Polymyalgia Rheumatica and Giant-Cell Arteritis

Polymyalgia rheumatica (PMR) and giant-cell arteritis (GCA) are related corticosteroid-responsive inflammatory conditions of older adults that likely represent a spectrum of the same underlying disease process — a substantial proportion of patients with one condition also have, or go on to develop, the other, and every patient with either diagnosis should be screened for symptoms of both at every visit.^[1] PMR causes bilateral aching and stiffness of the shoulder and hip girdles from low-grade synovitis and periarticular inflammation, while GCA is a granulomatous vasculitis of large and medium-sized arteries — chiefly the cranial branches of the aortic arch — that can occlude blood flow to the eye. GCA is an ophthalmologic and vascular emergency: once visual loss from GCA has occurred it is usually permanent, so the entire management principle is to start high-dose corticosteroids immediately on clinical suspicion, before any confirmatory test, to protect vision that has not yet been lost.

Both conditions are diagnosed clinically — there is no blood test specific to either PMR or GCA, and a temporal artery biopsy is confirmatory only for GCA, not PMR.

PMR and GCA — related but distinct presentations

Polymyalgia Rheumatica

Typical pain distribution in polymyalgia rheumatica — bilateral shoulder/neck and hip girdle regions. (Twisp, public domain, Wikimedia Commons)

• Bilateral aching and stiffness of the shoulders, neck, and hip girdles — shoulder involvement is the most common and usually the most severe.
• Acute onset; many patients can identify the specific day symptoms began.
• Morning stiffness lasting a substantial part of the morning, often prominent enough to wake the patient overnight with movement, and recurring after any period of inactivity during the day.
• Pain interferes significantly with activities of daily living — dressing, rising from a chair, reaching overhead.
• Systemic symptoms — low-grade fever, malaise, anorexia, weight loss, fatigue — may accompany the musculoskeletal features.

Giant Cell Arteritis

• New-onset headache, most often temporal or occipital, with scalp tenderness (pain on combing hair or resting the head on a pillow).
• Jaw or tongue claudication — pain that builds with chewing or talking and eases with rest — highly specific for GCA.
• Visual symptoms — transient monocular visual loss (amaurosis fugax), permanent monocular visual loss, diplopia, or blurred vision. Untreated, the fellow eye is at high risk of also losing vision within days.
• Upper-limb claudication or other large-vessel symptoms when the aortic arch branches are involved, resembling Takayasu arteritis.
• Systemic symptoms — fever, malaise, weight loss — occur in many patients.
• A recognized late complication is thoracic or abdominal aortic aneurysm, which can present years after the acute illness.

Because the two conditions overlap so heavily, ask every PMR patient specifically about headache, scalp tenderness, jaw claudication, and visual symptoms, and ask every GCA patient specifically about shoulder/hip girdle pain and stiffness — missing the overlap is a common, avoidable error.^[2]

• Age over 50 — both conditions are essentially confined to this age group, with the highest incidence between 70 and 80 years.
• Female sex — both conditions are more common in women than men.
• Northern European or Scandinavian ancestry, though both conditions occur in all populations.
• A first-degree relative with PMR or GCA.
• Existing PMR — a meaningful subset of patients develop concurrent or subsequent GCA.
• Existing GCA — many patients have concurrent or subsequent PMR symptoms.
• Smoking has been associated with an increased risk of GCA in observational data.

Conditions commonly confused with polymyalgia rheumatica

History

Characterize the pattern, distribution, and time course of pain and stiffness, and ask specifically about GCA symptoms (headache, scalp tenderness, jaw/tongue claudication, visual change) in every patient being assessed for PMR, and about PMR symptoms in every patient being assessed for GCA.

Physical examination

Suspected PMR: findings are usually nonspecific — reduced active range of motion of the neck and shoulders driven by pain rather than true weakness. Synovitis may be present in peripheral joints such as the wrists or knees, but should not involve the feet or ankles; involvement there points toward an alternative diagnosis. Marked pitting edema over the dorsum of both hands occurs in a distinct clinical subset. Proximal muscle tenderness may be present, but objective weakness should not occur — if weakness is present, reconsider myositis.

Suspected GCA: palpate both temporal arteries for pulse strength, thickening, and tenderness — a diminished or absent pulse with an appropriate history is highly suggestive of GCA. Check peripheral pulses, listen for bruits, and measure blood pressure in both arms; asymmetry suggests large-vessel involvement.

Laboratory tests

ESR and/or CRP are elevated in almost every patient with active PMR or GCA, but these markers are nonspecific — other causes of systemic inflammation (infection, malignancy) must be considered and excluded on clinical grounds. A small subset of patients have normal ESR and CRP despite active disease, so a normal result does not exclude either diagnosis when the clinical picture is otherwise convincing.^[4] CBC may show anemia and/or thrombocytosis.

