Polymyalgia rheumatica
Exam Tips
- Classic station clue: age >50 with bilateral shoulder/hip girdle pain and morning stiffness >45 minutes, but normal true muscle power.
- PMR diagnosis is clinical plus exclusion: always state baseline tests (FBC, U&E, LFT, calcium, TSH, CK, RF/anti-CCP, urinalysis, ESR/CRP).
- A good response to prednisolone 15 mg daily within about 1 week strongly supports PMR; poor response should trigger diagnostic reconsideration.
- Never miss giant cell arteritis: new headache, jaw claudication, scalp tenderness, visual symptoms = emergency high-dose steroid pathway.
- Inflammatory markers support diagnosis but can occasionally be normal in otherwise typical PMR; do not rely on ESR/CRP alone.
- For image-based viva discussion, describe typical ultrasound findings of bilateral subacromial/subdeltoid bursitis and biceps tenosynovitis as supportive (see standard rheumatology ultrasound figure sets).
Definition
Polymyalgia rheumatica (PMR) is an inflammatory syndrome of adults aged over 50 years, classically causing bilateral shoulder and/or pelvic girdle pain with prolonged morning stiffness. It is a clinical diagnosis supported by raised inflammatory markers and a marked early response to low-dose oral corticosteroid, after exclusion of mimics and urgent exclusion of giant cell arteritis.
Pathophysiology
The exact cause is unknown, but PMR is thought to arise from immune-mediated inflammation in peri-articular and synovial structures (especially subacromial/subdeltoid bursae, glenohumeral and hip synovium, and tendon sheaths). Cytokine-driven innate immune activation (notably IL-6 pathways) contributes to systemic symptoms and acute-phase marker elevation. This explains severe pain and stiffness with relatively preserved true muscle power (pain-limited effort rather than primary myopathy). PMR and giant cell arteritis likely sit on a disease spectrum of age-related immune dysregulation and vascular/synovial inflammation.
Risk Factors
- Age >50 years (peak incidence around 70-80 years)
- Female sex
- Northern European ancestry
- Possible seasonal/infective triggers (reported associations with respiratory pathogen peaks)
- Personal history or future development risk of giant cell arteritis
Clinical Features
Symptoms
- Bilateral shoulder girdle aching (often first symptom; may start unilateral then rapidly become bilateral)
- Pelvic girdle/hip pain, sometimes radiating to thighs or knees
- Morning stiffness >=45 minutes and stiffness after rest
- Difficulty turning in bed, rising from a chair, or lifting arms above shoulder level
- Night pain and sleep disturbance due to shoulder/hip discomfort
- Systemic upset: low-grade fever, fatigue, anorexia, weight loss, low mood
- Distal symptoms in some patients: hand/wrist swelling, carpal tunnel symptoms
Signs
- Restricted active shoulder movement due to pain (passive range may also be uncomfortable)
- Proximal tenderness (upper arms/shoulder girdle)
- No objective focal neurological deficit in uncomplicated PMR
- Muscle strength usually preserved when pain is controlled
- Possible peripheral synovitis (often wrists/knees) and pitting oedema of hands/feet
- Assess for giant cell arteritis signs: temporal tenderness, reduced temporal pulse, jaw claudication, visual symptoms
Investigations
Management
Lifestyle Modifications
- Give clear steroid counselling: take in the morning with food; carry a steroid treatment card; do not stop abruptly
- Promote progressive mobility/physiotherapy to reverse deconditioning and maintain shoulder/hip function
- Bone health optimisation: weight-bearing exercise, smoking cessation, alcohol moderation, falls prevention
- Monitor cardiovascular/metabolic risk during long-term steroid use (BP, glucose, weight)
- Safety-net urgently for giant cell arteritis symptoms (new headache, scalp tenderness, jaw claudication, visual disturbance)
Pharmacological Treatment
Oral corticosteroid (first-line)
- Prednisolone 15 mg orally once daily initially
- If inadequate early response, increase to prednisolone 20 mg once daily and reassess
Aim for lowest effective dose with gradual taper once controlled. Recheck symptoms and ESR/CRP at 3-4 weeks. Contraindications/cautions: active uncontrolled infection, poorly controlled diabetes, severe osteoporosis risk, peptic ulcer disease, psychosis history. If giant cell arteritis is suspected, treat as emergency with higher-dose steroid pathway and same-day specialist assessment to reduce risk of visual loss.
