Abstract

Toxoplasma gondii is the cause of toxoplasmosis. More than 60% of the world's population is infected with T. gondii. The prevalence of acute toxoplasmosis in pregnant women is 4.8 per 1000 women. The risk of fetal infection until 13 weeks of gestation is about 15% and after that the risk of infection increases and reaches 72% at 36 weeks of gestation. Fibrinogen is one of the most important acute phase proteins in pregnant women. Physiologically, there is an increase in blood procoagulant levels (include fibrinogen), but anticoagulant levels in the blood decrease during pregnancy and the performance of the fibrinolytic system weakens. In this condition, if the woman is infected with toxoplasmosis during pregnancy, the excessive elevation of coagulation factors may increase the risk of thromboembolism. T. gondii infection is known to increase IFN-γ secretion in sheep and rat experimental animals, then secrete fibrinogen-like protein 2 (fgl2) which plays a role in fibrin deposition and thrombosis. Fgl2 is a transmembrane prothrombinase that directly cleaves prothrombin to thrombin. The prothrombinase activity of Fgl2 was observed in abortion. Overall, the coagulation system gets stronger in pregnant women. However, the inflammatory process due to toxoplasmosis results in a prothrombic state situation associated with increased fibrinogen levels. Increased fibrinogen further increases inflammation. Excessive increases in fibrinogen increase the risk of thromboembolism that causes placental infarct and causes abortion.

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