In PSUMMIT 1 and 2, patients with PsA were randomized to placebo or ustekinumab 45 mg or 90 mg. Enthesitis was assessed at weeks 0 and 24 (Maastricht Ankylosing SpondylitisEnthesitis Score).
Among patients with baseline enthesitis and dactylitis, 62.4% achieved a Maastricht Ankylosing SpondylitisEnthesitis Score of 0 and 80.9% achieved a dactylitis count of 0, respectively.
A variety of clinical indices exist to assess enthesitis in PsA; however, the Leeds Enthesitis Index and Maastricht Ankylosing SpondylitisEnthesitis Score index have been the most frequently used indices in recent clinical trials.
Patients with PsA with active enthesitis were randomized 1:1 to receive either ustekinumab (UST; arm 1) or tumor necrosis factor inhibitors (TNFi; arm 2).
Common characteristics of patients who switched TNF inhibitors included female sex, older age, more severe disease, greater symptom burden, higher erythrocyte sedimentation rate, complete ankyloses, and enthesitis.
Clinics include enthesitis or dactylitis and extra-articular involvement as uveitis or inflammatory bowel disease, while treatment options range from nonsteroidal anti-inflammatory drugs (NSAIDs) to biologics, targeting TNF α or Th17.
The recent introduction of tumor necrosis factor (TNF) blockers in the treatment of spondyloarthritis has offered the most hope in not only relieving symptoms and signs of both peripheral arthritis and enthesitis but also spinal disease, which often has been refractory to other agents.
Nevertheless, a number of knowledge gaps exist regarding the role of IL-17A in the pathophysiology of spondyloarthritis in man, including its cellular origin, its precise role in discrete disease processes such enthesitis, bone erosion, and bone formation, and the reasons for the discrepant responses to IL-17A inhibition observed in certain other spondyloarthritis manifestations.
The use of different agents including JAK, IL-17, and IL-23 inhibitors contributes significantly to our understanding of enthesitis in terms of involved immune pathways.
Genetic evidence links the IL-23-IL-17 pathway to inflammation in these rheumatic diseases, and mechanistic data from mice support a functional role for IL-23-IL-17 pathway activation in the development of enthesitis and in entheseal bone formation.
Patients were assessed for CRP, musculoskeletal ultrasound (MSUS) in the form of grayscale ultrasound (GSUS), and power Doppler ultrasound (PDUS) for eight entheses and 34 joints to detect MSUS subclinical enthesitis and synovitis.
Genetic evidence links the IL-23-IL-17 pathway to inflammation in these rheumatic diseases, and mechanistic data from mice support a functional role for IL-23-IL-17 pathway activation in the development of enthesitis and in entheseal bone formation.
The use of different agents including JAK, IL-17, and IL-23 inhibitors contributes significantly to our understanding of enthesitis in terms of involved immune pathways.
Sleep disturbance is particularly associated with generalized pain, anxiety, enthesitis and levels of CRP and ESR in patients carrying the diagnosis of PsA.