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Giant cell arteritis

SNOMED: 414341000835 words•Updated 03/03/2026
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Exam Tips

  • In OSCE/viva, state immediately that suspected GCA is a same-day emergency and treatment should start before diagnostic confirmation if clinical suspicion is high.
  • Classic triad to mention: new headache in age >50, jaw claudication, and visual symptoms; add temporal artery abnormality and raised inflammatory markers.
  • A normal ESR/CRP does not completely exclude GCA; diagnosis is clinical plus imaging/biopsy.
  • Poor response to adequate prednisolone should trigger re-evaluation of the diagnosis.
  • Distinguish GCA from Takayasu arteritis by age and pattern: GCA is older adults with cranial features; Takayasu is younger with predominant large-vessel limb ischaemia.
  • Link to polymyalgia rheumatica in answers (common overlap, shared inflammatory biology).

Definition

Giant cell arteritis (GCA) is an immune-mediated granulomatous vasculitis of medium and large arteries, especially branches of the carotid artery (including temporal and ophthalmic territories) and sometimes the aorta and its major branches. It is a medical emergency because untreated arterial inflammation can cause rapidly irreversible ischaemic complications, particularly visual loss.

Pathophysiology

In genetically susceptible older adults, dendritic-cell and T-cell/macrophage activation in the arterial wall drives granulomatous inflammation with multinucleated giant cells, intimal hyperplasia, and luminal narrowing. This causes ischaemia (for example anterior ischaemic optic neuropathy, jaw claudication, stroke) and can also weaken the aortic wall, predisposing to aneurysm or dissection. GCA frequently overlaps with polymyalgia rheumatica, reflecting shared systemic IL-6-driven inflammation. See Figure: granulomatous inflammation of temporal artery wall and Figure: vascular territories at risk of visual ischaemia.

Risk Factors

  • Age 50 years or older (risk rises with age, especially 70-79 years)
  • Female sex (about 2-3 times more common than in men)
  • Northern European/Scandinavian ancestry
  • Coexisting polymyalgia rheumatica
  • Previous large-vessel inflammatory disease phenotype

Clinical Features

Symptoms

  • New-onset headache (often temporal, but can be occipital/parietal/generalized)
  • Scalp tenderness (for example pain when brushing hair)
  • Jaw claudication (masseter pain after chewing); less commonly tongue claudication
  • Visual disturbance: transient visual obscurations, amaurosis fugax, diplopia, visual field or colour vision change, sudden visual loss
  • Constitutional symptoms: low-grade fever, fatigue, anorexia, weight loss, low mood
  • Proximal pain and morning stiffness suggestive of polymyalgia rheumatica
  • Limb claudication, chest/back pain, or systemic symptoms suggesting extracranial large-vessel involvement

Signs

  • Temporal artery tenderness, thickening, nodularity, or reduced/absent pulsation
  • Occasional overlying erythema of temporal artery skin
  • Relative afferent pupillary defect or reduced visual acuity with ocular ischaemia
  • Fundoscopy may show optic disc pallor/oedema, retinal cotton-wool spots, retinal haemorrhages (often after visual loss)
  • Carotid/subclavian bruits
  • Inter-arm blood pressure difference or reduced peripheral pulses
  • Neurological deficits if TIA/stroke or peripheral neuropathy occurs

Investigations

Full blood count:Normocytic anaemia and/or thrombocytosis consistent with systemic inflammation
C-reactive protein (CRP):Usually raised; may be markedly elevated in active disease
Erythrocyte sedimentation rate (ESR):Usually raised (often high), though a normal result does not fully exclude GCA
Temporal and axillary artery ultrasound:Halo sign, stenosis, or occlusion supporting cranial/large-vessel GCA
Temporal artery biopsy:Granulomatous arteritis with giant cells and intimal hyperplasia; skip lesions can cause false negatives
CT angiography / MR angiography / PET-CT (specialist):Large-vessel aortitis, stenosis, aneurysm, or other extracranial involvement
Baseline monitoring before prolonged steroids or biologics:Glucose/HbA1c, renal and liver profile, bone risk assessment; for tocilizumab also neutrophils, platelets, lipids and infection screening (for example TB/hepatitis)

