25rhk023 10.3205/25rhk023 urn:nbn:de:0183-25rhk0235 Meeting Abstract Scholz Scholz Sophie Charlotte SC

Charité Universitätsmedizin Berlin, Department of Rheumatology and Clinical Immunology, Berlin Deutsches Rheumaforschungszentrum (DRFZ), Deutsches Rheumaforschungszentrum (DRFZ), Berlin

author Nitschke Nitschke Eduard E

Charité Universitätsmedizin Berlin, Department of Rheumatology and Clinical Immunology, Berlin Deutsches Rheumaforschungszentrum (DRFZ), Deutsches Rheumaforschungszentrum (DRFZ), Berlin

author Dreveton Dreveton Léa-Sophie LS

Charité Universitätsmedizin Berlin, Department of Rheumatology and Clinical Immunology, Berlin Deutsches Rheumaforschungszentrum (DRFZ), Deutsches Rheumaforschungszentrum (DRFZ), Berlin

author Glenzer Glenzer Annika A

Charité Universitätsmedizin Berlin, Department of Rheumatology and Clinical Immunology, Berlin Deutsches Rheumaforschungszentrum (DRFZ), Deutsches Rheumaforschungszentrum (DRFZ), Berlin

author Szelinski Szelinski Franziska F

Charité Universitätsmedizin Berlin, Department of Rheumatology and Clinical Immunology, Berlin Deutsches Rheumaforschungszentrum (DRFZ), Deutsches Rheumaforschungszentrum (DRFZ), Berlin

author Schrezenmeier Schrezenmeier Eva V. EV

Deutsches Rheumaforschungszentrum (DRFZ), Deutsches Rheumaforschungszentrum (DRFZ), Berlin Charité Universitätsmedizin Berlin, Department of Nephrology and Intensive Medical Care, Berlin

author Krönke Krönke Gerhard G

Charité Universitätsmedizin Berlin, Department of Rheumatology and Clinical Immunology, Berlin Deutsches Rheumaforschungszentrum (DRFZ), Deutsches Rheumaforschungszentrum (DRFZ), Berlin

author Dörner Dörner Thomas T

Charité Universitätsmedizin Berlin, Department of Rheumatology and Clinical Immunology, Berlin Deutsches Rheumaforschungszentrum (DRFZ), Deutsches Rheumaforschungszentrum (DRFZ), Berlin

author Stefanski Stefanski Ana-Luisa AL

Charité Universitätsmedizin Berlin, Department of Rheumatology and Clinical Immunology, Berlin Deutsches Rheumaforschungszentrum (DRFZ), Deutsches Rheumaforschungszentrum (DRFZ), Berlin

