Late-Onset Axial Spondyloarthritis Has Distinct Features

TOPLINE:

Patients with late-onset axial spondyloarthritis (axSpA) are less likely to be positive for human leukocyte antigen B27 (HLA-B27) and have a family history of SpA; they are more likely to present with peripheral arthritis.

METHODOLOGY:

• Researchers conducted a multicenter cross-sectional study including 2165 patients with a clinical diagnosis of axSpA who were identified from the Rheumatic Diseases Portuguese Register from June 2008 to December 2022.
• Patients with symptom onset at or after 45 years of age were referred as late-onset axSpA, whereas those with symptom onset before 45 years as early-onset axSpA.
• Overall, 273 had a diagnosis of late-onset axSpA (mean age at symptom onset, 51.4 years; 55% men) and 1892 had a diagnosis of early-onset axSpA (mean age at symptom onset, 28.9 years; 56% men).
• Independent associations between demographic, clinical, imaging, and treatment characteristics and late-onset axSpA were tested using multivariable logistic regression models.

TAKEAWAY:

• Patients with late-onset axSpA were less likely to be positive for HLA-B27 (51% vs 65%; P P P P
• Patients with late-onset axSpA had a higher likelihood of having peripheral arthritis than those with early-onset axSpA (36% vs 28%; P
• The odds of having late-onset axSpA were lower in patients with HLA-B27 positivity (adjusted odds ratio [aOR], 0.6; 95% CI, 0.4-0.7), a family history of SpA (aOR, 0.6; 95% CI, 0.4-0.9), inflammatory back pain (aOR, 0.5; 95% CI, 0.4-0.8), and acute anterior uveitis (aOR, 0.6; 95% CI, 0.4-0.9).
• Conversely, patients with peripheral arthritis had a higher likelihood of developing late-onset axSpA (aOR, 1.5; 95% CI, 1.1-1.9).

IN PRACTICE:

“In this study, we found that [late-onset axSpA] may represent a distinct phenotype with a weaker association with HLA-B27,” the authors wrote. “Whether [late-onset axSpA] comprises a subset of axSpA with a (possibly) different genetic or epigenetic background or rather translates difficulties in recognizing a less typical disease presentation and a population without a genetic marker which can make the diagnostic process more challenging merits further investigation,” they further added.

SOURCE:

The study was led by Margarida Lucas Rocha, MD, Department of Rheumatology, ULSA, Faro, Portugal. It was published online on October 29, 2024, in Joint Bone Spine.

LIMITATIONS:

No limitations were reported in the study.

DISCLOSURES:

No relevant funding information and conflicts of interest were disclosed by the authors.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication.