📋 Key Information Summary
- Polymyalgia rheumatica (PMR) is the most common inflammatory rheumatic disease in older Australians, with an incidence of ~80 per 100,000 person-years in those aged ≥50 years.
- The 2012 EULAR/ACR classification criteria (age ≥50, bilateral shoulder aching, elevated CRP or ESR, morning stiffness >45 minutes) should be used to support diagnosis after excluding mimics.
- Always assess for concurrent giant cell arteritis (GCA): new-onset headache, jaw claudication, visual symptoms, or temporal artery tenderness warrant urgent temporal artery ultrasound or biopsy.
- Low-dose prednisolone (12.5–25 mg/day) is first-line therapy; expect dramatic response within 1–2 weeks — failure to respond should prompt diagnostic review.
- Taper prednisolone slowly (reduce by 2.5 mg every 2–4 weeks to 10 mg, then 1 mg every 4–8 weeks); median time to remission off steroids is 1.5–2 years.
- Relapses (up to 50–60% of patients) typically occur during taper below 7.5 mg; treat with return to the last effective dose and re-taper more slowly.
- Methotrexate (10–15 mg/week PO) is the preferred steroid-sparing agent for relapsing, refractory, or steroid-dependent PMR, or when steroid toxicity is a concern.
- Bone protection is mandatory for all patients on glucocorticoids ≥3 months: calcium, vitamin D, and alendronate or risedronate (PBS-listed for steroid-induced osteoporosis).
- Monitor CRP/ESR at each visit; disease flares usually precede symptom recurrence by weeks.
- Aboriginal and Torres Strait Islander peoples may present later, have higher rates of comorbidities affecting treatment tolerance, and experience barriers to specialist rheumatology access in remote and regional Australia.
- Exclude serious mimics before committing to long-term steroids: malignancy (myeloma, lymphoma), infection (endocarditis), thyroid disease, and calcium pyrophosphate deposition disease.
- Dual-energy X-ray absorptiometry (DEXA) should be performed at baseline and annually while on glucocorticoids; MBS item 12310 covers DEXA for patients on oral corticosteroids.
Introduction & Australian Epidemiology
Polymyalgia rheumatica (PMR) is a common, glucocorticoid-responsive inflammatory rheumatic disorder characterised by aching and morning stiffness predominantly affecting the shoulder and pelvic girdles, neck, and torso. It is the most common inflammatory rheumatic condition in Australians aged ≥50 years and frequently coexists with giant cell arteritis (GCA).
PMR primarily affects older adults, with a peak incidence between 70 and 80 years. It is rare under the age of 50. Women are affected two to three times more frequently than men. In Australia, population-based data suggest an incidence of approximately 70–100 per 100,000 person-years in those aged ≥50, comparable to Northern European cohorts. The lifetime risk for an Australian woman is approximately 2–3%.
The aetiology remains incompletely understood but involves a complex interplay of genetic susceptibility (HLA-DRB1 associations), environmental triggers (including seasonal variation with higher incidence in spring/summer in some series), immunosenescence, and pro-inflammatory cytokine pathways — particularly interleukin-6 (IL-6), tumour necrosis factor-alpha (TNF-α), and interferon-gamma. The HLA-DRB1*04 allele is shared with GCA and confers higher relapse risk.
PMR imposes a significant treatment burden: even with optimal management, most patients require 1.5 to 2 years of glucocorticoid therapy. Steroid-related adverse effects — osteoporosis, diabetes, cataracts, adrenal insufficiency, weight gain, and increased infection risk — are the major drivers of morbidity and motivate the search for steroid-sparing strategies.
Diagnosis — 2012 EULAR/ACR Classification Criteria
PMR is a clinical diagnosis supported by laboratory markers of inflammation. There is no single pathognomonic test. The 2012 EULAR/ACR classification criteria, developed for use in research and validated in Australian cohorts, provide a structured scoring framework.
Diagnostic safety point: The 2012 EULAR/ACR criteria are classification criteria designed for research — they are not diagnostic criteria. Clinical judgement remains paramount. A steroid trial can be diagnostic, but always exclude GCA and serious mimics before initiating long-term glucocorticoids.
Core Criteria (required for scoring)
- Age ≥50 years
- New bilateral shoulder aching
- Abnormal CRP and/or ESR
2012 EULAR/ACR Scoring Items
| Criterion | Points (without ultrasound) | Points (with ultrasound) |
|---|---|---|
| Morning stiffness duration >45 minutes | 2 | 2 |
| Hip pain or limited range of motion | 1 | 1 |
| Absence of RF and/or ACPA | 2 | 2 |
| Absence of other joint involvement | 1 | 1 |
| ≥1 shoulder with subdeltoid bursitis and/or biceps tenosynovitis and/or glenohumeral synovitis (ultrasound) | — | 1 |
| Bilateral subdeltoid bursitis, biceps tenosynovitis, or glenohumeral synovitis (ultrasound) | — | 1 |
Interpretation
- Without ultrasound: a score of ≥4 has 93% sensitivity and 78% specificity for PMR.
- With ultrasound: a score of ≥5 has 91% sensitivity and 72% specificity for PMR.
- These criteria assume that other diagnoses (infection, malignancy, inflammatory arthritis) have been excluded.
Investigations to Support Diagnosis
Essential
ESR and/or CRP
ESR typically >40 mm/h (often 70–100); CRP elevated in >95%. Both may be normal in up to 5% of true PMR — do not exclude the diagnosis if clinical features are compelling.
Essential
FBC, LFTs (ALP often mildly elevated), UEC, calcium, glucose
Normochromic normocytic anaemia in ~50%. Mild ALP elevation in ~30%. Rule out hypercalcaemia and renal impairment affecting drug dosing.
Essential
Rheumatoid factor and ACPA
Both should be negative. A positive RF or ACPA raises suspicion for seronegative or seropositive rheumatoid arthritis. PBS item 69482 covers RF; item 69484 covers ACPA.
Available
Shoulder and hip ultrasound
May reveal subdeltoid bursitis, biceps tenosynovitis, glenohumeral synovitis, or hip synovitis. Widely available in Australian radiology practices. Enhances diagnostic confidence.
Available
MRI of shoulders/hips
Not routine, but useful when diagnosis uncertain. Can demonstrate peri-articular inflammation and soft-tissue oedema not seen on ultrasound. MBS item 63521 covers MRI shoulder.
Specialist
FDG-PET/CT
May differentiate PMR from malignancy or atypical inflammatory patterns. Not funded via MBS for PMR specifically; available at tertiary centres for clinical trials or complex cases.
Key Differential Diagnoses to Exclude
| Differential | Distinguishing Features |
|---|---|
| Late-onset rheumatoid arthritis | Symmetrical small-joint synovitis, RF/ACPA may be positive, erosive changes on X-ray |
| Inflammatory myopathy (polymyositis) | Proximal weakness >pain, elevated CK, abnormal EMG/muscle biopsy |
| Multiple myeloma | Bone pain, hypercalcaemia, renal impairment, raised total protein on serum protein electrophoresis |
| Hypothyroidism | Stiffness, fatigue, weight gain; TSH and free T4 diagnostic |
| Infective endocarditis | Fever, new murmur, positive blood cultures |
| Calcium pyrophosphate deposition | Acute or chronic inflammatory arthropathy, chondrocalcinosis on X-ray |
Association with Giant Cell Arteritis
PMR and giant cell arteritis (GCA) are closely related conditions sharing overlapping immunopathology, genetic predisposition (HLA-DRB1*04), and epidemiological profiles. Approximately 40–60% of patients with GCA have coexistent PMR, while 15–30% of PMR patients harbour subclinical or overt GCA.
Sight-threatening emergency: Untreated GCA can cause irreversible bilateral blindness. Any PMR patient with new headache, scalp tenderness, jaw claudication, visual disturbance (amaurosis fugax, diplopia), or limb claudication requires immediate investigation and high-dose glucocorticoid therapy — do not wait for biopsy confirmation.
Screening for GCA in PMR
- Every PMR patient must be screened for GCA symptoms at initial assessment and at every follow-up visit.
- Specific enquiries: new-onset headache (especially temporal), scalp tenderness on combing, jaw claudication with chewing, visual symptoms, arm/leg claudication.
- Physical examination: palpate temporal arteries for tenderness, reduced pulse, or nodularity.
When GCA is Suspected
1
Immediate high-dose glucocorticoids
Do not delay treatment for imaging. Start prednisolone 50–60 mg/day PO (or methylprednisolone 500 mg–1 g IV if visual symptoms). Refer to the med2date GCA article for full management details.
2
Temporal artery ultrasound within 7 days
The halo sign (oedematous, non-compressible vessel wall) has high specificity when performed by experienced sonographers. A negative ultrasound does not exclude GCA — proceed to biopsy if clinical suspicion remains.
3
Temporal artery biopsy
Gold standard diagnostic test. Sensitivity reduced by steroid pre-treatment, but skip lesions may be missed. Ideally performed within 1–2 weeks of starting steroids, though a positive result may still be found up to 4–6 weeks into treatment.
4
Imaging
CT angiography or MR angiography of the aorta and its branches to assess for large-vessel vasculitis, which may coexist in up to 30% of GCA patients and can be asymptomatic.
Implications for PMR Management
- PMR patients with concurrent GCA require higher starting doses of prednisolone (40–60 mg vs 12.5–25 mg for isolated PMR).
- Steroid taper is slower in GCA (minimum 12–24 months).
- Tocilizumab (IL-6 receptor inhibitor) is now PBS-listed for GCA in Australia (Authority Required) and may allow faster steroid tapering.
- Relapses of PMR in patients with concurrent GCA are common and may signal subclinical vasculitis flare — low threshold for re-escalation.
Steroid Therapy & Taper
Glucocorticoids remain the cornerstone of PMR therapy. An excellent response to low-dose prednisolone within 1–2 weeks is both therapeutic and diagnostic. Failure to respond should prompt diagnostic re-evaluation.
Initial Dose
Prednisolone
Solone® · Panafcortelone® · Generic · Glucocorticoid
Adult dose (isolated PMR)
12.5–25 mg/day PO (ESULAR/ACR recommends 12.5 mg; Australian practice often starts 15–20 mg). Use higher end (20–25 mg) for more symptomatic disease.
Adult dose (PMR + GCA)
40–60 mg/day PO; see GCA article for full protocol.
Route
Oral
Frequency
Once daily, in the morning with food (mimics physiological cortisol rhythm)
Renal adjustment
No dose adjustment required; monitor fluid retention and blood pressure
Hepatic adjustment
No adjustment; prednisolone does not require hepatic activation (unlike prednisone)
PBS status
✔ PBS General Benefit
Tapering Protocol
The goal is the lowest effective dose sustained for the shortest duration, balancing relapse prevention against steroid toxicity. No single taper schedule suits all patients; individualise based on disease activity and tolerability.
Recommended taper (isolated PMR):
1. Maintain initial dose for 2–4 weeks until CRP/ESR normalise and symptoms resolve.
2. Reduce by 2.5 mg every 2 weeks (or 1 mg/month for cautious taper) until 10 mg/day.
3. Below 10 mg: reduce by 1 mg every 4–8 weeks.
4. At 5 mg: consider alternate-day dosing or further 1 mg decrements every 8 weeks.
5. Discontinue when dose is ≤2.5 mg for ≥4 weeks without relapse.
Total treatment duration: typically 12–24 months; some patients require longer.
1. Maintain initial dose for 2–4 weeks until CRP/ESR normalise and symptoms resolve.
2. Reduce by 2.5 mg every 2 weeks (or 1 mg/month for cautious taper) until 10 mg/day.
3. Below 10 mg: reduce by 1 mg every 4–8 weeks.
4. At 5 mg: consider alternate-day dosing or further 1 mg decrements every 8 weeks.
5. Discontinue when dose is ≤2.5 mg for ≥4 weeks without relapse.
Total treatment duration: typically 12–24 months; some patients require longer.
Monitoring During Taper
- Check CRP and/or ESR at each visit (every 4–8 weeks during taper, more frequently in early treatment).
- Rising inflammatory markers often precede symptom relapse by 2–4 weeks — consider slowing the taper.
- Monitor blood pressure, glucose (HbA1c every 3–6 months), weight, and symptoms of steroid toxicity.
- Screen for adrenal insufficiency symptoms (fatigue, nausea, hypotension) as dose approaches physiologic replacement (5–7.5 mg/day).
- If adrenal insufficiency suspected: morning cortisol or short Synacthen test. Do not stop prednisolone abruptly.
Steroid Side Effects
| System | Adverse Effects | Monitoring |
|---|---|---|
| Musculoskeletal | Osteoporosis, avascular necrosis, proximal myopathy | DEXA at baseline and annually; FRAX score |
| Metabolic | Diabetes, weight gain, dyslipidaemia | Fasting glucose at baseline, then 3-monthly; HbA1c |
| Ophthalmological | Posterior subcapsular cataracts, glaucoma | Annual ophthalmology review if >7.5 mg >6 months |
| Cardiovascular | Hypertension, fluid retention | BP at each visit |
| Infectious | Increased risk of infection, reactivation of latent TB | Consider TB screening (IGRA) at baseline |
| Dermatological | Skin fragility, bruising, striae | Clinical assessment |
| Psychiatric | Insomnia, mood changes, psychosis (rare) | Patient enquiry at each visit |
Steroid-Sparing Agents
Not all PMR patients require steroid-sparing agents. However, they should be considered early in patients who relapse during taper, require prolonged moderate-dose steroids (≥7.5 mg prednisolone for ≥6 months), or have significant steroid-related comorbidities (diabetes, osteoporosis, glaucoma).
Methotrexate — First-Line Steroid Sparer
Methotrexate
Methoblastin® · Generic · Antimetabolite / DMARD
Adult dose
7.5–15 mg PO or SC once weekly (start 7.5–10 mg, increase to 15 mg if needed at 4–6 weeks)
Adjunct
Folic acid 5 mg PO weekly (taken 48 hours after methotrexate dose) — mandatory to reduce side effects
Onset of effect
6–12 weeks; continue concurrent prednisolone until steroid-sparing effect is evident
Renal adjustment
Contraindicated if eGFR <30 mL/min/1.73 m². Use with caution and reduced dose if eGFR 30–59.
Hepatic adjustment
Contraindicated in significant hepatic disease. Monitor LFTs fortnightly for 6 weeks, then monthly for 3 months, then 3-monthly.
PBS status
✔ PBS General Benefit
Evidence summary: The SEMAPHORE trial (2021) and systematic reviews demonstrate methotrexate reduces cumulative steroid dose, relapse rate, and steroid-related adverse effects in PMR. Benefits are most pronounced in relapsing or steroid-dependent disease.
Other Steroid-Sparing Options
Leflunomide
Arava® · Generic · DMARD (pyrimidine synthesis inhibitor)
Adult dose
20 mg PO daily (no loading dose in PMR). Considered when methotrexate is contraindicated or not tolerated.
PBS status
PBS Restricted Benefit
Tocilizumab
Actemra® · IL-6 receptor inhibitor (biologic DMARD)
Adult dose
162 mg SC weekly (or fortnightly). Emerging evidence from PMR-SPARE and other trials shows rapid CRP normalisation and steroid-sparing effect.
