Psoriatic arthritis (PsA) is a heterogeneous, chronic, progressive, inflammatory condition associated with enthesitis, dactylitis, and skin and nail psoriasis that can affect peripheral joints. However, axial involvement may also occur in PsA.1

In a recent review published in Seminars in Arthritis and Rheumatism, Poddubnyy and colleagues provided an overview on the clinical presentation, diagnosis, and treatment of axial PsA to improve rheumatologists’ knowledge of this phenotype.1

Risk Factors for Axial Involvement in PsA

Reported data of axial involvement in PsA are variable, with approximately 25% to 70% of patients with PsA experiencing axial involvement of their disease.1 The variability was found to be related to the various definitions of axial involvement in PsA; definitions can range from isolated unilateral sacroiliitis to criteria similar to those used for ankylosing spondylitis.1,2 Less than 5% of patients with PsA have axial disease alone; the majority of patients with axial PsA also have peripheral arthritis.2,3 


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Axial involvement in patients with PsA typically develops at a later stage in the disease course. Prevalence of axial disease increases with disease duration, with studies suggesting that up to 70% of patients with long-standing PsA may have axial involvement, compared with up to 28% of patients with early-stage PsA.4

The phenotype of axial PsA differs between men and women. Nas and colleagues reported that axial involvement is more common among women with PsA, suggesting that sex hormones, along with environmental factors, may play a role in disease incidence.5 Furthermore, the findings of the same study indicated that men with PsA have a better quality of life due to less spinal involvement, suggesting that differences in spinal involvement and mobility are associated with better functional outcomes among men.5

Data from the Corrona Psoriatic Arthritis/Spondyloarthritis registry have indicated that among patients with PsA, axial involvement was associated with significantly worse disease, including an increased risk for moderate to severe psoriasis, higher disease activity, and a greater effect on quality of life.6

Risk factors for developing axial involvement during early-stage PsA were found to include human leukocyte antigen (HLA)-B27 positivity, the presence of radiographic damage to peripheral joints, and an increased erythrocyte sedimentation rate (ESR); a family history of PsA was associated with a decreased risk of developing axial involvement at an early stage. The presence of nail dystrophy, a high number of radiographically damaged joints, periostitis, and elevated ESR levels were associated with an increased risk of developing axial involvement during late-stage PsA.7

Clinical Presentation – Differential Diagnosis of Axial PsA

The main manifestation of axial involvement of PsA is inflammatory back pain, characterized by pain in the hips or buttocks that improves with activity and worsens with rest, pain that occurs at night, pain that is responsive to nonsteroidal anti-inflammatory drugs (NSAIDs), and axial morning stiffness for more than 30 minutes. Additional potential symptoms of axial PsA include limited motion and tenderness around the sacroiliac joints. In some cases, axial PsA may be asymptomatic, usually in patients with long-standing PsA or newly onset PsA but at an older age.4,8

Overlapping features between axial PsA and axial spondyloarthritis (axSpA) often present a challenge in diagnosis for rheumatologists. In a study, Mease and colleagues reported that enthesitis, dactylitis, and nail psoriasis were significantly more common among patients with PsA with axial involvement compared with those without axial involvement.6

There are several differences in clinical, genetic, and radiographic features between patients with axial PsA and patients with axSpA. Patients with axial PsA are usually older at disease onset compared with those with axSpA. Peripheral involvement is seen in the majority of patients with axial PsA, but in less than 30% of those with axSpA. In contrast, inflammatory back pain is reported in most patients with axSpA and is significantly less frequent in those with axial PsA.1

Spinal magnetic resonance imaging (MRI) can be used as a diagnostic tool for axial involvement in patients with axSpA and those with PsA. Imaging has typically indicated that involvement of cervical spine and fusion of facet joints in cervical spine are more common among patients with axial PsA, while symmetric sacroiliitis and symmetrical and marginal syndesmophytes are more common among those with axSpA.1

A common risk factor for both axSpA and axial PsA is HLA-B27 positivity. Approximately 50% of patients with axial PsA vs 20% of those without axial involvement are more likely to test positive for HLA-B27. Axial PsA has also been associated with HLA-B08 and HLA-B38.1

What Are the Treatment Goals and Options for Axial PsA?

