The pathogenesis of pleural space loculation and fibrosis

Abstract

Organization of parapneumonic effusions may complicate pneumonia, and, annually, thousands of patients require procedures to treat intrapleural loculation and fibrosis. Surgical procedures are often used for the treatment, as fibrinolytic therapy is now not a routine and is undergoing reassessment. Investigation of mechanisms that underlie intrapleural loculation and fibrosis is therefore timely, as are studies on new strategies to medically address these problems with improved efficacy and safety. Contributions made over the past year include basic and translational studies unified by their broad focus on mechanisms by which the pleural compartment undergoes repair. Intrapleural single-chain urokinase was reported to effectively reverse intrapleural loculation when compared with commercially available agents in rabbits with tetracycline-induced pleurodesis. The ability of exogenous sclerosants to produce intrapleural loculation and fibrosis was compared. Overexpression of transforming growth factor beta in the pleural mesothelium promoted subpleural fibrosis, implicating the mesothelial cell in the pathogenesis of this lesion. A new model of pleurodesis in mice was reported, which could facilitate the use of transgenic animals to study the pathogenesis of pleural injury. New findings consolidate and extend the view that common mechanisms by which intrapleural organization occurs can be exploited to either generate pleurodesis or effectively reverse intrapleural loculation and fibrosis.