Session Type: ACR Poster Session A
Session Time: 9:00AM-11:00AM
Recent evidence suggests that chemokines and miRNAs are involved in the pathogenesis of antiphospholipid syndrome (APS). However, the specific role of these molecules in both cumulative thrombotic damage and in risk of thrombosis is still not well understood. The aim of this study was to explore the association between autoimmunity related chemokines and miRNAs with cumulative organ damage as well as the clinical risk of thrombosis in patients with APS.
Methods: This cross-sectional study included patients with APS Sapporo/Sydney criteria from a single outpatient rheumatology clinic. Demographic, clinical and clinimetric data (DIAPS, Damage Index in patients with Thrombotic Antiphospholipid Syndrome; aGAPSS, adjusted Global Anti-Phospholipid Syndrome Score and SLEDAI, Systemic Lupus Erythematosus Disease Activity Index) were recorded. Serum samples were obtained in the same visit and levels of chemokines BLC (B lymphocyte chemoattractant), IP10 (IFN-γ-induced protein 10), MCP-1 (monocyte chemoattractant protein-1) and MIG (monokine-induced-by-IFN-γ) were measured by multiplex bead array technology (Luminex MAGPIX System). In addition, relative expression of miR-19, miR-20, miR-126, and miR-155 was measured by qtPCR. Sera from healthy individuals were evaluated for reference. Normality analysis was performed with Kolmogorov-Smirnov test and comparisons were made with Mann-Whitney U test. Associations were evaluated with exact Fisher’s test and Spearman rho coefficient. ROCs were used to investigate miRNAs cut-off points. IBM SPSS version 23.0 was used for calculations.
Results: Sixty five APS patients were included, mean age was 43±14 years old, 73% were female and 53% primary APS. DIAPS correlates with number of thrombosis (0.381, p=0.003), anti-cardiolipin antibodies IgG (0.328, p=0.030), anti-β2GPI IgG (0.366, p=0.017) and BLC (0.385, p=0.015). Anti-cardiolipin IgG (0.395, p=0.010) and BCL (0.359, p=0.025) also correlates with aGAPSS. SLEDAI correlates with miR-126 (0.637, p=0.001) in secondary APS. The tissue factor related miRNAs, miR-19 (AUC=0.812, p<0.0001) and miR-20 (0.834 p< 0.0001) were able to differentiate patients from controls. Interestingly, miR-20 ≤ 0.0198 was associate to the presence of anticardiolipin (p=0.048) and a tendency of triple positivity (p=0.093) as well as recurrent thrombosis (p=0.075).
Conclusion: Our results suggest that BLC, miRNA-19 and miRNA-20 may be involved in the accrural damage in APS and risk of thrombosis. Wide and prospective studies to explore processes related to accumulation of chronic damage in APS are needed. The long time follow up for clinical end-points is the challenge for validating new potential circulating biological markers.
To cite this abstract in AMA style:Martinez-Martinez LA, Sanchez-Muñoz F, Chacon-Perez MJNN, Juarez-Vicuña Y, Ornelas NM, Beltran-Cortez A, Venegas Yañez RA, Fonseca Basurto J, Aranda Cano E, Amigo MC, Amezcua-Guerra LM. Serum Chemokines and miRNA Levels and Its Association with Cumulative Organ Damage in Patients with Antiphospholipid Syndrome: A Bench to Bedside Study [abstract]. Arthritis Rheumatol. 2018; 70 (suppl 10). https://acrabstracts.org/abstract/serum-chemokines-and-mirna-levels-and-its-association-with-cumulative-organ-damage-in-patients-with-antiphospholipid-syndrome-a-bench-to-bedside-study/. Accessed January 23, 2020.
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