RISK FACTORS: Age greater than 50, Presence of giant cell arteritis
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, improve muscle stiffness, and 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 for polymyalgia rheumatica are almost certainly ineffective in 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).
Diet: Ensure adequate calcium and vitamin D intake with corticosteroid use.
Activity: Generally, activity restriction is unnecessary.
DRUG(S) OF CHOICE
. Prednisone
. 10 mg/day initially (average initial effective dose 10-15 mg/d)
. Usually dramatic (diagnostic) response.
. May increase to 20 mg if no immediate response
. Begin slow taper at 4-6 weeks by only 1 mg every 1-4 weeks to a dose of 5-7.5 mg. Continue at this dose
for approximately 18 months to 2 years, if no recurrence of symptoms.
. After 18-24 months of treatment, attempt to taper by 1 mg every 2-4 weeks until drug discontinued. Patient
may, however, require steroids for 3 or more years.
. Increase prednisone for recurrence of symptoms (relapse common).
. Nonsteroidal anti-infl ammatory drugs (NSAIDs) often not helpful
ALTERNATIVE DRUGS NSAIDs have been used, rarely successful
PATIENT MONITORING
β’ Follow monthly initially and during taper of medication, every 3 months otherwise
β’ Follow ESR as steroids tapered
β’ Followup with patient for symptoms of giant cell arteritis. Educate patient to report such symptoms immediately (headache, visual and neurologic symptoms)
POSSIBLE COMPLICATIONS
β’ Medication - complications related to steroid use
β’ Disease - exacerbation of disease with taper of steroids; development of giant cell arteritis (may occur when PMR is being adequately treated)
EXPECTED COURSE/PROGNOSIS
β’ Average length disease is 3 years (range 1-10 years)
β’ Exacerbation if steroids tapered too fast
β’ Prognosis very good if treated (may gradually remit even if no treatment)
β’ Relapse common