Reduction of inflammation and prevention of damage are some of the main treatment goals for axial disease. Physiotherapy, NSAIDs, local glucocorticoid injections, and antitumor necrosis factor (anti-TNF) agents are the cornerstone of treatment. The anti-inflammatory effect of anti-TNF drugs may improve spinal flexibility, prevent functional limitations, maintain the ability to work, and decrease the risk for disease-associated complications.4

In addition, as there is evidence that interleukin (IL)-23/17 pathways play an important role in the inflammatory response, secukinumab, a monoclonal antibody against IL-17A, may be effective for axial inflammation in patients with PsA.1,4 Guselkumab, an IL-23 inhibitor may also have an important role among patients with axial involvement, but additional studies are required.1

Further, although monoclonal antibody ustekinumab, which is specific for IL-12 and IL-23, was not found to be efficacious in patients with axSpA, it may have a role in axial PsA. Janus kinase (JAK) inhibition may also be used for axial PsA treatment. However, there are currently no data to support the use of conventional synthetic disease-modifying anti-rheumatic drugs (DMARDs) or systemic steroids in axial PsA.1,4

Overall, additional studies are required to better understand the prognosis of axial involvement in patients with axial PsA.

“Highlighting the clinical characteristics, diagnostic tests, imaging characteristics, and prognosis of axial PsA provides rheumatologists with a better understanding of the disease and potential to identify axial PsA earlier,” Poddubnyy and colleagues noted in their review paper.1

References

  1. Poddubnyy D, Jadon DR, Van den Bosch F, Mease PJ, Gladman DD. Axial involvement in psoriatic arthritis: An update for rheumatologists. Semin Arthritis Rheum. 2021;51(4):880-887. doi:10.1016/j.semarthrit.2021.06.006
  2. Gladman DD. Axial disease in psoriatic arthritis. Curr Rheumatol Rep. 2007;9(6):455-60. doi:10.1007/s11926-007-0074-2
  3. Taylor WJ, Zmierczak HG, Helliwell PS. Problems with the definition of axial and peripheral disease patterns in psoriatic arthritis. J Rheumatol. 2005;32(6):974-977.
  4. Feld J, Chandran V, Haroon N, Inman R, Gladman D. Axial disease in psoriatic arthritis and ankylosing spondylitis: a critical comparison. Nat Rev Rheumatol. 2018;14(6):363-371. doi:10.1038/s41584-018-0006-8
  5. Nas K, Kiliç E, Tekeoğlu İ, The effect of gender on disease activity and clinical characteristics in patients with axial psoriatic arthritis. Mod Rheumatol. 2021;31(4):869-874. doi:10.1080/14397595.2020.1812870
  6. Mease PJ, Palmer JB, Liu M, et al. Influence of axial involvement on clinical characteristics of psoriatic arthritis: analysis from the Corrona Psoriatic Arthritis/Spondyloarthritis Registry. J Rheumatol. 2018;45(10):1389-1396. doi:10.3899/jrheum.171094
  7. Chandran V, Tolusso DC, Cook RJ, Gladman DD. Risk factors for axial inflammatory arthritis in patients with psoriatic arthritis. J Rheumatol. 2010;37(4):809-815. doi:10.3899/jrheum.091059
  8. Jadon DR, Sengupta R, Nightingale A. Axial disease in psoriatic arthritis study: defining the clinical and radiographic phenotype of psoriatic spondyloarthritis. Ann Rheum Dis. 2017;76(4):701-707. doi:10.1136/annrheumdis-2016-209853