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Dr Marwan Bukhari, Consultant Rheumatologist, University Hospitals of Morecambe Bay NHS Foundation Trust and Honorary Senior Lecturer, University of Manchester, and Dr Vanessa Quick, Consultant Rheumatologist, Luton & Dunstable University Hospital

Giant cell arteritis (GCA) is the most common idiopathic large vessel vasculitis and is characterised by granulomatous inflammation of the media of large and medium arteries in patients over the age of 50 years. It usually affects the arteries of the upper limb and thoracic aorta, but most commonly affects branches of arteries arising from the aortic arch, particularly cranial branches of the carotid arteries.1

Symptoms of GCA include headache, scalp tenderness, jaw and tongue claudication, as well as systemic features including malaise, weight loss, fever, night sweats, and tiredness.1,2 Visual symptoms, amaurosis fugax, blurring, and diplopia, may also occur and this may result in permanent visual loss, making it the most feared complication of GCA.2,3 Other serious complications include stroke,3 and aortic aneurysm.

Early recognition and treatment of GCA is important in order to prevent blindness and other ischaemic complications.2 Headache, scalp tenderness, jaw claudication, visual loss, and stroke are all classified as cranial manifestations of GCA.2 Patients presenting with a history of new visual loss (transient or permanent) or diplopia should be evaluated as soon as possible, on the same calendar day, by an ophthalmologist.2

Giant cell arteritis may be identified using clinical assessment and laboratory features, including raised inflammatory markers such as erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP). However, a definitive diagnosis can only be made following a positive temporal artery biopsy, or other positive imaging such as vascular ultrasound, magnetic resonance imaging (MRI), or positron emission tomography with computerised tomography (PET-CT) in the right clinical context.

The disease has a variable clinical course. It may respond to short-term treatment with high-dose glucocorticoids,2,4,5 and may be classified as ‘relapsing’ (often with multiple flares) or ‘refractory’ to treatment.4,5

Acute treatment of disease

Giant cell arteritis is considered a medical emergency because of the risk of blindness. Glucocorticoids, usually prednisolone, are the mainstay of treatment and are initially given at a dose varying between 40 mg and 60 mg daily, depending on the severity of the presentation and presence of ophthalmic complications, in order to induce remission in active GCA.2,4,5 The high-dose glucocorticoids are tapered to zero over approximately 12–24 months,2,4,5 although more recent guidelines support a more rapid dose reduction for patients at high risk of glucocorticoid toxicity and/or those receiving concomitant glucocorticoid-sparing therapy,2,5 i.e. a 6-month taper can be attempted for patients on tocilizumab.5

Patients with suspected GCA, who present with headaches and no predictors of neuro-ophthalmic complications may be started at a lower dose of 40 mg daily, while those with ischaemic symptoms including diplopia, amaurosis fugax, tongue claudication, or stroke are usually started on 60 mg daily. Co-morbidities such as uncontrolled diabetes, hypertension, or anxiety may justify a lower dose range. Intravenous methylprednisolone may also be initiated in patients with GCA if there is acute or intermittent visual loss.2,5

Relapsing and refractory GCA

There are no formal definitions of relapsing and refractory GCA in the British Society of Rheumatology (BSR) or NICE guidelines.2,4 The NHS England Blueteq form for tocilizumab provides a prescriptive definition in order for treatment to be reimbursed,6 and the recommendations from the European League Against Rheumatism (EULAR) also provide some wording (see Table 1).5

Relapsing GCA

Relapsing GCA may be defined as ‘a clear and evidenced recurrence of GCA symptoms or ischaemic complications in those who previously responded to treatment’ (see Table 1). While glucocorticoids remain the first-line treatment, relapses are common (one in three patients receiving glucocorticoids alone for at least a year still experience relapse).7

For symptoms that may signify a relapse of GCA during the glucocorticoid taper, the BSR advises further evaluation and, if judged to be due to GCA relapse, escalation of glucocorticoid treatment. For patients with:2

  • return of headache—return to previous higher prednisolone dose
  • jaw or tongue claudication—consider high-dose oral prednisolone (40–60 mg daily) with or without glucocorticoid-sparing agent
  • weight loss, fever, night sweats, anaemia, persistent acute phase response, new/recurrent polymyalgia rheumatica symptoms, limb claudication, abdominal pain, or back pain—investigate with vascular imaging (MRI, CT, or fluorodeoxyglucose PET-CT), and consider increasing oral prednisolone and/or adding a glucocorticoid-sparing agent. (Ultrasound scan [USS] may also be used.6) Patients with new visual loss or diplopia should be urgently evaluated by an ophthalmologist.

