Abstract
Every day the practitioner witnesses the results of obvious imbalances between coagulation and fibrinolysis, because they are central to the pathogenesis of cardiovascular disease, stroke, uncontrolled bleeding, and pulmonary thromboembolism. Astute observers have suspected that the deposition of fibrin in the distal air spaces may have a similar role in both acute and chronic lung disorders, typified by the adult respiratory distress syndrome (ARDS) and idiopathic pulmonary fibrosis, respectively. Diffuse alveolar damage, the pathologic counterpart of the early stages of ARDS, is characterized by widespread damage to the microvascular endothelial and alveolar epithelial cells, resulting in the formation of intraalveolar . . .