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Risk of Cancer according to Duration of Targeted Therapy Exposure in Spondyloarthritis: A Nationwide Cohort Study from the French Health Insurance Database

Arthritis & Rheumatology·August 17
RheumatologyConfirms priorAxial SpondyloarthritisCancerPsoriatic ArthritisSpondyloarthritisNationwide Cohort StudyIL-12/23 InhibitorIL-17 InhibitorIL-23 InhibitorJAK InhibitorTNF InhibitorAdult

Summary

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What was studied

This nationwide French cohort study examined whether duration of targeted therapy exposure (TNFi, IL-17i, IL-12/23i, IL-23i, JAKi) affects cancer risk in 56,591 adults with spondyloarthritis (including psoriatic arthritis and axial SpA), followed for a median of 5.0 years (2014–2024).

Key findings

Exposure >6 months/year vs. ≤6 months/year was associated with a **lower** overall cancer risk (wHR 0.86, 95% CI 0.75–0.99), driven primarily by hematological malignancies (wHR 0.65, 95% CI 0.42–0.99); no significant reduction was seen for solid cancers (wHR 0.92, 95% CI 0.79–1.07). Of 1,224 total cancers, 1,029 were solid and 116 hematological. Cumulative multi-year exposure was not associated with cancer risk.

Study limitations

- **Observational design**: residual confounding cannot be excluded despite inverse probability weighting. - **Database-based exposure**: therapy adherence is inferred from insurance claims, not directly measured. - **Heterogeneous SpA subtypes**: pooling psoriatic arthritis, axial SpA, and other subtypes may obscure subgroup-specific risks.

Clinical implications

Clinicians can reassure patients with SpA that prolonged targeted therapy use is not associated with increased cancer risk — and may even lower hematological malignancy risk. Cumulative years of exposure should not, on its own, prompt treatment discontinuation over cancer concerns.

Caveats

  • Causal inference relies on inverse probability weighting from claims data; unmeasured confounders (e.g., disease severity, concomitant medications) may not be fully accounted for.
  • The protective signal for hematological malignancies (wHR 0.65) is based on only 116 events, so this estimate should be interpreted cautiously — wide confidence intervals reflect limited precision.
  • The study pools multiple SpA subtypes and multiple drug classes (TNFi, IL-17i, IL-12/23i, IL-23i, JAKi) into a single exposure variable; drug-class-specific or subtype-specific cancer risks may differ and are not fully delineated in the abstract.

Related Questions

Explore related topics

Does TNF inhibitor use increase cancer risk in psoriatic arthritis or axial spondyloarthritis?How does JAK inhibitor exposure affect malignancy risk in inflammatory arthritis?Is it safe to continue biologic therapy long-term in spondyloarthritis patients with prior cancer risk factors?

Publication Details

Year
2026
Journal
Arthritis & Rheumatology
Sample Size
n=56,591
Source
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