PBS status
PBS Authority Required — approved for GCA, not yet PMR alone
When to start a steroid-sparing agent:
• Relapse during first steroid taper
• Prednisolone dose ≥7.5 mg/day required for >6 months
• Steroid-related adverse effects: new diabetes, fracture, cataracts, significant weight gain
• Pre-existing comorbidity exacerbated by steroids (diabetes, osteoporosis, glaucoma)
• Patient preference after discussion of risks/benefits
• Relapse during first steroid taper
• Prednisolone dose ≥7.5 mg/day required for >6 months
• Steroid-related adverse effects: new diabetes, fracture, cataracts, significant weight gain
• Pre-existing comorbidity exacerbated by steroids (diabetes, osteoporosis, glaucoma)
• Patient preference after discussion of risks/benefits
Agents NOT Recommended
- NSAIDs alone: Inadequate for PMR; may be used adjunctively for mild symptoms during taper.
- TNF inhibitors (infliximab, etanercept, adalimumab): Trials in PMR have been negative or inconclusive; not recommended.
- Azathioprine: Insufficient evidence; not standard of care for PMR.
Bone Protection
Glucocorticoid-induced osteoporosis (GIOP) is a major concern in PMR patients, who are already elderly and often have age-related bone loss. All patients commencing prednisolone ≥3 months require bone-protective measures. Australian guidelines (RACGP, Osteoporosis Australia) recommend risk stratification and prophylaxis.
Risk Assessment
- Perform FRAX® score calculation (adjusted for glucocorticoid dose) at baseline.
- DEXA scan at commencement of glucocorticoids (MBS item 12310) and annually while on treatment.
- Consider bone protection for all patients aged ≥70 or those with prior fragility fracture — these patients are automatically high-risk.
Universal Bone Protection Measures
Calcium + Vitamin D
Cal-DK2® · Ostelin® · Various generics
Adult dose
Calcium 500–1000 mg + Vitamin D3 800–1000 IU daily (adjust dietary intake)
PBS status
✔ Over-the-counter (OTC) — widely available
Alendronate
Fosamax® · Alendro® · Generic · Bisphosphonate
Adult dose
70 mg PO once weekly (fasting, upright position 30 min, with water only)
Renal adjustment
Contraindicated if eGFR <30 mL/min/1.73 m²
PBS status
✔ PBS General Benefit — for treatment of established osteoporosis in patients on systemic glucocorticoids ≥3 months
Risedronate
Actonel® · Generic · Bisphosphonate
Adult dose
35 mg PO once weekly (same fasting/position rules as alendronate)
PBS status
✔ PBS General Benefit — steroid-induced osteoporosis
High-Risk Patients — Additional Options
- Zoledronic acid (Aclasta®): 5 mg IV once yearly. PBS-listed for osteoporosis (Authority Required in some indications). Useful when oral bisphosphonates are not tolerated or compliance is a concern. Contraindicated if eGFR <35 mL/min/1.73 m².
- Denosumab (Prolia®): 60 mg SC every 6 months. PBS Authority Required for severe osteoporosis. Can be used in renal impairment (unlike bisphosphonates). Monitor calcium closely; rebound vertebral fractures may occur on discontinuation.
Bone protection is not optional in PMR: All patients on prednisolone ≥7.5 mg for ≥3 months should receive calcium, vitamin D, and a bisphosphonate. Reassess annually with DEXA. Do not discontinue bone protection until glucocorticoids are ceased and DEXA T-score is above −2.5.
Atypical & Relapsing PMR
Relapse
Relapse is common in PMR, affecting 50–60% of patients during or after glucocorticoid taper. Relapse is defined as recurrence of PMR symptoms with or without elevated inflammatory markers while on or after stopping glucocorticoids.
Features Suggesting Relapse
- Recurrence of bilateral shoulder and/or hip girdle aching and stiffness.
- Rising CRP and/or ESR (often precedes symptoms by 2–4 weeks).
- Fatigue, malaise, and reduced function.
- Typically occurs when prednisolone is tapered below 7.5 mg/day or after cessation.
Management of Relapse
1
Confirm it is a true relapse
Exclude infection, malignancy flare, new diagnosis (e.g., GCA), or non-inflammatory causes. Recheck CRP/ESR.
2
Re-escalate prednisolone
Return to the last dose that controlled symptoms (typically 10–15 mg). If symptoms resolve quickly (48–72 hours), confirms PMR relapse.
