The possible role of oxidative stress and paraoxonase (PON)/arylesterase (ARE) in the pathogenesis of acute immune thrombocytopenia. Following a triggering event such as infection or inflammation, antibody-coated platelets are destroyed by macrophages in the spleen and liver. The released foreign peptide fragments are presented to the T- and B-lymphocytes. While antibody synthesis continues with the stimulation of the B-lymphocytes, the peripheral thrombocyte destruction continues due to the cytotoxic T-lymphocytes activation. During the destruction of platelets in the reticuloendothelial system and the periphery, reactive oxygen species (ROS) are produced. Increasing ROS levels induces a decrease in the total antioxidant capacity (TAC) and an increase in the total oxidant status (TOS). As a result of this increased oxidative stress, deoxyribonucleic acid (DNA), protein, and lipid peroxidation ensues. Lipid peroxidation leads to formation of oxidized low-density lipoproteins (LDL). The released oxidized phospholipids and cholesterol esters interact with the free sulfhydryl groups of paraoxonase (PON), and inhibit the PON and arylesterase (ARE) activities. In addition, the PON activity is also reduced due to systemic inflammation. As a result, dysfunctional high-density lipoproteins (HDL) with impaired anti-atherogenic effects are produced. This impaired anti-atherogenic effect of HDL may increase the tendency to atherosclerosis.