Imaging

Plain radiographs of affected joints in suspected PMR can help exclude alternative diagnoses. Temporal artery ultrasound and MRI of the cranial arteries are emerging noninvasive alternatives to biopsy, but availability and diagnostic performance vary by centre, so temporal artery biopsy remains the diagnostic reference standard for GCA. CT or MR angiography of the neck, chest, abdomen, and pelvis is useful when large-vessel involvement is suspected, particularly if temporal artery biopsy is negative.^[2]

Temporal artery biopsy

Temporal artery biopsy in giant-cell arteritis — transmural granulomatous inflammation with multinucleated giant cells at the disrupted internal elastic lamina. (Nephron, CC BY-SA 3.0, Wikimedia Commons)

• Biopsy only if there is a genuine clinical suspicion of GCA — it is not routinely indicated for isolated PMR without GCA features.
• A unilateral biopsy of at least 1 cm on the more symptomatic side is the recommended initial approach.
• Because vessel involvement is focal and segmental (skip lesions), a normal biopsy does not exclude GCA — consider a contralateral biopsy if clinical suspicion remains high after a negative initial result.

• Achieve rapid, substantial symptom relief and normalize inflammatory markers.
• Prevent irreversible visual loss and other ischemic vascular complications in GCA.
• Restore functional status and quality of life.
• Use the lowest corticosteroid dose that controls disease activity, tapered as quickly as the disease allows, working toward eventual discontinuation.
• Minimize cumulative corticosteroid toxicity — bone, metabolic, ophthalmic, and infectious.
• Detect and manage relapse early, before it requires a full re-induction dose.

• Educate every patient at the outset that treatment is typically a multi-year process with a slow, deliberate taper — understanding this reduces self-directed premature discontinuation and improves adherence.
• Weight-bearing exercise, smoking cessation, and limiting alcohol intake to 1-2 drinks/day support bone health throughout the corticosteroid course.^[8]
• Prioritize dietary calcium and vitamin D intake, supplementing only the gap to reach target daily intake (see Pharmacologic Treatment Options).
• Home blood pressure monitoring, and home glucose monitoring in patients with diabetes or prediabetes, while on higher corticosteroid doses.
• Fall-prevention counselling — corticosteroid myopathy and osteoporosis together substantially raise fracture risk from a fall.
• Confirm vaccination status is up to date before starting significant immunosuppression, particularly before tocilizumab, upadacitinib, or methotrexate.
• Physiotherapy or occupational therapy referral for persistent stiffness, deconditioning, or reduced shoulder range of motion.
• For PMR shoulder pain that does not fully resolve with systemic tapering, consider whether a localized rotator cuff tendinitis, subacromial bursitis, or capsulitis is contributing — this is more likely when diagnosis or treatment was delayed, and often responds to a localized corticosteroid injection rather than indicating the systemic taper has failed (see Drug Tables).

Pregnancy

PMR and GCA occur almost exclusively in adults over 50, so pregnancy is not a practical concern for most patients — the following applies to the rare exception or to a steroid-sparing agent continued from another indication. Prednisone is compatible with pregnancy when clearly indicated for a serious maternal condition, used at the lowest effective dose. Methotrexate is contraindicated in pregnancy — it is teratogenic; stop it and use effective contraception, or switch to corticosteroid monotherapy, before a planned pregnancy. Tocilizumab, sarilumab, and upadacitinib have limited human pregnancy data and are generally avoided — upadacitinib in particular carries a specific fetal risk warning as a JAK inhibitor. Bisphosphonates and denosumab are avoided in pregnancy and when pregnancy is being planned, given bisphosphonates' long bone half-life and denosumab's effect on maternal-fetal calcium handling.

Breastfeeding

Low-dose prednisone is compatible with breastfeeding. Methotrexate is contraindicated. Data for tocilizumab, sarilumab, and upadacitinib in lactation are limited — individualize with specialist input.

Pediatrics

Not applicable — PMR and GCA occur almost exclusively in adults over 50. A similar presentation in a substantially younger patient should prompt evaluation for an alternative diagnosis before PMR or GCA is considered.

Older adults with comorbidities

Because this condition is essentially a disease of older adults, comorbidities should actively guide the initial corticosteroid dose: in patients with diabetes, hypertension, glaucoma, osteoporosis, or cardiovascular disease, select the lower end of the PMR dosing range (15 mg/day) as the starting dose where clinically reasonable, since these patients are also at the highest risk of corticosteroid-related complications.

