AB1017 SLE PATIENTS EXHIBIT WALL THICKENING IN MAJOR VEINS ACROSS THE BODY
Authors: H. Karadeniz, D. Yildirim, N. Ibrahimkhanli, H. N. Koc Kanik, İ. Vasi, R. Duran, R. C. Kardaş, B. Kaya, M. Cerit, H. N. Sendur, H. Küçük, A. Erden, B. Göker, M. A. Öztürk, A. Tufan
Journal: Annals of the Rheumatic Diseases (2024)

<h3>Background:</h3> Vascular disease significantly contributes to morbidity and mortality in individuals with systemic autoimmune diseases. The primary catalyst for accelerated vascular damage in Systemic Lupus Erythematosus (SLE) appears to be profound dysregulation in both innate and adaptive immune responses. It is well-established that there is an increased risk of venous thrombosis, particularly in cases complicated by antiphospholipid antibody syndrome (APS) in SLE. However, apart from a few case presentations related to mesenteric involvement with small vessel venulitis and renal venulitis, comprehensive studies about veins in SLE patients are lacking. Human Growth Differentiation Factor (HDGF15) and D-dimer are associated with venous thromboembolism [1]. P selectin is a biomarker of endothelial injury [2] and citrullinated histone 3 is a marker of NETosis [3] <h3>Objectives:</h3> The study aimed to characterize vein involvement in SLE with evaluation of vein wall thickness, vessel inflammation/injury markers, HDGF-15, CH3, p-selectin. We further investigated association between these characteristics and patient's clinical variables, autoantibodies, disease activity, and the presence of APS. <h3>Methods:</h3> In this cross-sectional study, 68 patients with SLE (mean age 41.3 ± 2.1 years) who fulfilled American College of Rheumatology 2019 Classification Criteria and followed at Gazi University were involved. SLE patients were dichotomized into three groups according to APS status: 1- those negative for APS antibodies (n=30), 2- those with positive APS antibodies (n=21) without history of thrombosis, and 3- those clinically diagnosed with APS according to the 2023 ACR/EULAR criteria (n=17). The results were compared with a healthy control group (n=20, mean age 41.2± 1.8 years) and patients diagnosed with rheumatoid arthritis with 2010 ACR/EULAR criteria (n=17, mean age 45.0±1.2 years). An experienced radiologist, who was blinded to clinical data, conducted neck, liver, and bilateral lower extremity venous and arterial Doppler ultrasonography on the same day of clinical assessment. Venous blood samples were obtained at the time of clinical evaluation and HDGF15, p-selectin, and CH3 levels were studied in SLE and healthy controls <h3>Results:</h3> The venous thicknesses in all evaluated veins werw significantly different between groups. Regardless of the positivity of APS antibodies or clinical status, venous thickness in SLE patients was greater than RA patients and healthy controls (Table 1). Venous thicknesses in patients with RA and healthy controls were comparable (p&gt;0.05). P-selectin, HDGF15, and CH3 levels were significantly higher in patients with clinical APS as compared to other SLE subgroups and lowest in healthy controls (p&lt;0.05 for all, Figure 1). Spearman analyses showed a positive correlation across all vascular thicknesses. Distinctively, the right superficial femoral vein thickness correlated with anti-beta-2 glycoprotein 1 (anti-2GP1) IgG antibody titers, and the portal vein thickness correlated positively with anti-cardiolipin IgM and anti-2GP1 levels. No association was observed between vein thicknesses and clinical activity parameters of SLE. <h3>Conclusion:</h3> Our findings indicate a widespread vein involvement in SLE patients, characterized by increased wall thicknesses. Subclinical vein inflammation, attributed to vein injury and NETosis, is particularly pronounced in individuals with SLE-APS. Assessment of HDGF15, p-selectin, and CH3 levels in SLE patients with positive thrombotic antibodies might help to anticipate patients at risk of venous complications. <h3>REFERENCES:</h3> [1] Hansen ES, et al., INVENT Consortium. Blood. 2020;136:1863-1870. [2] Setiadi H, et al. Blood Adv. 2019;3:168-183 [3] Li Y, et al. Front Cell Dev Biol. 2022;10:1071550. <b>Table 1.</b> <h3>Acknowledgements:</h3> <b>NIL.</b> <h3>Disclosure of Interests:</h3> <b>None declared.</b>