Refractory GCA

This may be defined as ‘inability to induce remission in patients with GCA despite optimal standard of care’ (see Table 1).

Table 1: Definitions of relapsing and refractory GCA5,6

NHS England SSC1894 - Blueteq form 2018


A patient with GCA who has previously responded to treatment, subsequently demonstrating one of the following:

  1. biopsy or imaging (e.g. USS/CT/MRA/PET-CT) evidence of currently active or progressive GCA
  2. evidence of definite ischaemic complications, such as acute ischaemic optic neuropathy, scalp necrosis, limb claudication, stroke or any other ischaemic or vascular complication due to GCA
  3. previous evidence of GCA (on biopsy or imaging, e.g. USS/CT/MRA/PET-CT) and clear recurrence of previous symptoms and/or increased inflammatory markers (e.g. CRP, ESR, PV) for which no other cause for increased inflammatory markers has been identified (e.g. active infection or other cause)


Inability to induce remission in a patient with GCA who has either:

  1. a definitive diagnosis of GCA (on biopsy or imaging (e.g. USS/CT/MRA/PET-CT)
  2. definite ischaemic signs or symptoms with a significant risk of end-organ damage or vascular damage, despite optimal standard care for which no other cause has been identified

EULAR 2018


EULAR recommends the use of the terms major relapse or minor relapse, as prognosis and treatment will differ depending on the presence of ischaemia and/or vascular damage:

Major relapse: Recurrence of active disease with either of the following:

  1. clinical features of ischaemia (including jaw claudication, visual symptoms, visual loss attributable to GCA, scalp necrosis, stroke, limb claudication)
  2. evidence of active aortic inflammation resulting in progressive aortic or large vessel dilatation, stenosis, or dissection

Minor relapse: Recurrence of active disease, not fulfilling the criteria for a major relapse


Inability to induce remission (with evidence of reactivation of disease, as defined below under ‘Active disease’) despite the use of standard care therapy

Active disease: 

  1. the presence of typical signs or symptoms of active LVV
  2. at least one of the following:
    1. current activity on imaging or biopsy
    2. ischaemic complications attributed to LVV
    3. persistently elevated inflammatory markers (after other causes have been excluded)

USS=ultrasound scan ; CT=computerised tomography; MRA=magnetic resonance angiography; PET-CT=positron emission tomography with CT; GCA=giant cell arteritis; CRP=C-reactive protein; ESR=erythrocyte sedimentation rate; PV=plasma viscosity; LVV=large vessel vasculitis.

Side-effects of glucocorticoids in GCA

Although glucocorticoids are efficacious in treating GCA, their side-effects are well-documented. These include osteoporosis, diabetes, skin thinning, muscle weakness, cataracts, glaucoma, high blood pressure, and mood or psychological disturbance.2,4,5,8–11

Patients with relapsing or refractory GCA are frequently treated with high doses of glucocorticoids tapered over varying time periods. This means that patients with GCA often experience high cumulative doses, which are associated with a considerable burden in terms of glucocorticoid-related adverse events.2,4,5,8–11

As the population affected is generally older, patients with GCA may have multiple co-morbidities and experience polypharmacy, therefore the impact of high cumulative doses or long-term steroid use may be increased.

In a UK primary care database, a third of patients (1034/3074) with GCA and at least 2-years follow up, had a total cumulative steroid dose of ≥10 g.8 In a UK clinical practice research datalink analysis of patients with GCA, patients with the highest cumulative dose of glucocorticoids of >10 g (10.1–20.0 g) versus ≤3 g gave an odds ratio of 2:1 of developing diabetes (95% CI 1.3,3.3) and 1.5 times increase in odds of osteoporosis (95% CI 1.1,2.1).9 Additional data from a study of 2497 veteran patients with GCA, in the United States, showed that for each 1 g increase in glucocorticoid exposure (approximately 67 days at an average dose of 15 mg), there is an increase in the hazard ratio of:10

  • 3% for developing cataracts (HR=1.03, 95% CI 1.02–1.05, p<0.001)
  • 5% for experiencing a bone-related adverse event (HR=1.05, 95% CI 1.03–1.06, p<0.001)
  • 5% for a new diagnosis of diabetes mellitus (HR=1.05, 95% CI 1.03–1.07, p<0.001)
  • 5% for developing glaucoma, (HR=1.05, 95% CI 1.01–1.08, p=0.005).

