Abstract
First part of the thesis summarizes current knowledge about platelet functions in systemic lupus erythematosus (SLE), their role in thrombotic complications, maintaining of disease activity and acceleration of atherogenesis. Experimental part consists of cross-section study of 63 SLE patients.
We examined organ manifestations of SLE, antiphospholipid antibodies, platelets morphology, thromboses or hemorrhages in history. Platelets aggregation was induced by low concentrations of ADP and epinephrine by aggregometry.
Each blood sample was examined by PFA-100 aggregometry too. Aggregation activity is altered is SLE platelets.
Tendency to higher aggregation activity is perceptible especially in patients non-treated by aspirin or NSAIDs and also in smokers. Aspirin therapy removed these differences.
Aspirin effect on platelet aggregation seems to be better in patients with more voluminous (activated) platelets.