What is giant cell arteritis?

Giant cell arteritis (GCA), also called temporal arteritis, is the most common primary systemic vasculitis in adults in high-income countries — affecting adults almost exclusively over 50 years (peak incidence 70-80 years, 3:1 female:male ratio). It is a granulomatous vasculitis of large and medium arteries, predominantly affecting the branches of the external carotid artery (temporal arteries, occipital arteries, posterior ciliary arteries) and the aorta and its branches. The characteristic symptoms: new severe headache (temporal or occipital); scalp tenderness (cannot brush hair without pain); jaw claudication (pain on chewing forcing rest); and — most feared — sudden visual loss from optic nerve ischaemia.

How quickly must GCA be treated?

If GCA is suspected — especially if the patient reports any visual symptoms (transient visual loss, diplopia, visual blurring) — high-dose corticosteroids must be given WITHIN HOURS. The anterior ischaemic optic neuropathy (AION) that causes permanent blindness can progress from "warning symptoms" (amaurosis fugax) to irreversible visual loss within hours to days. Do NOT: wait for a temporal artery biopsy result; wait for specialist referral; wait for the ESR result if clinical suspicion is high. Do: start prednisolone 60mg/day immediately (or IV methylprednisolone 500-1000mg if visual loss has already occurred). Temporal artery biopsy remains positive for up to 2-4 weeks after corticosteroids start — biopsy can be arranged after treatment begins.

What are the treatment options?

Standard treatment: prednisolone starting at 40-60mg/day (higher doses with visual symptoms); taper slowly over 12-24 months (too rapid tapering → relapse). Tocilizumab (Actemra): now first-line biologic in most guidelines; recommended as an adjunct to corticosteroids for patients who: have significant corticosteroid-related adverse effects; have relapsing disease; have high cumulative corticosteroid risk (diabetes, osteoporosis, hypertension, obesity). SC injection weekly or fortnightly; monitor for infections (including diverticulitis), neutropenia, lipids. Aspirin: low-dose aspirin (75-100mg) is recommended by some guidelines to reduce cranial ischaemic events — though evidence is mixed; discuss risk-benefit. Methotrexate: modest steroid-sparing effect; an alternative when tocilizumab is not available or tolerated.

What is polymyalgia rheumatica and how is it related to GCA?

Polymyalgia rheumatica (PMR) is a clinical syndrome of bilateral proximal (shoulder and hip girdle) aching and stiffness with elevated inflammatory markers (ESR, CRP), occurring almost exclusively in adults over 50. The stiffness is typically worst in the morning and lasts more than 45 minutes, making it hard to dress or get out of bed. Muscle strength is normal (unlike inflammatory myopathy). PMR and GCA are intimately related: approximately 40-50% of GCA patients have concurrent PMR features; approximately 15-20% of PMR patients develop GCA during follow-up. PMR requires only prednisolone 15mg — any PMR patient developing new headache, visual symptoms, jaw claudication or scalp tenderness must be urgently reassessed for GCA and started on 40-60mg if GCA is suspected.

Is GCA related to age?

Yes — profoundly. GCA almost never occurs under 50 years; peak incidence is 70-80 years. Incidence in the UK: approximately 2-3 per 10,000 persons over 50; approximately 7 per 10,000 over 70. It is significantly more common in Scandinavian/Northern European populations (possibly related to HLA-DRB1*04 association). It is rare in Asian and Black populations. The condition is associated with ageing of the immune system (immunosenescence) — granuloma formation reflecting an altered CD4+ T-cell response to arterial wall antigens. As populations age globally, GCA incidence is expected to increase.

How does GMJ News cover giant cell arteritis?

GMJ News covers the blindness emergency (treat within hours), tocilizumab GiACTA trial (first drug approved for GCA), temporal artery ultrasound halo sign, PMR co-occurrence, jaw claudication specificity, large vessel GCA and PET-CT, temporal artery biopsy (2-4 week window), AION pathophysiology, and corticosteroid tapering protocols. GCA — the most common systemic vasculitis in adults over 50 — is directly relevant to PHIG's rheumatology and emergency medicine programme and Georgia's ageing population health priorities.