There is therefore a need for immunosuppressive therapies that are able to induce long-term remission while minimising or avoiding the adverse effects of glucocorticoids. There continues to be a need for effective glucocorticoid-sparing therapies.

Other treatment options

Steroid-sparing agents

Recommendations from BSR and EULAR do not include the use of non-methotrexate (MTX) disease-modifying antirheumatic drugs (DMARDs) due to lack of robust efficacy from existing studies.2,5 The BSR guideline does, however, make a conditional recommendation for MTX in GCA: MTX might be considered for GCA, in combination with a glucocorticoid taper, in patients at high risk of glucocorticoid toxicity or who relapse.2 The guideline also states there is insufficient evidence to recommend any other oral immunosuppressive agent in GCA, including azathioprine, leflunomide or mycophenolate mofetil, and, furthermore, it does not recommend tumour necrosis factor inhibitors for GCA.2

The EULAR 2018 update found that data for other adjunctive therapies are either sparse (abatacept), derived from low-quality studies (ustekinumab, azathioprine, leflunomide, cyclophosphamide, dapsone, etanercept), or negative (adalimumab, infliximab, cyclosporine).5


Following publication of the results from the largest therapeutic trial of tocilizumab in giant cell arteritis (GiACTA),12 tocilizumab, a selective IL-6 receptor antagonist, was approved as the first licensed treatment for GCA by the US and European regulatory authorities in 2017. This trial investigated the efficacy and safety of tocilizumab in combination with a standardised 6-month prednisone* taper. Patients receiving placebo had one of two alternative prednisone tapering schedules, completing the taper by 26 weeks and 52 weeks if the patient remained relapse-free (see Figure 1).12

RoActemra supplement Figure 1

GiACTA part 1

The primary endpoint (see Figure 1) was achieved in 56% (56/100) of patients treated in the tocilizumab group + 26-week prednisone taper, whereas in the placebo groups this was achieved by 14% (7/50) and 18% (9/51) of patients tapering prednisone over 26 weeks and 52 weeks, respectively (p<0.001 for both analyses).12

In prespecified subgroup analyses:15

  • the proportion of patients with relapsing GCA who achieved sustained remission at 52 weeks was 53% (28/53) in the tocilizumab group + 26-week prednisone taper compared to 7% (2/27) and 14% (4/28) in the placebo groups with 26-week and 52-week prednisone taper, respectively
  • the proportion of patients with newly diagnosed GCA who achieved sustained remission at 52 weeks was 60% (28/47) in the tocilizumab group + 26-week prednisone taper compared to 22% (5/23) and 22% (5/23) in the placebo groups with 26-week and 52-week prednisone taper, respectively.

Over 52 weeks, 23% (23/100) of patients experienced flare in the tocilizumab group + 26-week prednisone taper compared to 68% (34/50) and 49% (25/51) of patients in the placebo groups with 26-week and 52-week prednisone tapers, respectively.12

Median cumulative glucocorticoid exposure was reduced by >50% in the tocilizumab + 26-week prednisone taper arm (1862 mg; n=100), compared with placebo and a 26-week prednisone taper arm (3296 mg; n=50) and with placebo and a 52-week prednisone taper arm (3818 mg; n=51).12

The percentages of patients with adverse events were similar in all the trial groups, but fewer patients reported serious adverse events in the group that received tocilizumab weekly + 26-week prednisone taper, 15% (15/100), versus 22% (11/50) in the placebo group with 26-week prednisone taper, and 25% (13/51) in the placebo group with 52-week prednisone taper.12

Twelve month cost-effectiveness data from GiACTA resulted in a positive recommendation in the NICE Technology Appraisal (TA518) for the use of tocilizumab for 1 year in patients with relapsing and refractory disease (see Box 1).4 The data also led to positive guidance from the Scottish Medicines Consortium (SMC), which allows the use of tocilizumab in all patients with GCA that fulfil its criteria of relapsing, refractory, and newly diagnosed patients (see Box 1).16

