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Abstract Number: 2487

Role Of IL-33 In The Development Of Premature Atherosclerosis In Psoriatic Arthritis Patients

Priscilla Ching-han Wong1, Qing Shang2, Cheuk-Man Yu2 and Lai Shan Tam2, 1Medicine and Therapeutics, Prince of Wales hospital, New Territories, Hong Kong, 2Department of Medicine & Therapeutics, The Chinese University of Hong Kong, Hong Kong, Hong Kong

Meeting: 2013 ACR/ARHP Annual Meeting

Keywords: Interleukins (IL) and psoriatic arthritis

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Session Information

Title: Spondylarthropathies and Psoriatic Arthritis: Clinical Aspects and Treatment III

Session Type: Abstract Submissions (ACR)

Background/Purpose: Interleukin 33 (IL-33) is a newly identified member of the IL-1 cytokine family.  It involves in T-cell mediated immune responses through the activation of the ST2 receptor that are widely expressed by the T helper 2 cells and mast cells.  Many previous studies have demonstrated the role of IL-33 in chronic autoimmune diseases.  Whether this may play a role in the pathogenesis of inflammation and accelerating atherosclerosis in psoriatic arthritis (PsA) has never been addressed.  

Methods: A prospective study of 89 PsA patients followed up by the Prince of Wale hospital were recruited with comprehensive measurements of the traditional and novel CV risk factors, markers of clinical disease activity and severity, laboratory markers of inflammation, intima-media thickness (IMT) and augmentation index (AIx).  Frozen plasma was retrieved for the measurement of IL-33.  66 patients came back for follow-up after 5 years and vascular assessments were repeated.  SPSS was used for statistical analysis

Results: Among the 89 patients, 50.6% were male and 49.4% were female. The mean age was 46.1.9 ± 11.8 years old and the mean disease duration was 9.2 ± 7.1.  IL-33 was measurable in only 54 out of 89 patients.  Among these 54 patients, the mean of the IL-33 was 3.97 ± 17.79 pg/ml.  IL-33 was associated with the mean IMT (r=0.273, p=0.011) and the maximum IMT (r=0.239, p=0.026), but it was not associated with AIx (r=-0.016, p=0.891).  IL-33 was also not associated with the traditional and novel CV risk factors, the markers of clinical disease activities and  severity, as well as the laboratory markers of inflammation. 

Conclusion: IL-33 could be a novel pathway in accelerating the progression of premature atherosclerosis in PsA patients affecting both structural (IMT) and functional (AIx) modification of the blood vessels, independent of the CV risk factors.


Disclosure:

P. C. H. Wong,
None;

Q. Shang,
None;

C. M. Yu,
None;

L. S. Tam,
None.

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