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Polymyalgia rheumatica

Last updated 28 Mar 2026 · Inflammatory Arthritis

Introduction

Polymyalgia rheumatica (PMR) is a common inflammatory disorder affecting adults aged >50 years, with median age of onset around 72 years. It is characterised by proximal muscle pain and morning stiffness affecting the shoulders, hip girdles, and neck. PMR is associated with giant cell (temporal) arteritis (GCA) in 15–20% of cases and may be a harbinger of subsequent GCA development.

The incidence of PMR in Australia is approximately 15–20 per 100,000 population annually. Early diagnosis and treatment with corticosteroids is essential to prevent progression to GCA and associated complications (vision loss, stroke). The majority of patients respond rapidly to prednisolone, typically achieving symptom resolution within weeks. However, prolonged treatment (often 1–2 years) is usually required, with careful steroid tapering to avoid relapse.

Pathophysiology

Aetiology and Pathogenesis

PMR is an inflammatory condition of unknown aetiology, likely involving both genetic predisposition and environmental triggers. The condition is characterised by T-cell mediated inflammation of the large arteries and bursae around the shoulders and hips, with elevation of inflammatory markers (ESR, CRP). Pathological studies reveal vasculitis of large elastic arteries, similar to giant cell arteritis but without the associated cranial arteritis features.

Association with Giant Cell Arteritis

  • PMR and GCA share common pathophysiology and genetic predisposition (HLA-DR4 association)
  • GCA occurs in 15–20% of PMR patients during follow-up
  • Conversely, 40–60% of GCA patients have concurrent or prior PMR symptoms
  • Risk of GCA is highest in the first 1–3 years after PMR diagnosis
  • All PMR patients require monitoring for GCA warning symptoms (headache, visual symptoms, jaw claudication)

Clinical Presentation

Typical Features

Onset: Typically subacute, developing over weeks to months. Pain: Bilateral, symmetrical pain and stiffness in the shoulders, hip girdles, neck, and lower back. Patients describe difficulty with arm raising, rolling over in bed, and rising from a chair. Morning stiffness: Often severe and prolonged (>1 hour), improving with activity and NSAIDs.

Systemic symptoms: Low-grade fever, fatigue, malaise, weight loss (5–10% body weight), and depression are common.

Key Examination Findings

Limited shoulder abduction/forward flexion due to pain and stiffness (not true weakness). Hip and groin discomfort with limitation of hip flexion and rotation. Normal muscle strength on standard testing (distinguishes from polymyositis/dermatomyositis). No rash or skin involvement (unlike dermatomyositis).

Investigations

  • Essential
    Inflammatory Markers: ESR and CRP
    ESR typically >50 mm/hr (often >100 mm/hr). CRP elevated (>100 mg/L common). Marked elevation is characteristic. Normal inflammatory markers make PMR diagnosis unlikely.
  • Essential
    Rheumatoid Factor and ANA
    Both typically negative in PMR. Presence of positive rheumatoid factor or ANA suggests alternative diagnosis (rheumatoid arthritis, systemic lupus erythematosus, connective tissue disease).
  • Essential
    Full Blood Count
    Mild anaemia is common (normocytic, normochromic). Thrombocytosis may be present. Significant anaemia or cytopaenia suggests alternative diagnosis.
  • Essential
    Creatine Kinase (CK)
    Normal CK excludes polymyositis/dermatomyositis. Elevated CK suggests muscle inflammation and alternative diagnosis.

Severity and Monitoring

MILD
Uncomplicated PMR
Typical proximal pain and stiffness. ESR >50 mm/hr. No systemic features suggesting GCA. Normal CK, rheumatoid factor negative.
Primary care with prednisolone; GP monitoring of inflammatory markers during tapering
MODERATE
PMR with Systemic Features
Prominent systemic symptoms (fever, weight loss, fatigue). Significantly elevated inflammatory markers (CRP >150 mg/L, ESR >100 mm/hr). Atypical distribution of pain.
Primary care with rheumatology consultation; careful monitoring for GCA complications
SEVERE
PMR with GCA Features
Red flags: new headache, visual symptoms, jaw claudication, scalp tenderness. Possible GCA. High inflammatory markers.
Emergency assessment; temporal artery ultrasound or biopsy; high-dose prednisolone (40–60 mg daily)

Directed Therapy

Corticosteroid Monotherapy (First-Line)

💊
Prednisolone
Prednisolone · Corticosteroid
Initial Adult Dose15–20 mg daily
RouteOral
Duration1–2 years (slow taper)
Tapering ScheduleAfter 2–4 weeks at 15–20 mg: reduce by 1–2 mg every 2–4 weeks to 10 mg; then slower taper. Adjust based on symptoms and inflammatory markers.
PBS Status✓ PBS General Benefit

Steroid-Sparing Therapy

💊
Methotrexate
Methotrexate · DMARD
Adult Dose10–15 mg weekly
RouteOral or subcutaneous
Duration6–12 months
NotesConsider if steroid-dependent (unable to taper below 7.5–10 mg) or steroid-intolerant. Folinic acid 5 mg daily (days 2–7) to reduce toxicity.
PBS Status✓ PBS Authority Required

Management of Giant Cell Arteritis

If GCA is diagnosed: Increase prednisolone to 40–60 mg daily, followed by slow taper based on clinical response and inflammatory markers. Refer to rheumatology specialist urgently. Consider temporal artery ultrasound or biopsy to confirm diagnosis. Monitor vision closely; visual symptoms require emergency assessment.

