Decision support only — not a substitute for rheumatology or the EULAR/ACR guidance. PMR is a clinical diagnosis with no confirmatory test, defined partly by a brisk steroid response, so two things matter most: rule out the mimics before committing, and screen for giant cell arteritis at every visit, since GCA can surface at any point. The steroid dose is far lower than GCA — don't conflate them. Verify all doses.
1 The treatment arc
Confirm the syndromeand exclude mimics
Age >50, bilateral shoulder/hip girdle pain, morning stiffness >45 min, raised ESR/CRP.
Take baseline bloods to exclude mimics first — CK (normal in PMR), RF/anti-CCP, TSH, FBC, ESR/CRP (§3).
Start steroidsexpect a dramatic response
Diagnosis supported.
Prednis(ol)one 12.5–25 mg daily (usually ~15 mg). An incomplete or slow response should make you doubt the diagnosis — genuine PMR responds within days.
Taper slowlyrelapse-prone
Symptoms and markers settled.
Reduce to 10 mg over ~4–8 weeks, then ~1 mg every 4 weeks while in remission. Total course usually 1–2 years; slow tapers relapse less.
Steroid-sparingif it won't behave
Relapsing, steroid-dependent, or high steroid-toxicity risk.
Methotrexate early; sarilumab for relapse on taper SAPHYR; tocilizumab (off-label) also steroid-sparing (§5).
Two rules that keep you out of trouble: ask about GCA symptoms at every visit (headache, jaw claudication, visual, scalp tenderness) — GCA and PMR travel together and GCA is the one that blinds; and remember the PMR dose (12.5–25 mg) sits well below the GCA dose (40–60 mg). NSAIDs and TNF inhibitors don't work in PMR — reaching for them is a sign the diagnosis is wrong.
2 Recognise & classify
The picture
- WhoAge >50 (mostly >65), women > men, more common in Northern European ancestry.
- CoreBilateral shoulder ± hip girdle pain and stiffness, worse in the morning (>45 min); difficulty rising, dressing, combing hair.
- SystemicFatigue, low-grade fever, weight loss, depression in some.
- LabsRaised ESR/CRP usually; a minority have normal markers. No confirmatory test.
2012 EULAR/ACR classification
- EntryAge ≥50, bilateral shoulder aching, and abnormal CRP/ESR (required).
- ScorePoints for morning stiffness >45 min, hip pain/limited movement, absence of RF/anti-CCP, and absence of other joint involvement (± ultrasound).
- NoteThese are classification criteria — supportive, not a substitute for clinical judgement and mimic exclusion.
3 Exclude the mimics — and read the steroid response
What else it could be
- RALate-onset/seronegative RA overlaps closely — peripheral synovitis, RF/anti-CCP point away from PMR.
- MyopathyInflammatory myositis → check CK; PMR has a normal CK and no true weakness (pain limits movement, not weakness).
- MalignancyDominant weight loss, atypical features, poor steroid response → look for cancer.
- OthersRS3PE, spondyloarthritis, hypothyroidism, OA/rotator-cuff disease, statin myopathy, infection (endocarditis), fibromyalgia.
The response is a diagnostic test
- GoodA rapid, near-complete response to ~15 mg supports the diagnosis.
- PoorIncomplete or absent response = reconsider — RA, myopathy, malignancy, or GCA hiding underneath.
- ReferAtypical features warrant specialist review: age <60, prominent peripheral arthritis, systemic symptoms, or low inflammatory markers.
4 The GCA overlap — the thing you must not miss
Screen at every visit
- AskNew headache, jaw claudication, visual symptoms, scalp tenderness — at diagnosis and every review.
- OverlapAround 15–20% of PMR patients develop GCA, and it can appear after PMR is established.
- If positiveAny cranial/visual feature → treat as GCA now: high-dose (or IV pulse) steroids and urgent work-up — don't stay on the PMR dose.
Two diseases, two doses
- PMR12.5–25 mg prednisolone — girdle syndrome, no ischaemic threat.
- GCA40–60 mg (IV pulse if visual) — sight-threatening; see the GCA sheet.
- The errorUnder-dosing emerging GCA at PMR doses risks vision; over-dosing PMR at GCA doses adds needless steroid harm.
5 Long-term treatment & steroid-sparing
Glucocorticoids still carry the disease, but relapse reaches up to three-quarters of patients and steroid toxicity is near-universal in this age group, so steroid-sparing is an active field. Sarilumab is the only approved add-on; everything else is conventional (methotrexate, leflunomide) or emerging.
Steroids & relapse
- TaperTo 10 mg, then ~1 mg/4 weeks; individualise to relapse. IM depot methylprednisolone is an alternative with lower cumulative dose.
- RelapseUp to ~three-quarters relapse — return to the last effective dose; don't chase markers alone.
- DurationMost 1–2 years; a substantial minority run longer or become steroid-dependent.
Steroid-sparing agents
- MethotrexateConventional first choice — consider early for relapse, prolonged therapy, or high steroid-toxicity risk. Leflunomide is a reasonable alternative if MTX isn't tolerated.
- SarilumabIL-6R inhibitor, the only approved steroid-sparer — sustained remission and roughly a third of the cumulative steroid vs placebo in relapsing PMR SAPHYR.
- EmergingRituximab (single infusion) showed glucocorticoid-free remission in a proof-of-concept RCT BRIDGE-PMR; tocilizumab (off-label), IL-17 and JAK inhibitors are in the pipeline.
Protect & monitor
- Steroid harmBone (bisphosphonate + Ca/vit D), PPI, glucose, BP, weight, mood — this is an elderly cohort on a long course.
- Follow-upEvery 4–8 weeks in year one, 8–12 weeks in year two, plus prompt access for flares or GCA symptoms.
- Don't useNSAIDs and TNF inhibitors are ineffective in PMR.
Guidelines. 2015 EULAR/ACR recommendations for the management of PMR (Dejaco et al — prednisone 12.5–25 mg initial, individualised slow taper, early methotrexate in selected patients, against NSAIDs/TNF inhibitors); 2012 EULAR/ACR provisional classification criteria; BSR/BHPR 2010 PMR guideline; eTG; PBS.
Trials. SAPHYR (sarilumab in relapsing PMR, NEJM 2023 — sustained remission 28% vs 10%, cumulative steroid ~777 vs 2044 mg); Caporali (methotrexate steroid-sparing, Ann Intern Med 2004); BRIDGE-PMR (rituximab, Lancet Rheumatol 2023 — proof-of-concept glucocorticoid-free remission); PMR-SPARE and other tocilizumab data; leflunomide observational cohorts; emerging IL-17 (secukinumab) and JAK-inhibitor (baricitinib, tofacitinib) trials.
Caveats. PMR is a clinical diagnosis with no confirmatory test — a poor steroid response is a red flag for an alternative (RA, myositis, malignancy) or concurrent GCA. Screen for GCA at every visit; the PMR steroid dose is far below the GCA dose. Sarilumab is FDA-approved for PMR; confirm Australian PBS availability, which may lag. Verify all doses. Companion to the GCA sheet and the rheumatology/bone set (osteoporosis).