Citation

Juneblad K, Rantapää-Dahlqvist S, Gerd-Marie A (2018) Biomarkers in Relation to Disease Manifestations in Psoriatic Arthritis. Int J Immunol Immunother 5:033. doi.org/10.23937/2378-3672/1410033

Copyright

© 2018 Juneblad K, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

RESEARCH ARTICLE | OPEN ACCESS DOI: 10.23937/2378-3672/1410033

Biomarkers in Relation to Disease Manifestations in Psoriatic Arthritis

Kristina Juneblad*, Solbritt Rantapää-Dahlqvist and Gerd-Marie Alenius

Department of Public Health and Clinical Medicine, Rheumatology, University Hospital, Sweden

Abstract

Background

In psoriatic arthritis (PsA), a complex disease with a lack of measurable laboratory parameters, there is a need for diagnostic and prognostic tools to meet the challenge of early diagnosis and assessment of disease severity.

Objective

To analyze whether soluble biomarkers could discriminate between disease phenotypes in PsA.

Methods

Two-hundred and seventy-four patients with established disease and 30 healthy controls were included in this cross-sectional study. Thirty-nine different serological biomarkers were investigated in relation to disease activity, disease manifestations and in comparison with controls. In addition to standard statistical methods, orthogonal partial least squares discriminant analysis (OPLS-DA) was used to investigate different phenotypes of PsA.

Results

Psoriatic arthritis activity was significantly associated with CRP (pc = 0.0008), IL-6 (pc = 0.001), IL-16 (pc = 0.007), calprotectin (pc = 0.014), IL-12/IL-23p40 (pc = 0.02), and ICAM-1 (pc = 0.045). Different PsA disease phenotypes were associated with different biomarkers, e.g., axial disease (with or without peripheral disease) was associated with IL-6 (pc = 0.044), IL-16 (pc = 0.044), MIP-1β (pc = 0.039) and polyarthritis was associated with IL-6 (pc = 0.0006), SAA (pc = 0.009), CRP (pc = 0.012) and IL-8 (pc = 0.04), although it was not possible to statistically separate the different phenotypes with OPLS-DA. An association was also seen in patients with PsA who, at any time had been prescribed bDMARD, (TNFβ (pc = 0.0001), TNFα (pc = 0.0003), calprotectin (pc = 0.0009), CRP (pc = 0.016) and lower levels of Tie-2 (pc = 0.027)). No significant differences were detected when PsA patients were compared with healthy controls.

Conclusions

In this study, inflammatory/pro-inflammatory biomarkers were associated with different disease phenotypes in PsA, however the impact of the various biomarkers is not evident as OPLS-DA analyses could not separate between groups.