Late-Onset Spondyloarthritis Presenting as Glucocorticoid-Resistant Polymyalgia Rheumatica: A Hitherto Underappreciated Entity in Which Tumor Necrosis Factor or Interleukin -17 Blockade May Have a Therapeutic Role

Objective Polymyalgia rheumatica (PMR) is an age-related inflammatory disease with shoulder/hip girdle involvement. Magnetic resonance imaging (MRI) reveals extracapsular/entheseal soft tissue involvement in both PMR and spondyloarthritis (SpA), with sacroiliac joint and perientheseal spinal bone marrow edema (BME) being characteristic of SpA. Therefore, some shared anatomic 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 observed at Leeds Teaching Hospitals NHS Trust with a diagnosis of psoriatic arthritis (PsA) or axial SpA were screened to identify those initially diagnosed with PMR from 2002 to 2024. Only those patients who retrospectively fulfilled the 2012 EULAR/American College of Rheumatology classification criteria or the Bird et al 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 62 [interquartile range (IQR) 58–69] years; 17 women and 14 men) presenting with typical PMR shoulder/hip girdle pain were subsequently classified as having 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 3 [IQR 1–4] years). Four of 27 tested patients were HLA–B27 positive. BME on MRI was detected in the spine and/or sacroiliac joints in 20 of 25 patients (80%) who underwent imaging (sacroiliac joint: 17 patients [68%]; spine: 15 patients [60%]). Clinical resolution with C-reactive protein (CRP) level normalization occurred in 21 of 31 patients following initial glucocorticoid (GC) therapy, but 7 of these 21 initial responders experienced disease flares or elevations in CRP levels. Therapy-wise, disease-modifying antirheumatic drugs (DMARDs) were used in 21 of 31 patients: 8 received conventional synthetic DMARDs, and 11 received biologic agents (8 anti–tumor necrosis factor agents, 3 interleukin-17 inhibitors), whereas the remaining 10 patients were treated with ≤10 mg/day of GCs.

Conclusion Late-onset SpA with PMR clinical presentations is characterized 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 biologic therapy efficacy in steroid-refractory PMR.