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Giant Cell Arteritis

GMJ News knowledge hub · last reviewed September 2026 · Georgian Medical Journal

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Giant cell arteritis (GCA) — a granulomatous vasculitis of large and medium vessels predominantly affecting adults over 50, causing severe temporal headache, jaw claudication and the risk of sudden, permanent, irreversible blindness from anterior ischaemic optic neuropathy in approximately 15-20% of untreated patients — is the most common primary systemic vasculitis in adults in high-income countries and represents an ophthalmic emergency: patients with visual symptoms require high-dose corticosteroids within hours, not after awaiting a temporal artery biopsy result (WHO). Tocilizumab (Actemra) — an IL-6 receptor antagonist — became the first drug specifically FDA and EMA approved for GCA in 2017 (GiACTA trial, NEJM): achieving sustained remission in 56% vs 14% of placebo patients at 52 weeks and dramatically reducing cumulative prednisolone dose — transforming what had previously been purely a corticosteroid-dependent condition.

Key messages

Blindness risk — treat within hours, not days

GCA with visual symptoms (amaurosis fugax, diplopia, visual blurring) must be treated with high-dose corticosteroids WITHIN HOURS — not after awaiting temporal artery biopsy results, blood test confirmation or specialist review. Anterior ischaemic optic neuropathy (AION) from GCA causes sudden, permanent, irreversible blindness. Prevention requires immediate action.

Tocilizumab — first drug approved specifically for GCA (FDA/EMA 2017)

The GiACTA trial (NEJM 2017): tocilizumab (anti-IL-6R) 162mg SC weekly or every 2 weeks vs placebo — 56% sustained remission at 52 weeks vs 14% placebo. Dramatically reduces cumulative corticosteroid dose and corticosteroid-related morbidity (diabetes, osteoporosis, hypertension). FDA/EMA approved 2017 — the first drug ever approved specifically for GCA, transforming a purely steroid-dependent condition.

Jaw claudication — the most specific GCA symptom

Jaw claudication (pain on chewing — particularly with tough foods like bread crust — that forces the patient to pause chewing) is caused by ischaemia of the masseter muscles from internal maxillary artery involvement. It is the most specific clinical symptom for GCA (specificity approximately 94%). Combined with temporal headache in a patient over 50 → ESR >50 → start steroids immediately.

PMR — the clinical companion of GCA

Polymyalgia rheumatica (PMR) co-occurs with GCA in approximately 40-50% of cases: bilateral shoulder and pelvic girdle aching and stiffness (worse in the morning, >45 minutes duration); normal muscle strength; dramatic response to low-dose prednisolone (15mg — vs 40-60mg for GCA). Approximately 15-20% of PMR patients develop GCA during follow-up. Any PMR patient developing new headache, visual symptoms or jaw claudication must be evaluated urgently for GCA.

Temporal artery biopsy — still the gold standard but not a reason to delay

Temporal artery biopsy (TAB): minimum 2-3cm segment of temporal artery (skip lesions occur) → histology showing granulomatous inflammation with giant cells, infiltration of the media, fragmentation of the internal elastic lamina. Sensitivity approximately 77-86% for positive biopsy. Key: TAB remains positive for up to 2-4 weeks after corticosteroids are started — do NOT delay starting treatment to wait for the biopsy. EULAR 2023: ultrasound (halo sign of the temporal arteries) is now the preferred first-line imaging, in many centres replacing biopsy.

Large vessel GCA — the underrecognised form

Approximately 40-60% of GCA patients have large vessel involvement (aorta, subclavian arteries, axillary arteries) — visible on FDG-PET/CT or MRA. Large vessel GCA may present differently: limb claudication; asymmetric arm blood pressures; absent radial pulse; aortic aneurysm (late complication). The temporal artery biopsy may be negative in large vessel predominant GCA — PET-CT is the key diagnostic investigation.

Key statistics

15-20%

of untreated GCA patients develop permanent blindness from AION

ESC/ACR

2017

year tocilizumab received FDA/EMA approval for GCA (first ever drug for GCA)

FDA/EMA 2017

56%

sustained remission at 52 weeks with weekly tocilizumab (GiACTA, NEJM 2017)

NEJM 2017

94%

specificity of jaw claudication for GCA diagnosis

ACR/EULAR

>50 years

GCA predominantly affects adults over 50; peak incidence 70-80 years; 3:1 female:male

EULAR

PMR in ~50%

of GCA patients — and 15-20% of PMR patients develop GCA during follow-up

EULAR

Giant cell arteritis — clinical manifestations and frequency

Source: EULAR/ACR. Headache most common; jaw claudication most specific; blindness the feared complication.