Box 1: NICE and SMC recommendations for the treatment of giant cell arteritis (GCA) in adult patients4,16

NICE April 2018

Tocilizumab, when used with a tapering course of glucocorticoids (and when used alone after glucocorticoids), is recommended as an option for treating giant cell arteritis in adults, only if:

  • they have relapsing or refractory disease
  • they have not already had tocilizumab
  • tocilizumab is stopped after 1 year of uninterrupted treatment at most and
  • the company provides it with the discount agreed in the patient access scheme

SMC September 2018

ADVICE: following a full submission assessed under the orphan medicine process

tocilizumab (RoACTEMRA®) is accepted for restricted use within NHS Scotland

Indication under review: the treatment of Giant Cell Arteritis (GCA) in adult patients

SMC restriction: treatment with tocilizumab is subject to a 12 month clinical stopping rule.

GiACTA part 2

Long-term data from GiACTA (part 2) have now been published and they highlight, in an observational setting, what happened to the patients in part 1 of the study when they stopped tocilizumab treatment at 12 months.13

The main endpoint for GiACTA part 1 was sustained remission,12 whereas in GiACTA part 2 the focus was on clinical remission, which was defined as the absence of flare (based on investigator’s assessment, the recurrence of signs/symptoms of GCA and/or ESR ≥30 mm/h attributable to GCA), and the main endpoint was maintained clinical remission, which was defined as ‘no flare’ reported during the entire part 2, up to the end of the study (week 156), regardless of treatment.13

Eighty-five patients originally assigned to the tocilizumab + 26 week prednisone taper group entered part 2 of the study, 95% (81/85) of whom were in clinical remission. For the placebo + 26-week prednisone taper, 44 patients entered part 2, with 75% (33/44) being in clinical remission; 46 patients in the placebo + 52 week prednisone taper entered part 2, with 74% (34/46) being in clinical remission. Of the patients in clinical remission at part 2 entry, 47% (38/81), 55% (18/33), and 59% (20/34) continued to be in remission at 3 years in the original tocilizumab + 26-week prednisone taper, placebo + 26-week prednisone taper and placebo + 52-week prednisone taper groups, respectively.13

Of these patients remaining in clinical remission at 3 years, 66% (25/38), 39% (7/18), and 50% (10/20) were treatment (tocilizumab and steroid) free in the original tocilizumab + 26-week prednisone taper, placebo + 26-week prednisone taper and placebo + 52-week prednisone taper groups, respectively.13

Over 3 years of the GiACTA study, median time to first flare was 575 days in the original tocilizumab + 26-week prednisone taper group, 162 days in the placebo + 26-week prednisone taper group, and 295 days in the placebo + 52-week prednisone taper group. No new safety signals were observed with tocilizumab exposure in GCA patients during the 3-year study.13

How this data impacts on clinical treatment pathways is yet to be determined. However, the current data may give clinicians, and their patients, confidence that even after only 12 months of treatment, patients on tocilizumab may continue to remain in remission for up to 3 years. Further analysis of the cost-effectiveness of the 3-year data would be of benefit and may support future reimbursement.

Tocilizumab: recommendations for use and reimbursement

Guidance on the use of tocilizumab in patients with GCA has also been issued by BSR and EULAR:2,5

  • BSR: Strong recommendation: tocilizumab can be considered for GCA, in combination with a glucocorticoid taper, especially in patients at high risk of glucocorticoid toxicity or who relapse2
  • EULAR: adjunctive therapy [using tocilizumab] should be used in selected patients with GCA (refractory or relapsing disease, the presence of, or an increased risk of, glucocorticoid-related adverse effects or complications). Additional commentary within the guideline states, ‘In patients treated with tocilizumab, the published rapid 26-week steroid taper may be attempted in order to significantly reduce the cumulative dose’.5


In order for patients with GCA, who fulfil the criteria in NICE TA518 to receive treatment with tocilizumab,4 NHS England have developed a Blueteq form that hospital trusts must use to request reimbursement as part of NHS commissioning.6 The form states that patients must have either relapsing or refractory GCA and also requests additional criteria, including a definitive diagnosis, that must be fulfilled before patients can receive drug treatment.

