionally, this publication does not imply the Federal or Department of Defense endorsement of any product.

Past Contributors

Michael S Beeson, MD, MBA, FACEP Professor of Emergency Medicine, Northeastern Ohio Universities College of Medicine and Pharmacy; Attending Faculty, Akron General Medical Center

Michael S Beeson, MD, MBA, FACEP is a member of the following medical societies: American College of Emergency Physicians, Council of Emergency Medicine Residency Directors, National Association of EMS Physicians, and Society for Academic Emergency Medicine