HHE 2018 | Page 187

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 .

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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

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