The easiest cases to be approved are those where patients have a documented positive biopsy or diagnosis confirmed by imaging (such as USS/CT/magnetic resonance angiography [MRA]/PET-CT). Patients without a documented diagnosis, for example those who were treated with glucocorticoids prior to a definitive diagnosis, can still be considered for tocilizumab treatment if they meet other criteria, such as evidence of definite ischaemic complications, or previous evidence of GCA (on biopsy or imaging), and they have clear recurrence of previous symptoms and/or increased inflammatory markers. In these cases, clinicians report successful reimbursement attempts when they have discussed the case as part of a multidisciplinary team (MDT) meeting.

The recommendation from NICE specifically only permits treatment/reimbursement for 12 months, which has limited the use of tocilizumab in England.4 In Scotland, the SMC recommendation also states there is a 12-month restriction, however within the commentary of the guidance document it also provides flexibility on the continuation of treatment: ‘based upon the chronic nature of GCA, treatment beyond 52 weeks should be guided by disease activity, physician discretion, and patient choice’.16 The process in Scotland for reimbursement is simpler as the Blueteq process does not exist in NHS Scotland. Clinician feedback is that local NHS Boards have more flexibility to decide on patient eligibility and length of treatment.

Case studies have been included providing examples of how funding has been achieved for a patient in England with relapsing GCA (see Box 2, case study 1) and a patient with refractory GCA (see Box 2, case study 2).

Box 2: Case studies

Study 1

  • A 71-year-old Caucasian woman presented in July 2017 with a 2-month history of polymyalgia, night sweats, and weight loss, then one week of bitemporal/occipital headache, bitemporal tenderness, and left-sided jaw claudication. Prednisolone 60 mg daily was commenced, bloods were drawn and she was urgently referred to the local GCA FTP clinic where she was seen the next day
  • Positive findings on examination included bilateral temporal artery tenderness and limited active shoulder abduction to 80 degrees bilaterally. Pre-prednisolone bloods in primary care revealed CRP 54 mg/l, ESR 17 mm/h, and platelets 457x109/l. Vascular ultrasound showed a florid bilateral temporal artery halo sign, confirming the diagnosis of GCA. Axillary artery ultrasound was normal
  • All GCA symptoms resolved after 3 weeks prednisolone 60 mg daily and CRP normalised to 2 mg/l. The BSR GCA prednisolone regimen was then attempted. However, from November 2017 to June 2018 she suffered from grumbling, low-grade active disease (mild intermittent GCA headache and CRP >5 mg/l) and two frank GCA relapses (GCA headache, night sweats, CRP 7–25 mg/l) requiring a slowing of reduction, or increase in prednisolone dose, despite addition of methotrexate 20 mg weekly. Prednisolone dose increases were limited by multiple glucocorticoid-related toxicities, including weight gain, Cushingoid habitus, severe anxiety, pre-diabetic hyperglycaemia, hypertension, and osteopenia
  • In November 2018, on 7 mg prednisolone daily, she relapsed again (headache, temporal tenderness, night sweats, CRP 7 mg/l). Repeat vascular ultrasound revealed a positive right temporal artery halo sign. Symptoms resolved when prednisolone was increased to 12.5 mg daily. Tocilizumab had now been approved by NICE for relapsing and refractory GCA,4 and an application for tocilizumab was approved by the local MDT. The patient commenced 1 year of tocilizumab 162 mg subcutaneous weekly, with a planned GiACTA prednisolone reduction regimen, starting from 12.5 mg daily. In December 2019 she had been prednisolone-free for over 6 months without GCA flare or adverse effect from tocilizumab. Her anxiety, hypertension, and weight had improved. Her Cushingoid habitus and pre-diabetic hyperglycaemia had resolved.


  • The case was approved by the local MDT because the NICE definition for relapsing GCA was fulfilled: she had a secure diagnosis of GCA, was deemed to have received optimal standard care, and had developed clear recurrence of previous symptoms for which no other cause was identified
  • Biopsy or imaging confirmation of GCA is only required on one occasion at diagnosis or flare: specialist-led GCA FTPs including vascular ultrasound facilitate this at diagnosis, so that confirmation is not mandated at flare, when it is more challenging to obtain, however, for this patient the presence of a halo at flare strengthened this case
  • Optimal standard care has not been defined by NICE, but should follow local protocol, based on published guidelines such as that from BSR; lower dose prednisolone regimens may still constitute optimal care if dose reduction is required in those who develop glucocorticoid toxicity
  • Neither NICE, SMC, nor NHS England mandate the use of a conventional DMARD before tocilizumab,4 but some MDTs may consider it as an alternative treatment option if there are no ongoing ischaemic symptoms or complications and no persistent extensive disease on imaging, although evidence for efficacy is weak. In this case, methotrexate was used before tocilizumab was licensed.