Glossary of key terms

Anterior ischaemic optic neuropathy (AION)
Ophthalmology/NeurologyGCA-induced ischaemia of the posterior ciliary arteries → ischaemia of the optic nerve head → sudden, painless visual loss (typically as an altitudinal field defect — loss of the upper or lower visual field). GCA is the most common cause of AION in adults over 50 (arteritic AION). Non-arteritic AION (NAION) — more common — results from small vessel disease in hypertension/diabetes without GCA. Fundoscopy in arteritic AION: pale, swollen optic disc. Once visual loss from AION occurs, it is almost always permanent and irreversible — treatment prevents the fellow eye from being affected, not recovering the lost vision. Amaurosis fugax (transient monocular vision loss — seconds to minutes) is the warning sign preceding AION.

Tocilizumab (Actemra) for GCA
FDA 2017/RocheA recombinant humanised anti-IL-6R monoclonal antibody — blocking IL-6 signalling. In GCA, IL-6 drives the granulomatous vasculitis and systemic inflammation. GiACTA trial (Stone et al., NEJM 2017): SC tocilizumab 162mg weekly or fortnightly + 26-week prednisolone taper vs placebo + standard prednisolone taper. Primary endpoint: sustained remission at 52 weeks. Results: weekly tocilizumab 56%; fortnightly 53%; placebo 14-23% (two prednisone taper regimens). Cumulative prednisolone dose dramatically lower with tocilizumab (1,862mg vs 3,296mg). Adverse effects: neutropenia; hyperlipidaemia; liver enzyme elevation; infections (including diverticulitis — significant risk).

Temporal artery ultrasound (halo sign)
EULAR/RadiologyHigh-resolution B-mode ultrasound of the temporal (and axillary) arteries can detect the dark, hypoechoic halo surrounding the inflamed artery wall — called the halo sign — caused by oedema of the arterial wall in active GCA. Sensitivity approximately 77-90%; specificity approximately 96% for the temporal artery halo sign. EULAR 2023 updated recommendations: ultrasound is the preferred first-line diagnostic investigation for GCA in centres with expertise — replacing temporal artery biopsy in many cases. The axillary artery is also commonly involved in GCA and should be included in US examination.

Polymyalgia rheumatica (PMR)
EULAR/ACRA clinical syndrome of: bilateral aching and stiffness of the shoulder girdle (deltoid areas); hip and pelvic girdle (hip abductors, proximal thighs); morning stiffness >45 minutes; elevated ESR/CRP; normal muscle enzymes (CK/aldolase normal — unlike inflammatory myopathy). Dramatic response to prednisolone 15mg/day — relief within 24-72 hours (a diagnostic test in practice). Starting dose: 15mg (GCA requires 40-60mg). Risk of GCA during PMR follow-up: approximately 15-20%. PMR is one of the most common rheumatological conditions in adults over 50 (incidence ~50/100,000 in UK Caucasians >50 years).

Large vessel GCA — PET-CT diagnosis
ESC/RadiologyFDG-PET/CT (fluorodeoxyglucose positron emission tomography) images metabolic activity of inflamed vessel walls — the aorta, subclavian, axillary and femoral arteries show increased FDG uptake in large vessel GCA. Sensitivity approximately 80-90% for large vessel GCA at diagnosis (before steroids are started). PET-CT is the preferred investigation when: temporal artery biopsy and ultrasound are negative but clinical suspicion remains high; large vessel involvement is suspected (arm claudication, asymmetric blood pressures). Note: FDG-PET must be performed before or within the first few days of corticosteroid therapy — steroids rapidly normalise the FDG uptake.

ESR and CRP in GCA
Laboratory/DiagnosisErythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) are almost universally elevated in GCA: ESR typically >50 mm/h (often >100 mm/h — the "80-100 club"); CRP often >30-50 mg/L. Absence of raised ESR (<50 mm/h): occurs in approximately 5-10% of GCA — a normal ESR does not exclude GCA. CRP is more sensitive than ESR in early or treated GCA. After starting corticosteroids: both normalise rapidly (days to weeks) — normalization is the therapeutic target. Elevated CRP at symptom resolution is associated with higher relapse risk.

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