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giant cell arteritis

large-vessel vasculitis affecting the temporal and other cranial arteries — a medical emergency because of the risk of irreversible visual loss. treat with high-dose steroids immediately

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About This Page

This is a clinician-written, evidence-based summary aligned to the 2026 MLA Content Map. It is intended for medical students and junior doctors preparing for the UKMLA. Always cross-reference with NICE guidance, local protocols, and clinical judgement.

The Bottom Line

  • Large-vessel vasculitis predominantly affecting branches of the external carotid artery (temporal, occipital) in patients >50 years
  • MEDICAL EMERGENCY: risk of permanent visual loss (anterior ischaemic optic neuropathy) — up to 20% if untreated
  • Key symptoms: new-onset headache (temporal), jaw claudication (most specific symptom), scalp tenderness, visual disturbance
  • Start high-dose prednisolone IMMEDIATELY on clinical suspicion: 40–60 mg/day (or IV methylprednisolone if visual symptoms)
  • Temporal artery biopsy is the gold standard for diagnosis. USS showing "halo sign" increasingly used as first-line

Overview

Giant cell arteritis (GCA, temporal arteritis) is a granulomatous vasculitis of large and medium arteries, predominantly affecting the cranial branches of arteries originating from the aortic arch. It is the most common primary systemic vasculitis in adults over 50. The superficial temporal artery is the classically affected vessel, but GCA can involve any large artery (aorta, subclavian, axillary — "large vessel GCA"). The most feared complication is permanent visual loss from anterior ischaemic optic neuropathy (AION), which occurs in ~15–20% of untreated patients and is usually irreversible. This makes GCA a medical emergency requiring immediate high-dose steroids.

Epidemiology

GCA almost exclusively affects those over 50 years (mean age ~73). Female:male ratio is approximately 2.5:1. Incidence in the UK is approximately 20 per 100,000 per year in those over 50. It is closely related to PMR: ~50% of GCA patients have PMR symptoms, and ~15–20% of PMR patients develop GCA. Most common in White European populations, particularly those of Scandinavian descent.

Clinical Features

Symptoms
New-onset headache: typically temporal, unilateral or bilateral — different from any previous headache
Jaw claudication: pain in jaw muscles on chewing that eases with rest (MOST SPECIFIC symptom for GCA)
Scalp tenderness: pain on combing hair, wearing hat, or lying on pillow
Visual disturbance: transient visual loss (amaurosis fugax), diplopia, or permanent visual loss (AION)
PMR symptoms: bilateral shoulder/hip girdle pain and stiffness (coexist in ~50%)
Systemic features: malaise, fever, weight loss, fatigue
Signs
Temporal artery tenderness, thickening, beading, or reduced pulsation on palpation
Scalp tenderness
Visual field defect or reduced visual acuity (AION)
RAPD (relative afferent pupillary defect) — if optic nerve affected
Pale swollen optic disc on fundoscopy (AION)
Asymmetric blood pressures or bruits (large vessel involvement)

Investigations

First-line
ESR and CRPTypically markedly raised (ESR >50 mm/hr, often >80–100). CRP also raised. Normal ESR does not completely exclude GCA but makes it less likely
FBCNormocytic anaemia, thrombocytosis
Temporal artery USS (colour Doppler)Non-invasive, fast. "Halo sign" (dark hypoechoic area around temporal artery lumen) = vessel wall oedema. Sensitivity ~77%, specificity ~96%. Increasingly used as first-line imaging test (BSR 2020)
Second-line
Temporal artery biopsyGold standard. Shows granulomatous inflammation with giant cells, intimal hyperplasia, fragmentation of internal elastic lamina. Should be performed within 2 weeks of starting steroids (histology may normalise after 2–6 weeks). Negative biopsy does not exclude GCA (skip lesions — 30% false negative rate)
Specialist
PET-CT or MRAIf large vessel GCA suspected (aortitis, subclavian involvement). Shows vessel wall inflammation
LFTsALP may be raised (hepatic involvement) — part of the clinical picture
1
Immediate treatment — do NOT delay
  • WITHOUT visual symptoms: prednisolone 40–60 mg/day orally
  • WITH visual symptoms or visual loss: IV methylprednisolone 500 mg–1 g/day for 3 days, then oral prednisolone 60 mg/day
  • Start IMMEDIATELY on clinical suspicion — do NOT wait for biopsy or results
  • Start bone protection: bisphosphonate, calcium, vitamin D
  • PPI for gastric protection
2
Steroid tapering
  • Taper gradually over 1–2 years: reduce by 10 mg every 2 weeks to 20 mg, then by 2.5 mg every 2–4 weeks to 10 mg, then by 1 mg/month
  • Monitor ESR/CRP with each reduction — relapse triggers dose increase
  • Total treatment duration typically 1–2 years (some need longer)
3
Steroid-sparing agents
  • Tocilizumab (anti-IL-6): NICE-approved for relapsing/refractory GCA or to reduce steroid exposure (NICE TA518)
  • Methotrexate: may be used as steroid-sparing agent (evidence less strong than for tocilizumab)
4
Monitoring
  • Urgent ophthalmology assessment if ANY visual symptoms
  • Monitor for steroid side effects: glucose, BP, bone health
  • Long-term: screen for aortic aneurysm (annual CXR or CT if large vessel involvement suspected)
  • Low-dose aspirin: consider for cardiovascular risk reduction (some guidelines recommend)

Complications

  • Permanent visual loss: ~15–20% if untreated (AION). Usually irreversible. Contralateral eye at risk within days-weeks if untreated — the urgency of treatment
  • Aortic aneurysm: 17-fold increased risk — screen with imaging. Can cause aortic dissection
  • Stroke: From vertebral/carotid artery involvement
  • Steroid complications: Osteoporosis, diabetes, infections, cataracts — major concern with prolonged high-dose steroids
  • Relapse: ~50% during steroid taper — may require dose increase or steroid-sparing agent
UKMLA Exam Tips
  • 1New headache + jaw claudication + raised ESR + age >50 = GCA. Treat IMMEDIATELY — do not wait for biopsy
  • 2Jaw claudication is the MOST SPECIFIC symptom for GCA
  • 3Visual loss from GCA is a MEDICAL EMERGENCY — IV methylprednisolone 500 mg–1 g if visual symptoms
  • 4Prednisolone dose: GCA = 40–60 mg/day (high). PMR = 15 mg/day (low). Know the difference
  • 5Temporal artery biopsy: gold standard but negative biopsy does NOT exclude GCA (skip lesions)
  • 6USS "halo sign": hypoechoic ring around the artery = vessel wall oedema. Increasingly used first-line
  • 7Tocilizumab (anti-IL-6): NICE-approved steroid-sparing agent for GCA
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Verified Sources & References

BSR 2020 — Guideline for diagnosis and treatment of GCA
NICE TA518 — Tocilizumab for GCA