eMedicine Specialties > Rheumatology > Vasculitis

Polymyalgia Rheumatica: Treatment & Medication

Author: Ehab R Saad, MD, FACP, FASN, MA, Assistant Professor, Department of Medicine, Medical College of Wisconsin
Coauthor(s): Gloria Fioravanti, DO, Program Director, Clinical Assistant Professor, Department of Internal Medicine, Saint Luke's Hospital of Bethlehem, Temple University School of Medicine; Allen Samuels, MD, Consulting Staff, Department of Internal Medicine, Division of Rheumatology, St Luke's Hospital, Lehigh Valley Hospital, Pocono Medical Center
Contributor Information and Disclosures

Updated: Aug 20, 2009

Treatment

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

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

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.


Prednisone (Deltasone, Meticorten, Orasone)

Has the capacity to dramatically reduce inflammatory manifestations for the following reasons: (1) inhibition of the function of leukocytes and tissue macrophages, which diminishes their ability to respond to antigens and mitogens; (2) inhibition of phospholipase A2, resulting in decreased prostaglandin and leukotriene synthesis; (3) inhibition of cyclooxygenase II expression, which may be the enzyme more involved in the inflammatory effects of eicosanoids; and (4) decreased activity of kinins and decreased histamine release by basophils, leading to decreased capillary permeability.
Controversy remains regarding dose and duration of treatment. Dose depends on patient's weight and severity of symptoms. Expect relief of symptoms in 24-72 h. Dose should be increased if symptoms are not well controlled within 1 wk, and a diagnosis of giant cell arteritis may need to be pursued. Tapering should be guided by clinical response. Normalization of laboratory values are helpful but should not set the guidelines for decreasing or stopping the treatment. In contrast to other rheumatic diseases, alternate-day administration of corticosteroids in polymyalgia rheumatica has been largely unsuccessful.

Adult

0.2-0.3 mg/kg/d PO (10-15 mg/d) initial; maintain effective dose for 2-4 wk after patient becomes asymptomatic; generally, effective dose can be lowered by 1-2.5 mg/d q2-4wk to find the minimum dose needed to maintain symptom suppression; once 10-mg dose is reached, taper by 1 mg/d decrements q4wk

Pediatric

Not applicable

Coadministration with estrogens may decrease prednisone clearance; concurrent use with digoxin may cause digitalis toxicity secondary to hypokalemia; phenobarbital, phenytoin, and rifampin may increase metabolism of glucocorticoids (consider increasing maintenance dose); monitor for hypokalemia with coadministration of diuretics; decreases effects of salicylates and toxoids (for immunizations)

Documented hypersensitivity; viral infection; peptic ulcer disease; hepatic dysfunction; connective tissue infections; fungal or tubercular skin infections; GI disease

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Abrupt discontinuation of glucocorticoids may cause adrenal crisis; hyperglycemia, edema, osteonecrosis, myopathy, peptic ulcer disease, hypokalemia, osteoporosis, euphoria, psychosis, myasthenia gravis, growth suppression, and infections may occur with glucocorticoid use; aspirin should be used cautiously in conjunction with corticosteroids in patients with hypoprothrombinemia

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.


Ibuprofen (Ibuprin, Motrin)

DOC for patients with mild to moderate pain. Inhibits inflammatory reactions and pain by decreasing prostaglandin synthesis.

Adult

200-400 mg PO q4-6h while symptoms persist; not to exceed 3.2 g/d

Pediatric

Not applicable

Coadministration with aspirin increases risk of inducing serious NSAID-related adverse effects; probenecid may increase concentrations and, possibly, toxicity of NSAIDs; may decrease effect of hydralazine, captopril, and beta-blockers; may decrease diuretic effects of furosemide and thiazides; may increase PT when taking anticoagulants (instruct patients to watch for signs of bleeding); may increase risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently

Documented hypersensitivity; peptic ulcer disease; recent GI bleeding or perforation; renal insufficiency; high risk of bleeding

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Caution in congestive heart failure, hypertension, and decreased renal and hepatic function; caution in coagulation abnormalities or during anticoagulant therapy


Naproxen (Anaprox, Aleve, Naprosyn, Naprelan)

For relief of mild to moderate pain; inhibits inflammatory reactions and pain by decreasing activity of cyclooxygenase, which results in a decrease of prostaglandin synthesis.

