Anti-citrullinated protein antibodies are linked to erosive disease in an observational study of patients with psoriatic arthritis

Frank Behrens, Michaela Koehm, Diamant Thaçi, Holger Gnann, Gerd Greger, Bianca Maria Wittig, Harald Burkhardt, Frank Behrens, Michaela Koehm, Diamant Thaçi, Holger Gnann, Gerd Greger, Bianca Maria Wittig, Harald Burkhardt

Abstract

Objective: ACPAs are associated with bone destruction in RA. The aim of this study was to evaluate the association between ACPA and bone destruction in patients with a distinct inflammatory disorder, PsA.

Methods: We used baseline data from a large observational study of PsA patients preparing to initiate treatment with adalimumab to analyse demographic and disease characteristics by ACPA status. To ensure a homogeneous PsA study population, only patients with active psoriatic skin manifestations who met Classification of Psoriatic Arthritis criteria for PsA were included in the analyses, thereby minimizing the risk of including misdiagnosed RA patients. Multiple logistic regression analyses were used to explore potential associations between ACPA seropositivity and bone destruction.

Results: Of 1996 PsA patients who met the strict inclusion criteria, 105 (5.3%) were positive for ACPA. ACPA-positive patients had significantly higher swollen joint counts and 28-joint DAS values than ACPA-negative patients and significantly higher rates of erosive changes and dactylitis. Multiple logistic regression analysis confirmed the association of ACPA seropositivity with a 2.8-fold increase in the risk of erosive disease.

Conclusion: As has been previously shown for RA, ACPA is associated with bone destruction in PsA, suggesting that the osteocatabolic effect of ACPA is not confined to RA but is also detectable in the different pathogenetic context of a distinct disease entity.

Trial registration: ClinicalTrials.gov, NCT01111240.

Keywords: adalimumab; anti-citrullinated protein antibodies; erosions; observational study; osteoporosis; psoriatic arthritis.

© The Author 2016. Published by Oxford University Press on behalf of the British Society for Rheumatology.

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Source: PubMed

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