New knowledge concerning the role of inflammation in activation of fibrinolysis and in discoordination of its components interaction has been presented in the review. Considerable attention was given to molecular mechanisms of the haemostatic protein involvement in the acute phase of inflammation. An analysis of their level changes according to inflammation state has been proposed for thrombogenic risk assessment. Abundant consumption of plasminogen in situ as a result of coagulation induced by moderate level of inflammation is the first critical point in thrombus formation. Activated protein C leakage during severe inflammation is another trigger of thrombogenesis leading to possible death.