Background Lack of measures of disease activity and prognosis is a key challenge in spondyloarthritis (SpA). Several soluble biomarkers have been proposed, but very few have been found to relate to MRI activity and add to the diagnostic value of CRP.(1) Leukocytes are key players in SpA disease activity.(2) The soluble form of CD18 (sCD18) has been found to be shed from leukocytes in inflammation and to be present in the blood.(3)
Objectives This study examines the association of sCD18 in the blood and SpA disease activity.
Methods Plasma from a study population with 84 SpA patients at baseline and 33 patients at three-year follow-up and a control group of age and gender matched normal healthy volunteers (NHV) were studied. The samples were analyzed for sCD18 by a time resolved immunoflourometric assay (TRIFMA) using the KIM185 antibody as capture antibody and the KIM127 antibody as detection antibody as previously described.(3)
Results The level of sCD18 was decreased in plasma from SpA patients compared to plasma from NHV (p<0.0005). The level of sCD18 showed inverse correlations to the clinical parameters clinician defined disease activity on a 100-mm visual analog scale (VAS) (p<0.05) and Bath Ankylosing Spondylitis Metrology Index (BASMI) (p<0.005) and the paraclinical measures CRP (p<0.005) and sacroiliac joint (SIJ) MRI activity score (p<0.05). Interestingly, CRP did not show any significant relation to clinical findings or MRI activity in this study. Patients with BASMI improvement at three-year follow-up also had increases in sCD18 concentration compared to patients without BASMI improvements (p<0.05).
Conclusions sCD18 is associated with clinical findings, CRP and SIJ MRI activity in SpA. sCD18 could be a novel disease activity marker in SpA directly measuring leukocyte activity.
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Gjelstrup LC, Boesen T, Kragstrup TW, Jorgensen A, Klein NJ, Thiel S, et al. Shedding of large functionally active CD11/CD18 Integrin complexes from leukocyte membranes during synovial inflammation distinguishes three types of arthritis through differential epitope exposure. J Immunol. 2010;185(7):4154-68.
Disclosure of Interest None Declared
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