author German Medical Science GMS Publishing House

Düsseldorf

610 20250917 engl This is an Open Access article distributed under the terms of the Creative Commons Attribution 4.0 License. Dieser Artikel ist ein Open-Access-Artikel und steht unter den Lizenzbedingungen der Creative Commons Attribution 4.0 License (Namensnennung). M0627 023 Deutsche Gesellschaft für Rheumatologie Deutsche Gesellschaft für Orthopädische Rheumatologie 53. Kongress der Deutschen Gesellschaft für Rheumatologie (DGRh), 39. Jahrestagung der Deutschen Gesellschaft für Orthopädische Rheumatologie (DGORh) Deutscher Rheumatologiekongress 2025 Experimentelle & Translationale Rheumatologie Wiesbaden 20250917 20250920 ET.01 TextIntroduction: Antiphospholipid syndrome (APS) is a systemic autoimmune disorder primarily characterized by thrombotic events and/or obstetric complications, in the presence of persistent antiphospholipid antibodies. Thrombocytopenia was recently incorporated into the 2023 revised ACR/EULAR criteria for APS . Type I interferon (IFN) upregulation has been identified as a potential contributor to clinical disease in a subset of APS patients . However, the relationship between type I IFN and thrombocytopenia in this population has yet to be further delineated.The primary objective of this study was to investigate a possible association between thrombocytopenia and elevated type I IFN in APS patients.Methods: A retrospective analysis was conducted among 211 APS patients seen in our department between 2017 and 2024. Clinical manifestations, with a particular focus on thrombocytopenia, and laboratory characteristics (specifically autoantibody profiles and SIGLEC-1 expression on monocytes as a surrogate marker for elevated type I IFN ) were evaluated. The relationship between type I IFN, thrombocytopenia, and other disease manifestations was assessed using the Mann-Whitney U test and Spearman’s correlation for statistical analysis.Results: Among the 211 APS patients, 56 were identified as having experienced thrombocytopenia during the observational period (20 with primary APS and 36 with secondary APS associated with systemic lupus erythematosus (SLE)). APS patients with thrombocytopenia exhibited higher SIGLEC-1 expression levels on monocytes compared to those without thrombocytopenia, with an inverse correlation observed between platelet count and SIGLEC-1 expression (Figure 1A). Additionally, thrombocytopenic patients showed elevated levels of anti-Cardiolipin IgG antibodies (p = 0.0039) and a trend towards increased anti-β2-Glycoprotein IgG antibodies (p = 0.051). Notably, the enhanced type I IFN signature was significant only in primary APS patients with thrombocytopenia (Figure 1B), with no significant difference observed in the secondary APS cohort (Figure 1C). APS patients with thrombocytopenia also demonstrated a higher overall disease burden, with distinct clinical presentations between primary and secondary APS. In comparison to non-thrombocytopenic patients, primary APS patients with thrombocytopenia exhibited a higher incidence of venous thromboembolic events (55% vs. 35.48%) and a lower occurrence rate of arterial events (15% vs. 29%). In contrast, secondary APS patients with thrombocytopenia experienced a greater frequency of mixed venous and arterial events (27.78% vs. 12.9%) as well as obstetric complications (19.44% vs. 17.74%).Conclusion: The data suggest that type I IFN may play a key pathogenic role in thrombocytopenia in primary APS. Furthermore, APS patients with thrombocytopenia exhibit higher autoantibody profiles and more severe disease manifestations, particularly in relation to thromboembolic and obstetric complications. These findings warrant confirmation in prospective studies and could inform the development of targeted therapeutic strategies for APS. Barbhaiya M Zuily S Naden R Hendry A Manneville F Amigo MC Amoura Z Andrade D Andreoli L Artim-Esen B Atsumi T Avcin T Belmont HM Bertolaccini ML Branch DW Carvalheiras G Casini A Cervera R Cohen H Costedoat-Chalumeau N Crowther M de Jesus G Delluc A Desai S De Sancho M Devreese KM Diz-Kucukkaya R Duarte-Garcia A Frances C Garcia D Gris JC Jordan N Leaf RK Kello N Knight JS Laskin C Lee AI Legault K Levine SR Levy RA Limper M Lockshin MD Mayer-Pickel K Musial J Meroni PL Orsolini G Ortel TL Pengo V Petri M Pons-Estel G Gomez-Puerta JA Raimboug Q Roubey R Sanna G Seshan SV Sciascia S Tektonidou MG Tincani A Wahl D Willis R Yelnik C Zuily C Guillemin F Costenbader K Erkan D ACR/EULAR APS Classification Criteria Collaborators The 2023 ACR/EULAR Antiphospholipid Syndrome Classification Criteria 2023 Arthritis Rheumatol 1687-702 Barbhaiya M, Zuily S, Naden R, Hendry A, Manneville F, Amigo MC, Amoura Z, Andrade D, Andreoli L, Artim-Esen B, Atsumi T, Avcin T, Belmont HM, Bertolaccini ML, Branch DW, Carvalheiras G, Casini A, Cervera R, Cohen H, Costedoat-Chalumeau N, Crowther M, de Jesus G, Delluc A, Desai S, De Sancho M, Devreese KM, Diz-Kucukkaya R, Duarte-Garcia A, Frances C, Garcia D, Gris JC, Jordan N, Leaf RK, Kello N, Knight JS, Laskin C, Lee AI, Legault K, Levine SR, Levy RA, Limper M, Lockshin MD, Mayer-Pickel K, Musial J, Meroni PL, Orsolini G, Ortel TL, Pengo V, Petri M, Pons-Estel G, Gomez-Puerta JA, Raimboug Q, Roubey R, Sanna G, Seshan SV, Sciascia S, Tektonidou MG, Tincani A, Wahl D, Willis R, Yelnik C, Zuily C, Guillemin F, Costenbader K, Erkan D; ACR/EULAR APS Classification Criteria Collaborators. The 2023 ACR/EULAR Antiphospholipid Syndrome Classification Criteria. Arthritis Rheumatol. 2023 Oct;75(10):1687-702. DOI: 10.1002/art.42624 http://dx.doi.org/10.1002/art.42624 Xourgia E Tektonidou MG Type I interferon gene expression in antiphospholipid syndrome: Pathogenetic, clinical and therapeutic implications 2019 J Autoimmun 102311 Xourgia E, Tektonidou MG. Type I interferon gene expression in antiphospholipid syndrome: Pathogenetic, clinical and therapeutic implications. J Autoimmun. 2019 Nov;104:102311. DOI: 10.1016/j.jaut.2019.102311 http://dx.doi.org/10.1016/j.jaut.2019.102311 Biesen R Demir C Barkhudarova F Grün JR Steinbrich-Zöllner M Backhaus M Häupl T Rudwaleit M Riemekasten G Radbruch A Hiepe F Burmester GR Grützkau A Sialic acid-binding Ig-like lectin 1 expression in inflammatory and resident monocytes is a potential biomarker for monitoring disease activity and success of therapy in systemic lupus erythematosus 2008 Arthritis Rheum 1136-45 Biesen R, Demir C, Barkhudarova F, Grün JR, Steinbrich-Zöllner M, Backhaus M, Häupl T, Rudwaleit M, Riemekasten G, Radbruch A, Hiepe F, Burmester GR, Grützkau A. Sialic acid-binding Ig-like lectin 1 expression in inflammatory and resident monocytes is a potential biomarker for monitoring disease activity and success of therapy in systemic lupus erythematosus. Arthritis Rheum. 2008 Apr;58(4):1136-45. DOI: 10.1002/art.23404 http://dx.doi.org/10.1002/art.23404 0

1 1 Figure 1: (A) Siglec-1 values relecting type I IFN were compared between APS patients with thrombocytopenia and without thrombocytopenia Mean with SEM, Mann-Whitney test.; Correlation of platelet number and Siglec-1 values in APS patients Spearman correlation. Created with GraphPad Prism 9. (B) Comparison of Siglec-1 expression between primary APS patients with thrombocytopenia and without thrombocytopenia Mean with SEM, Mann-Whitney test. (C) Siglec-1 expression levels of secondary APS patients with thrombocytopenia versus those without thrombocytopenia Mean with SEM, Mann-Whitney test. * for p<0,05; ** for p<0,01

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