Renal impairment

Methotrexate is contraindicated in significant renal impairment. Oral bisphosphonates are generally avoided at very low creatinine clearance — denosumab is a reasonable alternative, but correct hypocalcemia and monitor calcium closely given the higher hypocalcemia risk in renal impairment.

Hepatic impairment

Use methotrexate with caution, or avoid, in significant hepatic impairment. Monitor liver enzymes closely with tocilizumab, which can cause transaminase elevation requiring dose interruption.

Reassess symptoms and repeat ESR/CRP at every dose-taper step. An isolated rise in ESR or CRP without a corresponding clinical relapse is not, by itself, sufficient justification to increase the corticosteroid dose — treat the patient, not the number. If a genuine relapse occurs, increase to the lowest previously effective dose, maintain it for about 1 month, then resume the taper more gradually.

Most patients need close follow-up (clinical review and inflammatory markers) every few weeks during the induction and early taper phases, spacing out as the dose stabilizes at a low maintenance level.

1. Confirm adherence and the correct dose before assuming a treatment failure — nonadherence to a complex, slowly-changing taper schedule is common.
2. PMR not substantially improved within about 1 week of an adequate corticosteroid dose: reconsider the diagnosis — rescreen for GCA symptoms and review the differential diagnosis (myositis, fibromyalgia, rheumatoid arthritis, malignancy, CPPD arthropathy).
3. Relapse during taper (recurrent symptoms with or without a rise in ESR/CRP): increase to the lowest previously effective dose, maintain for about 1 month, then resume the taper more gradually.
4. Frequent relapse, or inability to taper prednisone below 7.5 mg/day: add a steroid-sparing agent — tocilizumab or upadacitinib for GCA; tocilizumab, sarilumab, or methotrexate for PMR.
5. GCA with new ischemic symptoms despite treatment (new visual change, jaw claudication, limb claudication): treat as a new emergency — same-day reassessment, IV pulse corticosteroids if not already used, and urgent vascular/ophthalmology input.
6. Suspected large-vessel complication (upper-limb claudication, aortic symptoms): obtain CT or MR angiography and arrange vascular referral.
7. Genuine corticosteroid intolerance preventing adequate dosing: prioritize earlier initiation of a steroid-sparing agent and involve rheumatology.

• Waiting for temporal artery biopsy results before starting corticosteroids in suspected GCA.
• Treating GCA-related headache or visual symptoms as a routine migraine or ophthalmologic complaint without asking about jaw claudication or scalp tenderness.
• Using alternate-day corticosteroid dosing — associated with a higher relapse rate than daily dosing.
• Increasing the corticosteroid dose based on an isolated ESR/CRP rise without a corresponding clinical relapse.
• Assuming PMR that fails to improve within about a week is simply under-dosed rather than reconsidering the diagnosis.
• Missing GCA symptom screening in a patient managed for PMR, or PMR symptom screening in a patient managed for GCA.
• Prescribing methotrexate without co-prescribing folic acid.
• Forgetting bone-protective therapy in a patient starting a multi-month or multi-year corticosteroid course.^[9]
• Using a TNF-alpha inhibitor (adalimumab, etanercept, infliximab) for PMR or GCA — trial evidence shows no benefit in either condition.
• Starting a statin specifically to treat GCA — no demonstrated disease-modifying effect on GCA itself.
• Skipping latent tuberculosis and hepatitis B/C screening before starting tocilizumab or upadacitinib.
• Stopping corticosteroids abruptly once symptoms improve, rather than following the taper schedule.

How to use this table: Doses are adult doses and require patient-specific confirmation (renal/hepatic function, weight, allergy history). Pediatric dosing is weight-based per the current product monograph unless stated. Drug pricing is intentionally omitted. Select any drug name to open its complete Pharmasist Drug Database page.

Corticosteroids

Conventional steroid-sparing immunomodulators

Biologic and targeted steroid-sparing agents

TNF-alpha inhibitors — not recommended for PMR or GCA

Randomized trial evidence shows no benefit in either condition; reserve these agents for their approved indications (e.g., rheumatoid arthritis).

Antiplatelet therapy

Glucocorticoid-induced osteoporosis prevention

Assess fracture risk as soon as possible after starting a corticosteroid course expected to last more than 3 months; the unadjusted 10-year fracture-probability estimate from a tool such as FRAX should be adjusted upward for doses above a low/moderate range and downward for lower doses.

Gastrointestinal protection

For patients on concurrent ASA/NSAID plus corticosteroid therapy, given the additive GI bleeding risk.

Infection prophylaxis

Evidence note: Drug inventory, dosing, adverse effects, and comments reflect current Canadian practice, cross-checked against the 2025 EULAR recommendations and current Health Canada product indications.^[1]