Steroid-sparing therapy (specialist-guided, relapsing disease)
- Methotrexate 10-15 mg once weekly (oral or subcutaneous)
- Folic acid 5 mg once weekly (on a different day from methotrexate)
Consider in frequent relapse or prolonged steroid requirement. Safety: teratogenic, marrow/hepatic toxicity, pneumonitis risk; monitor FBC, LFT, renal function; avoid in significant liver disease and severe renal impairment unless specialist-directed.
Bone and GI protection during prolonged steroids
- Alendronic acid 70 mg orally once weekly (if fracture risk indicates)
- Calcium carbonate with colecalciferol (for example, calcium 1-1.2 g plus vitamin D about 800 IU daily)
- Omeprazole 20 mg once daily when GI ulcer risk is elevated
Bisphosphonates are contraindicated in oesophageal stricture/achalasia, inability to remain upright for 30 minutes, hypocalcaemia, and severe renal impairment. Correct hypocalcaemia before treatment.
Complications
- Giant cell arteritis (including risk of irreversible visual loss and large-vessel ischaemic complications)
- Relapsing or chronic steroid-dependent PMR course
- Adverse effects of long-term corticosteroids: osteoporosis/fracture, diabetes, hypertension, cataracts, glaucoma, infection risk, skin fragility, mood disturbance, adrenal suppression
- Functional decline from pain, stiffness, and deconditioning
Prognosis
Overall prognosis is usually good, with many patients improving dramatically within 24-72 hours of starting prednisolone. However, relapse is common and treatment often continues for at least 9-12 months, with many patients requiring 3-5 years of tapering therapy. PMR itself is not strongly linked to excess mortality, but morbidity is driven by relapses, coexisting giant cell arteritis, and steroid toxicity.
Sources & References
🏥BMJ Best Practice(1)
💊BNF Drug References(1)
- Prednisolone[management.pharmacological]
✅NICE Guidelines(1)
- Polymyalgia rheumatica[overview]
📖Textbook References(20)
- David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1327)[context]
- David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1804, 1805)[context]
- David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1805, 1806)[context]
- David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1116)[context]
- David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1155, 1156)[context]
- David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1757, 1758)[context]
- David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1805)[context]
- David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1474, 1475)[context]
- David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1130, 1131)[context]
- David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1156, 1157)[context]
- David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1155, 1156)[context]
- David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1156)[context]
- David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1819, 1820)[context]
- Oxford Handbook of Clinical Diagnosis (Huw Llewelyn, Hock Aun Ang, Keir Lewis etc.) (Z-Library).pdf(pp. 440, 441)[context]
- Oxford Handbook of Clinical Diagnosis (Huw Llewelyn, Hock Aun Ang, Keir Lewis etc.) (Z-Library).pdf(pp. 441)[context]
- Oxford Handbook of Clinical Diagnosis (Huw Llewelyn, Hock Aun Ang, Keir Lewis etc.) (Z-Library).pdf(pp. 674, 675)[context]
- [Oxford Medical Handbooks] Ian Wilkinson, Tim Raine, Kate Wiles, Anna Goodhart, Catriona Ha - Oxford Handbook of Clinical Medicine (2017, Oxford University Press) - libgen.li.pdf(pp. 572, 573)[context]
- [Oxford Medical Handbooks] Ian Wilkinson, Tim Raine, Kate Wiles, Anna Goodhart, Catriona Ha - Oxford Handbook of Clinical Medicine (2017, Oxford University Press) - libgen.li.pdf(pp. 899, 900)[context]
- [Oxford Medical Handbooks] Ian Wilkinson, Tim Raine, Kate Wiles, Anna Goodhart, Catriona Ha - Oxford Handbook of Clinical Medicine (2017, Oxford University Press) - libgen.li.pdf(pp. 553)[context]
- [Oxford Medical Handbooks] Ian Wilkinson, Tim Raine, Kate Wiles, Anna Goodhart, Catriona Ha - Oxford Handbook of Clinical Medicine (2017, Oxford University Press) - libgen.li.pdf(pp. 572, 573)[context]