A multidisciplinary study of the role of genetic and acquired autoimmune abnormalities in the onset of systemic manifestations of antiphospholipid syndrome.

Antiphospholipid syndrome(APS)is characterized by arterial or venous thrombosis and repeated fetal losses in the presence of antiphospholipid antibodies (aPL). Multiple agents could be involved as causative factors in the development of APS. The reseach includes six thematic groups: 1.To determine prevalence aPL type and level (LA,aCL,ß2GPI) in patients with thrombotic and non-thrombotic manifestations of the disease. 2.Analysis of gene polymorphisms which are important for the T(H)17 and regulatory T cells differentiation in APS patients, and their correlation with the disease manifestations and severity. 3.Determination of aPL association with the innate thrombophilia(deficiency of AT,PC,PS,FXII,polymorphisms FV Leiden,prothrombin 20210,and MTHFR)and characteristics of clinical expression. 4.Determination of aPL role in the development of induced atherosclerosis,using the latest technology methods:64 MSCT,which would present the extent and location of changes in blood vessels. 5.To determine the importance of oxidative stress, markers of inflammation, endothelial adhesion receptor molecules induction and activation, as additional factors in the pathophysiology and multifactorial etiology of APS thrombosis. 6.To continue in obtaining the national APS patients’ registry with the possibilities of it participating in international studies. 7. To overview the patient outcomes with various APS therapeutic protocols.