Adult

500 mg PO followed by 250 mg q6-8h; not to exceed 1.25 g/d

Pediatric

Not applicable

Coadministration with aspirin increases risk of inducing serious NSAID-related adverse effects; probenecid may increase concentrations and, possibly, toxicity of NSAIDs; may decrease effect of hydralazine, captopril, and beta-blockers; may decrease diuretic effects of furosemide and thiazides; may increase PT when taking anticoagulants (instruct patients to watch for signs of bleeding); may increase risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently

Documented hypersensitivity; peptic ulcer disease; recent GI bleeding or perforation; renal insufficiency

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Acute renal insufficiency, interstitial nephritis, hyperkalemia, hyponatremia, and renal papillary necrosis may occur; patients with preexisting renal disease or compromised renal perfusion risk acute renal failure; leukopenia occurs rarely, is transient, and usually returns to normal during therapy; persistent leukopenia, granulocytopenia, or thrombocytopenia warrants further evaluation and may require discontinuation of drug


Ketoprofen (Orudis, Oruvail, Actron)

For relief of mild to moderate pain and inflammation. Small dosages are initially indicated in small and elderly patients and in those with renal or liver disease. Doses of more than 75 mg do not increase therapeutic effects. Administer high doses with caution and closely observe patient for response.

Adult

25-50 mg PO q6-8h prn; not to exceed 300 mg/d

Pediatric

Not applicable

Coadministration with aspirin increases risk of inducing serious NSAID-related adverse effects; probenecid may increase concentrations and, possibly, toxicity of NSAIDs; may decrease effect of hydralazine, captopril, and beta-blockers; may decrease diuretic effects of furosemide and thiazides; may increase PT when taking anticoagulants (instruct patients to watch for signs of bleeding); may increase risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Caution in congestive heart failure, hypertension, and decreased renal and hepatic function; caution in coagulation abnormalities or during anticoagulant therapy

More on Polymyalgia Rheumatica

Overview: Polymyalgia Rheumatica
Differential Diagnoses & Workup: Polymyalgia Rheumatica
Treatment & Medication: Polymyalgia Rheumatica
Follow-up: Polymyalgia Rheumatica
References
Further Reading
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Keywords

polymyalgia rheumatica, PMR, giant cell arteritis, GCA, collagen diseases, muscle pain, morning stiffness, HLA-DR4, interleukin-2, IL-2, interleukin-6, IL-6, remitting seronegative symmetrical synovitis with pitting edema, RS3PE, carpal tunnel syndrome, malaise, fatigue, depression, nonerosive synovitis, tenosynovitis, bursitis, proximal myalgia of the hip, shoulder girdles, HLA-DR4 haplotype

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Contributor Information and Disclosures

Author

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

Coauthor(s)

Gloria Fioravanti, DO, Program Director, Clinical Assistant Professor, Department of Internal Medicine, Saint 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.

Medical Editor

Kristine M Lohr, MD, MS, Program Director, Professor, Department of Internal Medicine, Division of Rheumatology and Women's Health, University of Kentucky School of Medicine
Kristine M Lohr, MD, MS is a member of the following medical societies: American College of Physicians, American College of Rheumatology, and American Medical Women's Association
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Elliot Goldberg, MD, Dean of the Western Pennsylvania Clinical Campus, Professor, Department of Medicine, Temple University School of Medicine
Elliot Goldberg, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians, and American College of Rheumatology
Disclosure: Nothing to disclose.

CME Editor

Alex J Mechaber, MD, FACP, Associate Dean for Undergraduate Medical Education, Associate Professor of Medicine, University of Miami Miller School of Medicine
Alex J Mechaber, MD, FACP is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians-American Society of Internal Medicine, and Society of General Internal Medicine
Disclosure: Nothing to disclose.

Chief Editor

Herbert S Diamond, MD, Professor of Medicine, Temple University 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: medifocus Honoraria Review panel membership; health dialogs Honoraria Consulting; West Penn Allegheny Health System None Board membership

 
 
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