Rheumatology · Systemic Inflammatory Disorders
The facts most likely to be tested
Polymyalgia rheumatica typically presents in patients older than 50 years with bilateral aching and morning stiffness lasting longer than 45 minutes in the shoulders, hip girdle, and neck.
The diagnosis is strongly supported by a significantly elevated erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) in the setting of characteristic clinical symptoms.
Polymyalgia rheumatica is clinically associated with giant cell arteritis (GCA), requiring clinicians to screen for temporal headache, jaw claudication, and visual disturbances.
The first-line treatment for uncomplicated polymyalgia rheumatica is low-dose oral prednisone (typically 15–20 mg daily).
A dramatic and rapid clinical response to low-dose corticosteroids is a hallmark feature that helps confirm the diagnosis.
Patients with polymyalgia rheumatica do not exhibit muscle weakness on physical examination, which helps distinguish the condition from polymyositis.
Long-term management requires slow tapering of corticosteroids over several months to prevent disease relapse.
Vignette unlocked
A 72-year-old woman presents to the clinic complaining of a 3-week history of severe stiffness and aching in her shoulders and hips that is worst in the morning and takes over an hour to improve. She reports difficulty rising from a chair and brushing her hair. She denies muscle weakness, fever, or weight loss. Physical examination reveals normal muscle strength in all extremities but pain-limited range of motion in the shoulders. Laboratory studies show an ESR of 85 mm/hr and a normal creatine kinase level.
What is the most appropriate initial management for this patient?
Initiation of low-dose oral prednisone
The patient's age, classic distribution of stiffness, and elevated ESR are diagnostic for polymyalgia rheumatica, which is treated with low-dose corticosteroids.
Full handout
High yield triage
Etiology / Epidemiology
Affects patients >50 years old; strong association with Giant Cell Arteritis.
Clinical Manifestations
Bilateral proximal muscle stiffness and pain in the shoulders and hips; morning stiffness >30 minutes.
Diagnosis
Diagnosis of exclusion; ESR >40 mm/hr is the classic diagnostic marker.
Treatment
Low-dose prednisone is the first-line treatment; rapid symptomatic relief is diagnostic.
Prognosis
Excellent prognosis; monitor for vision loss if associated with Giant Cell Arteritis.
Full handout
Epidemiology & Etiology
Primarily affects individuals >50 years old, with a peak incidence in those >70. It is rare in patients under 50. There is a significant genetic predisposition and a well-documented link to Giant Cell Arteritis (temporal arteritis).
Pertinent Anatomy
Inflammation primarily involves the synovial joints and bursae of the shoulder and pelvic girdles. The condition is characterized by synovitis and bursitis rather than true muscle inflammation (myositis).
Pathophysiology
The exact etiology remains idiopathic, involving a systemic inflammatory response. Cytokine-mediated inflammation, specifically IL-6, drives the acute phase response. This leads to the characteristic elevation of inflammatory markers without true muscle fiber necrosis.
Clinical Manifestations
Patients present with bilateral proximal muscle stiffness and aching in the shoulders, hips, and neck. Morning stiffness lasting >30 minutes is a hallmark feature. Red flags include jaw claudication, scalp tenderness, or visual disturbances, which mandate immediate evaluation for Giant Cell Arteritis.
Diagnosis
Diagnosis is clinical, supported by an ESR >40 mm/hr or elevated CRP. Muscle enzymes (CK) are typically normal, which helps distinguish this from polymyositis. Ultrasound may show subacromial bursitis or biceps tenosynovitis.
Treatment
Low-dose prednisone (10–20 mg/day) is the treatment of choice. Patients typically experience dramatic improvement within 24–72 hours. Tapering too rapidly risks disease flare; maintenance therapy is often required for 1–2 years.
Prognosis
The prognosis is excellent with treatment, though relapses are common during tapering. The most critical complication is the development of Giant Cell Arteritis, which carries a risk of permanent blindness.
Differential Diagnosis
Polymyositis: elevated CK and muscle weakness rather than stiffness
Fibromyalgia: absence of elevated inflammatory markers
Rheumatoid Arthritis: involvement of distal small joints
Hypothyroidism: elevated TSH and normal inflammatory markers
Giant Cell Arteritis: presence of cranial symptoms and visual loss