Those with an abnormal accumulation of air within the pleural space (a pneumothorax) can bleed into the cavity, which occurs in about 5% of cases of spontaneous pneumothorax, especially when lung bullae rupture. The resulting combination of air and blood within the pleural space is known as a hemopneumothorax. Bone growth in exostosis can create sharp edges, which can result in hemothorax by damaging adjacent arteries. It can occur postpartum due to the change in thoracic pressure during labor. Vascular
Vascular causes of hemothorax include rupture of the descending aorta, in which case it initially involves the left pleural and mediastinal area due to the close vicinity of the pleural cavity. Rarely, a rupture of the thoracic aorta can result in a hemothorax, but the bleeding usually occurs in the pericardial space. Spontaneous tearing of blood vessels is more likely to occur in those with disorders that weaken blood vessels such as some forms of Ehlers-Danlos syndrome, disorders that lead to malformed blood vessels as seen in Rendu-Osler-Weber syndrome, or in bleeding disorders such as hemophilia and Glanzmann thromboastenia. Other rare causes of hemothorax include neurofibromatosis type 1 and extramedullary hematopoiesis. Catamenial
Rarely, hemothoraces can arise due to extrapelvic endometriosis, a condition in which tissue similar to the lining that normally covers the inside of the uterus forms in unusual locations outside the pelvis.
Bosutinib (rINN/USAN; codenamed SKI-606, marketed under the trade name Bosulif) is a small molecule BCR-ABL and src tyrosine kinase inhibitor used for the treatment of chronic myelogenous leukemia. Originally synthesized by Wyeth, it is being developed by Pfizer. Mechanism
It is an ATP-competitive Bcr-Abl tyrosine-kinase inhibitor with an additional inhibitory effect on Src family kinases (including Src, Lyn and Hck). It has also shown activity against the receptors for platelet derived growth factor and vascular endothelial growth factor. Bosutinib inhibited 16 of 18 imatinib-resistant forms of Bcr-Abl expressed in murine myeloid cell lines, but did not inhibit T315I and V299L mutant cells.Bosutinib is metabolized through CYP3A4. Medical uses
Bosutinib received US FDA and EU European Medicines Agency approval in September 2012, and March 2013, respectively for the treatment of adults with Philadelphia chromosome-positive (Ph+) chronic myelogenous leukemia (CML) with resistance, or intolerance to prior therapy. Contraindications
Bosutinib has two known absolute contraindications, which are: known hypersensitivity to bosutinib and liver impairment. Interactions
Bosutinib is both a substrate and an inhibitor of P-glycoprotein (P-gp) and CYP3A4. Hence P-gp and CYP3A4 inhibitors may increase plasma levels of bosutinib. Likewise CYP3A4 inducers may reduce plasma concentrations of bosutinib. It may also alter the metabolism and uptake (into the GIT by means of its P-gp inhibitory effects) of other drugs that are substrates for P-gp and CYP3A4. Notes
See also
Discovery and development of Bcr-Abl tyrosine kinase inhibitors

References
External links
"Bosutinib". Drug Information Portal. U.S. National Library of Medicine.