Study 2

  • An 82-year-old man was referred in November 2015 with sudden-onset complete left visual loss following 2 weeks of unilateral headache, tenderness of the scalp, and jaw pain. He recalled many months of increasing stiffness of the torso, shoulder, and hip girdle when he could not turn over in bed. ESR was measured at 52 mm/h and CRP was 64 mg/l. Ophthalmology review confirmed left acute ischaemic optic neuropathy. Glucocorticoids were commenced at a dose of 60 mg daily and, due to administrative error, the patient did not have a temporal artery biopsy and was not seen in rheumatology clinic until February 2016 while he remained on that dose. The dose of prednisolone was tapered according to local protocol, but headache and polymyalgic symptoms returned, associated with a rise in CRP, every time the dose was reduced below 7.5 mg daily. Bone density was in the osteopenic range, but despite this he sustained a fracture of T11
  • In January 2019, 4 years after diagnosis, he was still on 7.5 mg prednisolone daily and his fracture risk assessment tool (FRAX) score indicated that he would benefit from treatment with bisphosphonates. He was unable to tolerate methotrexate 10 mg weekly due to nausea
  • His case was discussed at the local specialist centre MDT, funding was agreed for tocilizumab, and prednisolone was tapered over 3 months to nil; at the time of writing the patient had received 11 months of tocilizumab therapy without GCA flare, or any adverse events.


  • A positive tissue biopsy or imaging is not essential in all cases; evidence of definite ischaemic complications due to GCA can be used instead to escalate to further treatment (i.e. tocilizumab)
  • Neither NICE, SMC, BSR, EULAR, nor NHS England make any recommendations about the use of methotrexate before tocilizumab when treating patients with GCA
  • Based on the current evidence, there is a strong recommendation to use tocilizumab, in combination with a glucocorticoid taper, especially in patients at high risk of glucocorticoid toxicity or who relapse
  • Fractures can occur in osteopenic patients: in one study, before the routine use of bone protection with glucocorticoids, nearly 40% GCA patients developed fractures11 —all patients with GCA should be considered for bone protection at diagnosis, such as a calcium and vitamin D supplement and bisphosphonate.

GCA=giant cell arteritis; FTP=fast-track pathway; CRP=C-reactive protein; ESR=erythrocyte sedimentation rate; MDT=multidisciplinary team; DMARD=disease-modifying antirheumatic drug


In conclusion, the treatment of GCA is continuing to evolve and there continues to be increasing guidance on how best to manage patients. Tocilizumab, in combination with a glucocorticoid taper, is strongly recommended by current guidelines as a treatment option that may benefit patients with GCA, specifically those with relapsing and refractory disease or at high risk of glucocorticoid toxicity.2,5 In Scotland, tocilizumab can also be used in patients with new-onset GCA.16


* Prednisone and prednisolone are both glucocorticoids that work in a similar way. Prednisone is a prodrug which is metabolised by 11-β-hydroxysteroid dehydrogenase liver enzymes to prednisolone.

Conflicts of interest

Dr Bukhari has been sponsored to attend regional, national and international meetings by Roche/Chugai and other pharmaceutical companies. He has received honoraria for speaking and attended advisory boards with Roche/Chugai and other pharmaceutical companies. He has received honoraria from educational groups Revalidaid and TREG consultants.

Dr Quick has received honoraria for educational/advisory services or travel support from Roche and other pharmaceutical companies.

