Ljudmila Stojanovich received her PhD in Medicine, with the thesis “Neuropsychiatric manifestations in patients with Systemic Lupus Erythematosus” in 1999. She is the scientific director in the Bezhanijska Kosa, University Medical Center of Belgrade University, where she is currently a Research Professor. Her research focuses on Systemic Lupus Erythematosus, Antiphospholipid Syndrome, and Vaccination in patients with Autoimmune Rheumatic diseases. She is an author of three monographs and of about 250 articles on various aspects of Rheumatic disorders, published in international and domestic journals and in conference proceedings. She is in Editorial Boards/Reviewer in the “Current Contests” or “Science citation index”, like Lupus, Cellular and Molecular Neurobiology, The Journal of Vaccine, The Journal of Rheumatology, Allergologia et Immunopathologia and others. She is a member of number International Project, like of “the European Forum on Antiphospholipid Antibodies”, “Multicentre Studies Antiphospholipid Antibodies, Infections and Autoimmune Diseases”. She is a mentor/Supervisor of a numbers of post-doc students.


Introduction: Antiphospholipid syndrome (APS) patients suffer from various cardiovascular manifestations with the presence of antiphospholipid antibodies (aPL). APS may manifest itself as a primary disease (PAPS) or as a secondary disease, most commonly in the context of Systemic Lupus Erythemathosus (SLE). Patients and methods: We analyzed 488 patients: 346 PAPS and 142 patients with secondary APS (398 female and 90 male, 45.03±13.61 years). aPL analysis included analysis of aCL (IgG/IgM), ß2GPI and LA. In all patients echocardiography study was performed in order to reveal presence of pseudoinfective endocarditis or valve thickening or dysfunction not related to age. Results: In our study group, there was 38.7% pts with aCL IgG antibodies, 53.1% with aCL IgM, 34.1% with ß2GPI IgG, 41.8% ß2GPI IgM and 53.2% with LA. There was no statisticaly significant difference between overall cardiac manifestations and the type of aPL. Highly statistically significant difference was revealed considering presence of aCL-IgG and aCL-IgM antibodies and pseudoinfective endocarditis (p=0.004, p=0.003 respectively) and presence of aCL-IgG and valvular dysfunction (p=0.023). Valvular manifestations in our cohort were significantly related to titers of aCL antibodies. The level of aCL IgG (p=0.005, Pearson +0.138) were in positive correlation with presence of pseudoinfective endocarditis. Conclusion: Our study showed that presence of anticardiolipin antibodies in APS patients brings higher probability of valvular changes development. Higher titers of aCL IgG bring greater probability of pseudoinfective endocarditis development in our APS cohort.

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