3
Re-taper more slowly
Use a slower taper rate (e.g., 1 mg per month below 10 mg). Consider alternate-day dosing.
4
Initiate steroid-sparing agent
Methotrexate 10–15 mg/week is preferred for second or subsequent relapse, or if on ≥7.5 mg for >6 months.
Atypical Presentations
A minority of patients present with atypical features that can complicate diagnosis or suggest an alternative diagnosis.
| Atypical Feature | Consideration |
|---|---|
| Peripheral arthritis (hands, wrists, knees) | Consider late-onset rheumatoid arthritis (LORA), remitting seronegative symmetrical synovitis with pitting oedema (RS3PE), or overlap syndrome |
| Normal ESR and CRP | Seen in ~5% of PMR. Do not exclude diagnosis. Consider occult malignancy, fibromyalgia, or statin myopathy. |
| Distal swelling with pitting oedema | RS3PE syndrome (remitting seronegative symmetrical synovitis with pitting oedema) — responds to low-dose steroids, may be PMR variant |
| Onset <50 years | PMR extremely rare <50; strongly consider alternative diagnoses including malignancy and inflammatory arthritis |
| Poor steroid response | Re-evaluate diagnosis. Consider myeloma, hypothyroidism, malignancy, fibromyalgia, or corticosteroid myopathy causing apparent relapse |
| Systemic features (fever, weight loss, night sweats) | Consider occult malignancy (lymphoma, myeloma), infection (endocarditis), or concurrent GCA |
Steroid-Resistant or Steroid-Dependent PMR
- Definition: Failure to reduce prednisolone below 10 mg/day without relapse after two attempts, or inability to discontinue after 2 years.
- Re-evaluate the diagnosis thoroughly — perform imaging, consider malignancy screen, and assess for concurrent GCA.
- Initiate methotrexate if not already commenced. Leflunomide as second-line.
- Consider tocilizumab in specialist centres for refractory cases (off-label for PMR; PBS-authorised for GCA).
- Refer to rheumatology if not already under specialist care.
Special Populations
Pregnancy
PMR and pregnancy:
PMR is essentially a disease of older adults and extremely rare in women of childbearing age. If it occurs, prednisolone is the safest glucocorticoid in pregnancy (Category A). Methotrexate is teratogenic (Category X) and must be ceased at least 3 months before conception. Leflunomide also teratogenic — requires washout with cholestyramine.
Paediatrics
PMR in children:
PMR does not occur in children. Bilateral shoulder/hip pain in a child suggests juvenile idiopathic arthritis, infection, malignancy, or mechanical causes. PMR is defined as occurring in individuals aged ≥50 years.
Elderly (≥75 years)
Steroid side effects amplified:
Higher rates of steroid-induced diabetes, osteoporotic fractures, cataracts, and adrenal insufficiency. Start bone protection from day one. Consider lower starting dose (12.5 mg) and slower taper. Earlier use of methotrexate may be justified.
Polypharmacy:
Review concurrent medications. NSAIDs should be avoided (renal/GI risk). Monitor for drug interactions with anticoagulants and hypoglycaemics.
Renal Impairment
Prednisolone:
No dose adjustment, but monitor fluid retention, potassium, and glucose closely.
Methotrexate:
Contraindicated if eGFR <30; dose reduction if eGFR 30–59. Monitor FBC closely.
Bisphosphonates:
Contraindicated if eGFR <30. Use denosumab as alternative.
Hepatic Impairment
Prednisolone:
Preferred over prednisone as it does not require hepatic conversion. No dose adjustment but monitor for fluid retention and hepatotoxicity.
Methotrexate:
Avoid in significant liver disease (risk of hepatotoxicity). Monitor LFTs closely; stop if transaminases >3× ULN.
Immunocompromised
Steroid + DMARD caution:
Combined immunosuppression increases infection risk. Screen for latent TB (IGRA) before starting methotrexate. Ensure vaccinations are up to date (influenza, pneumococcal, COVID-19, herpes zoster/shingles) before commencing immunosuppressive therapy.
