HHE Rheumatology and musculoskeletal supplement 2018 | Page 15

for investigation and treatment. Vascular US can
detect characteristic sonographic findings, which
allows for a diagnosis of GCA without the need
to progress to temporal artery biopsy (TAB).
Specifically the ‘Halo’ sign is indicative of an
acutely inflamed vessel wall. This is seen as a
homogenous, hypo-echoic wall thickening, which
should be appreciable in both the longitudinal
and transverse planes, and does not disappear on
compression with the ultrasound probe. 6 Vascular
US has multiple advantages. Visualising the entire
length of the temporal arteries bilaterally can
give increased sensitivity compared with TAB,
as it minimises the problem of skip lesions.
Furthermore, it is widely available and well
tolerated by patients. There is also reasonable
evidence to suggest that additional ultrasound
of the axillary and subclavian arteries assessing
intima-medial complex thickness would be
a useful screening tool for LV-GCA. 7 At the axillary
artery, an intima-medial complex >1.0mm is
considered abnormal. 8 US changes in acute GCA
typically start to diminish after initiation of
glucocorticoid treatment;however observed
changes at the axillary arteries can persist for
months. 9 The role of vascular US in monitoring
and follow-up is yet to be determined. Further
studies on the persistence of sonographic findings
and effect of glucocorticoids are required.
Cross-sectional imaging may be useful for
assessing disease extent in LV-GCA, as well as
monitoring vascular complications. However there
is currently no consensus on the best modality.
This is a decision that is influenced by practical
constraints as well as clinical considerations.
18
F-FDG PET-CT, MRI and CT have all been utilised.
High-resolution MRI has comparable sensitivity
and specificity to TAB in detecting GCA, as well as
identifying cranial vessel involvement other than
the temporal artery. 10 However these facilities are
not widely available. 18 F-FDG PET-CT attributes the
FDG signal to a precise anatomic location, and is
therefore useful in establishing disease extent and
severity. It is particularly useful in situations where
there is ongoing concern of LV-GCA despite prior
negative tests, or to exclude differential diagnoses
such as infection or malignancy. Athough it should
be interpreted with caution because FDG signal is
attenuated by glucocorticoid use and increased
with vascular re-modelling and atherosclerosis. 11
This could lead to under- and over-diagnosis of
active inflammation, respectively.
Treatment options in GCA
Initial treatment of new onset GCA remains
high-dose glucocorticoids, at a dose of either 1mg/
kg, or a dose equivalent to 40mg prednisolone for
uncomplicated disease and 60mg prednisolone
for those with ischaemic and sight-threatening
presentations. 3 Methylprednisolone pulses may be
required initially for those with severe visual
complications. 3 Yet the traditional view that this
will provide a complete response in all patients
is not borne out in clinical practice. From the
GiACTA trial baseline data, 17% of the overall
cohort was classified as having disease refractory
to glucocorticoids. 12 In PMR, a related condition,
some groups of patients also respond less well
to glucocorticoids, with only 45–55% having
a complete response, 25–27% with a partial
figure 1
Treatment algorithm for LVV ( target refractory group highlighted in the red box)
GCA, TAK Isolated PMR
High dose GC Low dose GC
Outcome
Remission
Relapse
Refractory disease
GC tapering with
monitoring
Adverse effects
intolerance
Adjunctive therapy
Conventional
immunosuppressants
Biologics
Adapted from reference 4
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