Biologic therapy: If steroid-dependent or steroid-intolerant GCA, tocilizumab (IL-6 receptor antagonist) has been shown to reduce relapse rates and steroid requirements. Requires specialist rheumatology input.

Acute Management

Initial Assessment

When PMR is suspected:

  • Detailed history: Age >50 years, onset and distribution of pain, morning stiffness duration, systemic symptoms (fever, weight loss, fatigue), vision symptoms or headache (red flags for GCA).
  • Thorough examination: Assess shoulder and hip range of motion, palpate for tenderness, general appearance (unwell vs well).
  • Blood tests: ESR, CRP, rheumatoid factor, ANA, creatine kinase, FBC, renal function, liver function (baseline before steroid initiation).

Red Flags for GCA

Urgent assessment needed if: New headache (especially temporal), visual symptoms (blurred vision, amaurosis fugax), jaw claudication (jaw pain with chewing), scalp tenderness, systemic symptoms suggesting infection (high fever, lymphadenopathy).

Monitoring and Follow-Up

Baseline Assessment Before Starting Prednisolone

Prior to corticosteroid initiation, obtain: (1) DEXA scan (assess bone density). (2) Blood pressure monitoring. (3) Liver and renal function. (4) Glucose tolerance — perform HbA1c if relevant risk factors.

Regular Monitoring During Treatment

Frequency: Review at 4–6 weeks after starting prednisolone to assess response. Then review every 8–12 weeks during tapering. ESR and CRP every 4–8 weeks to guide dose adjustments.

Key measures: Symptoms (pain, stiffness). Inflammatory markers (ESR/CRP should normalise with treatment). Side effects of steroid therapy. Bone health (consider calcium, vitamin D, and bisphosphonate if long-term use with low bone density).

Relapse Management

30–50% of PMR patients experience relapse during steroid tapering. If relapse occurs: increase prednisolone to previous effective dose; restart taper at a slower pace; consider addition of methotrexate if multiple relapses occur.

Special Populations

👴 Older Adults (>70 years)
Steroid sensitivityOlder patients often require lower initial doses (12–15 mg prednisolone); titrate carefully. Monitor for steroid-induced side effects (osteoporosis, myopathy, mood disturbance) more closely.
ComorbiditiesReview medication interactions. Monitor glucose (steroid-induced hyperglycemia). Assess cardiovascular risk (steroid-induced hypertension).
⚠️ Immunocompromised Patients
Infection riskPrednisolone increases infection risk. Ensure up-to-date vaccinations before steroid initiation. Monitor for infection symptoms during therapy.
Aboriginal and Torres Strait Islander Health Considerations

PMR is less common in Aboriginal and Torres Strait Islander populations due to younger median age of the population. However, when diagnosed, management is complicated by higher rates of comorbidities (diabetes, hypertension, chronic kidney disease), which increase steroid-related complications.

Diagnostic Delay
Limited access to laboratory tests (ESR, CRP) in remote areas may delay diagnosis. Utilise clinical diagnosis in conjunction with available tests. Arrange telehealth consultation with rheumatologist.
Steroid-Related Complications
Higher baseline rates of diabetes and hypertension make steroid-induced hyperglycemia and hypertension more problematic. Tighter blood glucose and BP monitoring. Lower initial steroid doses if possible. Screen for diabetes before steroid initiation (HbA1c).
GCA Screening
Temporal artery ultrasound may not be available in remote communities. Train local healthcare workers to recognise GCA red flags. Arrange urgent telehealth assessment if GCA is suspected.
Treatment Adherence
Long-term steroid tapering (1–2 years) requires multiple appointments. Simplified follow-up schedule where possible. Involve Aboriginal health workers as care coordinators. Use SMS reminders for appointments.

Stewardship and Key Points

Key Messages

  • Early recognition and diagnosis is critical: Classical presentation (proximal pain, morning stiffness, elevated ESR/CRP in patient >50 years) should prompt immediate consideration of PMR.
  • Prednisolone is highly effective: Rapid response to low-dose prednisolone is expected; failure to improve should prompt review of diagnosis.
  • All PMR patients require GCA surveillance: Screen at every visit for red flags (headache, visual symptoms, jaw claudication, scalp tenderness). Low threshold for urgent investigation if GCA symptoms develop.
  • Slow steroid taper is essential: Rapid reduction in steroid dose increases relapse risk. Typical tapering takes 1–2 years.
  • Monitor for steroid toxicity: Weight gain, osteoporosis, infections, mood disturbance, and hyperglycemia are common. Implement preventative measures (calcium/vitamin D, bisphosphonates if needed).

Avoiding Diagnostic Errors

Consider alternative diagnoses if: Normal inflammatory markers — suggests non-inflammatory aetiology. Elevated CK — suggests polymyositis/dermatomyositis. Positive rheumatoid factor/ANA — suggests rheumatoid arthritis or connective tissue disease. Age <50 years — PMR is rare; look for other causes.

References

  • 01
    Dasgupta B, Borg FA, Hassan N, et al. BSR and BHPR guidelines for the management of polymyalgia rheumatica. Rheumatology. 2010;49(1):186-190.
  • 02
    Mackie SL, Dejaco C, Appenzeller S, et al. British Society for Rheumatology guideline for the diagnosis and management of polymyalgia rheumatica. BMJ Open. 2023;13(1):e066421.
  • 03
    Matteson EL, Hunder GG. Temporal arteritis (giant cell arteritis) and polymyalgia rheumatica. Nat Rev Dis Primers. 2020;6(1):6.
  • 04
    Australian and New Zealand Society for Geriatric Medicine. Polymyalgia rheumatica in older adults: Australian perspective. 2022 Update.