Aboriginal and Torres Strait Islander Health Considerations
Aboriginal and Torres Strait Islander Health
Aboriginal and Torres Strait Islander peoples may experience PMR differently due to higher background rates of comorbid chronic disease, barriers to specialist access, and the impact of racism and social disadvantage on healthcare engagement. Culturally safe, patient-centred care is essential.
Quick Reference — PMR Management at a Glance
New bilateral shoulder girdle pain + stiffness in patient >50
Check CRP, ESR, RF, ACPA
Exclude GCA, RA, myeloma, hypothyroid
Confirmed PMR (EULAR/ACR criteria)
Prednisolone 12.5–20 mg/day PO
Expect response in 1–2 weeks
Bone protection — ALL patients
Ca²⁺ + Vit D daily + Alendronate 70 mg weekly
DEXA at baseline, then annually
Taper schedule
↓ 2.5 mg q2–4 wk → 10 mg → then ↓ 1 mg q4–8 wk
Monitor CRP at each step
Relapse
↑ to last effective dose; consider Methotrexate 10–15 mg/wk
Re-taper slowly
📚 References
- 1. Dasgupta B, Cimmino MA, Maradit-Kremers H, et al. 2012 provisional classification criteria for polymyalgia rheumatica: a European League Against Rheumatism/American College of Rheumatology collaborative initiative. Ann Rheum Dis. 2012;71(4):484–492.
- 2. Dejaco C, Singh YP, Perel P, et al. 2015 recommendations for the management of polymyalgia rheumatica: a European League Against Rheumatism/American College of Rheumatology task force collaborative initiative. Arthritis Rheumatol. 2015;67(10):2569–2580.
- 3. Buttgereit F, Dejaco C, Matteson EL, Dasgupta B. Polymyalgia rheumatica and giant cell arteritis: a systematic review. JAMA. 2016;315(22):2442–2458.
- 4. Caporali R, Cimmino MA, Ferraccioli G, et al. Prednisone plus methotrexate for polymyalgia rheumatica: a randomized, double-blind, placebo-controlled trial. Ann Intern Med. 2004;141(7):493–500.
- 5. Bonelli M, Radner H, Kerschbaumer A, et al. Tocilizumab in patients with new onset polymyalgia rheumatica (PMR-SPARE): a phase 2/3 randomised controlled trial. Ann Rheum Dis. 2022;81(6):831–837.
- 6. Australian Institute of Health and Welfare (AIHW). Rheumatic and musculoskeletal disease in Aboriginal and Torres Strait Islander peoples. AIHW, Canberra; 2019.
- 7. Royal Australian College of General Practitioners (RACGP). Recommended guidelines for the management of glucocorticoid-induced osteoporosis. RACGP, Melbourne; 2017.
- 8. Kermani TA, Warrington KJ, Cuthbertson D, et al. Disease relapses among patients with giant cell arteritis: a prospective, longitudinal cohort study. J Rheumatol. 2015;42(7):1213–1217.
- 9. Department of Health and Aged Care. Schedule of Pharmaceutical Benefits. Commonwealth of Australia, Canberra. Available at: pbs.gov.au. Accessed 2025.
- 10. Cimmino MA, Zaccaria A. Epidemiology of polymyalgia rheumatica. Clin Exp Rheumatol. 2000;18(4 Suppl 20):S9–S11.
- 11. Gonzalez-Gay MA, Vazquez-Rodriguez TR, Lopez-Diaz MJ, et al. Epidemiology of giant cell arteritis and polymyalgia rheumatica. Arthritis Care Res. 2009;61(10):1454–1461.
- 12. RHDAustralia (ARF/RHD writing group). The 2020 Australian guideline for prevention, diagnosis and management of acute rheumatic fever and rheumatic heart disease. 2nd edn. Menzies School of Health Research, Darwin; 2020. [Referenced for remote and Indigenous health service delivery models.]