Community acquired pneumonia (CAP) is still one of the most important causes of morbidity in adults. (1) In severe cases, parapneumonic effusions or empyema may develop. In these patients, a transitional fibrin neomatrix constitutes part of the acute inflammatory response as seen in sepsis. (2) The increased vascular permeability, mediated by several cytokines, such as IL-1, IL-6, IL-8, tumor necrosis factor (TNF), and platelet activator factor, allows migration of inflammatory cells, an increased fluid accumulation and bacterial invasion into pleural space. (3) At this stage, activation of the coagulation cascade leads to procoagulant activity and decreased fibrinolysis with deposition of fibrin in the pleural space. The activation of the fibrinolytic system produce the D-dimer and follow by increased other procoagulant markers like thrombin anti thrombin, fragment 1.2 (4-5) Several studies showed that the plasma D-dimer levels were increased even in community-acquired pneumonia patients. Moreover, others reported that Serum levels of AT-III, D-D and CRP at admission appear to be useful biomarkers for assessing the severity of CAP. However, no data exists about the fibrinolytic profile in patients with CAP alone in compare to CAP with parapneumonic effusion with and without empyema.