POS0431 BASELINE VASCULAR ULTRASOUND OF PMR PATIENTS AT TIME OF DIAGNOSIS STRATIFIES RELAPSE RISK AT 6 MONTHS
Authors: S. Cowley, P. Harkins, C. Kirby, R. Conway, D. Kane
Journal: Annals of the Rheumatic Diseases (2024)

<h3>Background:</h3> It has been reported that up to a quarter of patients with polymyalgia rheumatica (PMR) have subclinical giant cell arteritis (GCA). It is currently uncertain if this finding at diagnosis may predict clinical outcomes or stratify the risk of progression to GCA. <h3>Objectives:</h3> The objective of this study was to determine if the presence of US-identified subclinical GCA in PMR can stratify the risk of PMR relapse and progression to GCA&gt;. <h3>Methods:</h3> 75 newly diagnosed PMR patients who met a clinical diagnosis for PMR were examined with ultrasound of their temporal and axillary arteries at time of diagnosis. US of all 6 branches of the superficial temporal arteries and both axillary arteries was performed using a GE P9 device. Sonographic abnormalities considered indicative of vasculitis in the temporal arteries included the halo sign and non-compressible arteries with a thickened intima-media complex. An intima-media thickness of 0.42mm for the common superficial temporal branch, 0.34mm for the frontal branch, and 0.29mm for the parietal branch was considered positive. In the axillary arteries, a halo sign, and an intima-media thickness of &gt;1.0mm was considered positive [1]. Clinical, ultrasound and laboratory characteristics were recorded at baseline, 1 month, 3 months and 6 months. <h3>Results:</h3> 75 patients with a clinical diagnosis of PMR and 54 patients with a diagnosis of GCA (to act as a comparator group) were enrolled in the study. 69/75 (92%) of the PMR patients met the 2012 ACR/EULAR PMR classification criteria (those who did not meet this classification were primarily due to prior corticosteroid use in primary care resulting in normal ESR/CRP). All 54 GCA patients met the 2022 ACR/EULAR GCA classification criteria. 14/75 (18.7%) of patients with PMR had evidence of subclinical GCA on ultrasound of their temporal and axillary vessels. The mean initial prednisolone dose initiated for pure PMR was 18.7mg, while those with subclinical GCA in PMR were started on a mean of 23.5mg prednisolone and those with GCA were on average started on 45.5mg of prednisolone. 72% of patients with GCA were commenced on tocilizumab adjunct treatment as were one each in the subclinical GCA in PMR group and pure PMR group due to frailty and poorly controlled diabetes mellitus in both cases. Patients with US-identified subclinical GCA in PMR had more PMR relapses than those with pure PMR or GCA patients in the first 6 months. 42.8% of those with subclinical GCA in PMR relapsed compared to 26.2% of the pure PMR group, OR 1.6, 95% CI 0.5-4.9, p=0.38. They were also more likely to have a relapse than those in the GCA group where only 3.7% had a relapse in the first six months of treatment, OR 11.5, 95% CI 2.1-63.6, p=0.0049. Those with US-identified subclinical GCA in PMR were more likely to progress to GCA which occurred in 14.5% vs 0% of the pure PMR group in the first six months OR 21.1, 95% CI 0.96-466, p=0.05. PMR relapses while on steroid treatment occurred in 17/22 patients (77%) with steroid doses ranging from 2mg to 30mg, with a median of 8mg. The most common relapse time point was at the six-month mark. 2/22 patients with PMR relapsed while on tocilizumab (one with pure PMR and one with subclinical GCA in PMR) and 3/22 relapsed while on no treatment. Those patients with subclinical GCA in PMR relapsed at an earlier time point than those with pure PMR, 2.8 months vs 4.2 months average, p=0.22. <h3>Conclusion:</h3> Patients with subclinical GCA in PMR had more clinical relapses of PMR in the first six months of treatment than patients with pure PMR. They also were more likely to progress to GCA than their pure PMR counterparts. PMR relapses occurred at an earlier time point in those with US-identified GCA in PMR. Vascular US scanning of patients with a new diagnosis of PMR may help to risk stratify these patients at the time of diagnosis. <h3>REFERENCES:</h3> [1] Dejaco, C., et al., <i>EULAR recommendations for the use of imaging in LVV in clinical practice.</i> Ann Rheum Dis, 2018. <b>77</b>(5): p. 636-643. <h3>Acknowledgements:</h3> Meath Foundation, Tallaght Hospital Dublin <h3>Disclosure of Interests:</h3> Sharon Cowley Janssen, Novartis, Patricia Harkins Janssen, Colm Kirby: None declared, Richard Conway Abbvie, Fresenius Kabi, Galapagos, Janssen, UCB, Viatris, Abbvie, Celltrion, Janssen, Nordic Pharma, Novartis, David Kane Janssen, Novartis.