Key points

  • GCA is an unpleasant disease that mainly affects adults over the age of 50—patients may benefit from high-dose glucocorticoids in an acute presentation to avoid severe, life-changing complications
  • While the acute use of glucocorticoids is likely to be beneficial, glucocorticoid doses should be reduced as quickly as possible to avoid glucocorticoid-related side-effects and longer-term morbidity
  • There are now alternative treatment options; tocilizumab is recommended by NICE, SMC, EULAR, and BSR for use in patients with GCA if they meet the relevant criteria
  • Reimbursement for the use of tocilizumab:
    • in England, patients with relapsing GCA and refractory GCA are eligible for reimbursement
    • in Scotland patients with newly diagnosed, relapsing and/or refractory GCA are eligible for reimbursement
  • To apply for tocilizumab funding, it is not always necessary to have a documented positive biopsy or diagnosis of GCA confirmed by imaging if the patient meets other criteria, such as evidence of definite ischaemic complications (for example, acute ischaemic optic neuropathy, scalp necrosis, limb claudication, stroke, or any other ischaemic or vascular complication due to GCA)
  • Data from GiACTA part 2 have highlighted possible outcomes after 12 months of tocilizumab treatment, and cost-effectiveness analyses over the longer study period should be undertaken as soon as possible
  • Following approval by the SMC and NICE, respectively, there is more flexibility to use tocilizumab after 12 months in Scotland than there is in England
  • Neither NICE, SMC, BSR, EULAR, nor NHS England make any recommendations on the use of methotrexate before tocilizumab when treating patients with GCA
  • Based on the current evidence, BSR has given a strong recommendation to use tocilizumab: ‘tocilizumab can be considered for GCA, in combination with a glucocorticoid taper, especially in patients at high risk of glucocorticoid toxicity or who relapse’2
  • There has been a recent increase in approvals for tocilizumab in GCA patients, and it appears that it is becoming easier for clinicians, working as part of the MDT, to navigate the process better in order to get patients the treatment they need
  • Many clinicians are happy to support their peers with any concerns they may have about treatments and/or the application process.


  1. Koster M, Matteson E, Warrington K. Rheumatology 2018; 57 (suppl. 2); ii32–ii42.
  2. Mackie S, Dejaco C, Appenzeller S et al. Rheumatology 2020; 59 (3): e1–e23.
  3. Vodopivec I, Rizzo J. Rheumatology 2018; 57 (suppl._2); ii63–ii72.
  4. NICE. Tocilizumab for treating giant cell arteritis. Technology Appraisal 518. NICE, 2018. Available at:
  5. Hellmich B, Agueda A, Monti S et al. Ann Rheum Dis 2020; 79: 19–30.
  6. NHS England. Specialised Services Circular_SSC1894. Blueteq form. Technology Appraisal 518: Tocilizumab for treating giant cell arteritis. Issued July 2018.
  7. Mainbourg S, Addario A, Samson M et al. Arthr Care Res 2019; 10.1002/acr.23901 
  8. Petri H, Nevitt A, Sarsour K et al. Arthr Care Res 2015; 67 (3): 390–395.
  9. Wilson J, Sarsour K, Collinson N et al. Semin Arthr Rheum  2017; 46 (6): 819–827.
  10. Broder M, Sarsour K, Chang E et al. Semin Arthr Rheum 2016; 46 (2): 246–252.
  11. Proven A, Gabriel S, Orces C et al. Arthr Rheum (Arthr Care Res) 2003; 49 (5): 703–708.
  12. Stone J, Tuckwell K, Dimonaco S et al. N Engl J Med 2017; 377 (4): 317–328.
  13. Stone J, Bao M, Han J et al. Ann Rheum Dis 2019; 78 (suppl. 2): A145
  14. Unizony S, Dasgupta B, Fisheleva E et al. Int J Rheumatol 2013;
  15. Roche data on file: RCUKACTE01691
  16. Scottish Medicines Consortium. Tocilizumab, 162mg solution for injection in pre-filled syringe and pre-filled pen (RoActemra®). SMC2014 For the treatment of Giant Cell Arteritis (GCA) in adult (published September 2018).
This promotional supplement to Guidelines in Practice has been commissioned and funded by Roche Products Limited and Chugai Pharma UK Limited. Roche and Chugai suggested the topic, and selected and briefed the clinicians who have written this article. Roche and Chugai have carried out full review to ensure compliance with UK regulations. The views and opinions of the authors are not necessarily those of Guidelines in Practice, its publisher, advisers, or advertisers. No part of this publication may be reproduced in any form without the permission of the publisher. 

Job code: RCUKACTE01980a

Date of preparation: April 2020