rheumatology and
musculoskeletal
Treating giant cell arteritis
Giant cell arteritis remains a clinical emergency, which can
lead to irreversible sight loss. New ‘Fast Track Pathways’, diagnostics
and treatments are improving the standard of care and outcomes
Fiona Coath
MBChB MRCP
Faidra Laskou
MBBS MRCP
Bhaskar Dasgupta
MBBS MD FRCP
Rheumatology
Department, Southend
University Hospital, UK
Giant cell arteritis (GCA) remains a rheumatology
emergency. Critical ischaemia of the temporal
arteries can lead to anterior ischaemic optic
neuropathy and irreversible sight loss. This is
a significant cause of morbidity among these
patients, not least due to subsequent loss of
independence and depression. If the symptoms
of GCA are recognised promptly and treated
appropriately, then the incidence of this
catastrophic event could be reduced. There is
increasing evidence regarding the efficacy and
positive outcomes of ‘Fast Track Pathways’. This is
a process whereby patients are offered rapid access
to specialist clinical assessment, with the goal of
providing a secure diagnosis in as many patients
as possible. Glucocorticoid therapy can then be
continued or importantly stopped if inappropriate.
Evidence from current services of this type has
shown significant reduction in morbidity. For
example, at Southend Hospital, the incidence of
sight loss has been reduced from 37% to 9%. 1 Similar
results have been replicated in other centres.
Presentation and classification
In clinical practice, it is clear there are subgroups
within GCA. Recognition of these subgroups is
important to determine additional investigations
and management. It is no longer sufficient to label
this simply as a ‘headache’ disease. Some patients
may have isolated cranial GCA, presenting with
headaches and ischaemic symptoms such as jaw
or tongue claudication and uniocular visual
disturbance. However many are found to have
more extensive large vessel involvement, termed
large vessel giant cell arteritis (LV-GCA). With the
advent of improved imaging techniques, the
estimated prevalence of this group is greater than
previously recognised; 12–37% depending on the
modality used. 2 A clinical suspicion of LV-GCA can
be prompted by patients presenting with more
predominant constitutional symptoms, including
unintentional weight loss, and night sweats and
fevers, or in patients who have already developed
symptoms of vascular compromise such as limb
claudication secondary to stenotic disease. In
reality, there is a significant degree of symptom
overlap between cranial GCA, LV-GCA and
polymyalgia rheumatica (PMR), and it may be
more accurate to think of them as a spectrum
of disease rather than discrete conditions. 3
Another clinically significant method of
classification is ‘response to treatment’. Figure 1
divides patients into four groups: remission;
relapse; refractory disease; and adverse effects
or intolerance. 4 It is these latter three groups,
outlined in the red box, for which there is
currently an unmet need for effective disease
modifying and glucocorticoid-sparing treatment.
Observational cohort studies report flares in
34–62% of GCA patients, with only 15–20%
achieving sustained remission with GC alone. 3
Investigations
Advances in vascular ultrasound (US) have
transformed the management of GCA in recent
years. EULAR now recommends it as the first-line
investigation in acute GCA if there is appropriate
equipment and expertise available. 5 Vascular US
forms a significant part of ‘Fast Track Pathway’
clinics, as it potentially offers a ‘one-stop shop’
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