Management

Lifestyle Modifications

  • Treat as same-day emergency pathway; do not delay glucocorticoids while awaiting tests if suspicion is high
  • Safety-net urgently for any visual symptoms (same-day ophthalmology/emergency review)
  • Cardiovascular risk reduction (smoking cessation, BP/lipid/diabetes optimisation, exercise as tolerated)
  • Steroid harm minimisation: weight-bearing activity, falls prevention, calcium/vitamin D intake, vaccination planning (avoid live vaccines on significant immunosuppression)

Pharmacological Treatment

Immediate glucocorticoid induction (no visual symptoms)

  • Prednisolone oral 40-60 mg once daily

Start immediately when GCA is strongly suspected; urgent specialist review via fast-track pathway (same day if possible, within 3 working days). Taper slowly under specialist/shared-care guidance.

Visual symptoms or visual loss emergency treatment

  • Methylprednisolone intravenous 500 mg to 1 g once daily for 3 days (specialist regimen)
  • If IV not possible: Prednisolone oral 60-100 mg once daily for up to 3 consecutive days while urgent transfer arranged

Transient or permanent visual loss/diplopia requires same-day ophthalmology assessment. Aim is prevention of further irreversible visual loss, including in the fellow eye.

Steroid-sparing therapy in relapsing/refractory disease (specialist)

  • Tocilizumab 162 mg subcutaneous once weekly (with glucocorticoid taper)

Consider in selected patients to reduce cumulative steroid exposure. Contraindications/cautions include active serious infection; monitor neutrophils, platelets, liver enzymes and lipids; avoid live vaccines during therapy.

Prevention of treatment-related adverse effects

  • Alendronic acid 70 mg orally once weekly
  • Colecalciferol with calcium as per product dosing
  • Omeprazole 20 mg once daily when GI risk is present

Assess fracture risk and GI risk early in prolonged steroid courses. Check bisphosphonate suitability (for example oesophageal disorders, inability to remain upright, severe renal impairment). Monitor for steroid complications: hyperglycaemia, hypertension, infection, mood change/psychosis, cataract, glaucoma, osteoporosis.

Surgical / Interventional

  • Endovascular or open surgical repair for thoracic/other aortic aneurysm or dissection when indicated by vascular specialists
  • Intervention for critical large-artery stenosis in selected cases (specialist vascular decision)

Complications

  • Permanent visual loss (partial or complete), including bilateral involvement risk if untreated
  • Aortic aneurysm (often thoracic) and aortic dissection
  • Large-artery stenosis causing limb claudication or cerebrovascular insufficiency
  • Stroke or transient ischaemic attack
  • Myocardial infarction, heart failure, and peripheral arterial disease risk increase
  • Scalp necrosis
  • Peripheral neuropathy or cranial nerve palsies
  • Adverse effects of long-term corticosteroids (diabetes, fractures/osteoporosis, weight gain, bruising, cataract/glaucoma, infection)

Prognosis

Most patients improve quickly after starting glucocorticoids, but relapse is common (up to about 50%) and prolonged treatment is typical (often 1-2 years, sometimes longer low-dose therapy). Overall survival is usually similar to age-matched populations, but long-term surveillance is important because large-vessel complications, particularly aortic aneurysm/dissection, remain increased.

Sources & References

💊BNF Drug References(2)

✅NICE Guidelines(1)

📖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. 1839)[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. 1158, 1159)[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. 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. 1092)[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. 273)[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. 1090)[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. 1158, 1159)[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. 274, 275)[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. 935, 936)[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. 1839)[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. 552, 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. 570, 571)[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. 877, 878)[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. 903, 904)[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. 794, 795)[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. 878)[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. 904)[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. 877, 878)[context]
  • [Williams, Bailey and Love's Short Practice of Surgery] Norman Williams, Christopher Bulstrode, P Ronan O'Connell - Bailey & Love's Short Practice of Surgery 26E (2013, CRC Press) - libgen.li.pdf(pp. 863)[context]

Sources

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