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  1. N. J. Kleinrensink1,2,
  2. W. Foppen2,
  3. N. Seddiqi2,
  4. H. Vonkeman3,
  5. K. Suijkerbuijk4,
  6. M. Jansen1,
  7. P. De Jong2,
  8. M. W. Heijstek1,
  9. J. Spierings1
  1. 1UMC Utrecht, Department of Rheumatology & Clinical Immunology, Utrecht, Netherlands
  2. 2UMC Utrecht, Department of Radiology, Utrecht, Netherlands
  3. 3Medisch Spectrum Twente, Department of Rheumatology, Enschede, Netherlands
  4. 4UMC Utrecht, Department of Medical Oncology, Utrecht, Netherlands


Background Patients with psoriatic arthritis (PsA) have an increased risk of cardiovascular disease, possibly due to a chronic inflammatory state.

Objectives The main objective of this study was to investigate whether vascular inflammation, measured with 18-fluorodeoxyglucose positron emission tomography/computed tomography (PET/CT), is elevated in PsA patients.

Methods We included 75 PsA patients with active peripheral arthritis (≥2 tender and swollen joints) from an ongoing clinical trial (EudraCT 2017-003900-28), and a retrospective group of 40 controls with melanoma, without distant metastases and not receiving immunotherapy. Both PsA patients and controls were aged 18-75 years. The main outcome measure was aortic vascular inflammation, which was measured using target-to-background-ratios (TBR) on PET/CT. Clinical disease activity in PsA was assessed with joint counts, body surface area and the composite measure Disease Activity index for PsA. Laboratory assessments included the inflammatory parameters C-reactive protein and Erythrocyte Sedimentation Rate. Vascular inflammation was compared between PsA patients and controls in univariate analysis with an unpaired t-test with equal variances. A multiple linear regression analysis was performed to adjust for age, gender, body mass index and mean arterial pressure (MAP). Associations of clinical parameters of disease activity in PsA with vascular inflammation were assessed using Spearman’s correlation coefficient.

Results Vascular inflammation was increased in PsA patients in comparison with controls (mean TBR for entire aorta respectively 1.53±0.15 and 1.42±0.13; P<0.001; Figure 1). This association remained significant after adjusting for gender, age, body mass index and mean arterial pressure (P=0.002). In individuals with PsA, vascular inflammation was not associated with disease-related parameters. There were no significant differences between PsA patients and controls regarding age, mean arterial pressure (MAP) and history of CVD. PsA patients had a higher BMI in comparison with healthy controls (Table 1).

Conclusion Aortic vascular inflammation was increased in patients with active PsA compared with controls. This evidence suggests that inflammation in PsA is not limited to skin and joints, but also involves the cardiovascular system.

Table 1.

Patients’ characteristics

Figure 1.

Increased vascular inflammation in the entire aorta and all separate aortic segments, assessed with the TBR, in PsA (n=75) in comparison with controls (n=40).

Acknowledgements This work was supported by Pfizer (New York, New York, USA). The collaboration project is cofunded by the PPP Allowance made available by Health~Holland, Top Sector Life Sciences & Health, to stimulate public–private partnerships (grant number: LSHM17074).

The TOFA-PREDICT Author Group:

A. van Tubergen,

K. Hermans,

M.E. Hettema,

M.R. Kok,

R.J. Bisoendial,

A.W.R. van Kuijk,

J. Wiegel,

T.L.T.A. Jansen,

A.C. Comarniceanu,

L. Geurts – van Bon,

L.G. Schipper,

S.T.A. van Bijnen,

S. Wijngaarden,

A. Herman.

Disclosure of Interests Nienke J. Kleinrensink: None declared, Wouter Foppen Grant/research support from: WF has received research grants from NovoNordisk and Pfizer which were paid to the institution., Negina Seddiqi: None declared, Harald Vonkeman Grant/research support from: Prof. H. Vonkeman reports having received grants, consulting fees or honorarium from AbbVie, Boehringer Ingelheim, Novartis, Pfizer, UCB, Janssen and Galapagos; all outside the submitted work., Karijn Suijkerbuijk Consultant of: Bristol-Myers Squibb, Merck Sharp and Dome, Abbvie, Pierre Fabre, Novartis, Sairopa. All paid to institution and outside the submitted work, Grant/research support from: Novartis, Roche, Merck Sharp and Dome. All paid to institution and outside the submitted work., Mylène Jansen: None declared, Pim de Jong Consultant of: Vifor Pharma and Philips Healthcare, Marloes W. Heijstek: None declared, Julia Spierings: None declared.

  • Psoriatic arthritis
  • Cardiovascular disease
  • Imaging

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