Late-Onset Spondylarthritis Presenting as Glucocorticoid-Resistant Polymyalgia Rheumatica: A hitherto underappreciated entity where TNF or IL-17 Blockade may have a Therapeutic Role.

Abstract

BACKGROUND Polymyalgia rheumatica (PMR) is an age-related inflammatory disease with shoulder-hip girdle involvement. Magnetic resonance imaging (MRI) reveals extracapsular/entheseal soft tissue involvements in both PMR and spondyloarthritis (SpA) with sacroiliac joint and peri-entheseal spinal bone marrow oedema (BMO) being characteristic of SpA. Therefore, some shared anatomical topography might be expected to result in similar clinical features. Herein we describe the clinical and imaging features of SpA initially diagnosed as PMR. METHODS Patients followed at Leeds Teaching Hospitals NHS Trust with a diagnosis of psoriatic arthritis (PsA), or axial SpA (axSpA) were screened to identify those initially diagnosed with PMR from 2002 to 2024. Only those patients who retrospectively fulfilled the 2012 EULAR/ACR classification criteria or the Bird criteria for PMR were included. Clinical data relevant to initial PMR diagnosis, imaging features, follow-up and treatment data were collected, as well as radiographic or MRI features that established the final diagnosis. RESULTS Thirty-one patients [median age in years (IQR): 62 (58-69); 17 females and 14 males] presenting with typical PMR shoulder/hip girdle pain were subsequently classified as SpA-spectrum disorders. The SpA diagnosis was made in 12 patients within three months of presentation, and in 19 patients during the remaining follow-up period [median (IQR): 3 (1-4) years]. Four of 27 tested patients were HLA-B27 positive. BMO on MRI was detected in the spine and/or sacroiliac joints in 20 of 25 imaged patients (80%) (sacroiliac joint: 17 patients [68%], spine: 15 patients [60%]). Clinical resolution with CRP normalisation occurred in 21 of 31 patients following initial glucocorticoid (GC) therapy, but 7 of these 21 initial responders experienced disease flares or CRP elevations. Therapy-wise, disease-modifying antirheumatic drugs (DMARDs) were used in 21 of 31 cases: 8 received conventional DMARDs, and 11 received biologic agents (eight anti-TNFs, three IL-17 inhibitors), while the remaining 10 patients were treated with 10 mg/day or less GC therapy. CONCLUSION Late-onset SpA with PMR clinical presentations is characterised by failure to respond to or taper GC therapy and is often identified by SpA-specific osteitis patterns on MRI. We propose that a PMR-SpA overlap may account for biological therapy efficacy in steroid-refractory PMR.