Showing papers on "Blood coagulation disorder published in 2014"
TL;DR: This chapter will describe gene delivery via portal vein administration in mice and dogs to correct the blood coagulation disorder hemophilia B.
Abstract: The liver is a very complex organ with a large variety of functions, making it an attractive organ for gene replacement therapy Many genetic disorders can be corrected by delivering gene products directly into the liver using viral vectors In this chapter, we will describe gene delivery via portal vein administration in mice and dogs to correct the blood coagulation disorder hemophilia B Although there are multiple delivery routes for both viral and non-viral vectors in animals, portal vein administration delivers vectors directly and efficiently into the liver Complete correction of murine hemophilia B and multi-year near-correction of canine hemophilia B have been achieved following portal vein delivery of adeno-associated viral (AAV) vectors expressing factor IX from hepatocyte-specific promoters Peripheral vein injection can lead to increased vector dissemination to off-target organ such as the lung and spleen Below, we will describe portal vein injection delivery route via laparotomy
8 citations
TL;DR: This work reports on a patient who showed rapid resolution of ASDH with coagulopathy and discusses such a rare case with speculation of the coagULopathy as a factor to promote this phenomenon.
Abstract: Acute subdural hematoma (ASDH) constitutes one of the most critical emergencies in neurosurgery and rapid spontaneous resolution of ASDH is an infrequent phenomenon. Several mechanisms have been attributed to explain this phenomenon including redistribution of subdural blood, dilution by cerebral spinal fluid and brain atrophy. Rapid resolution of ASDH related to coagulopathy is a rare phenomenon; to our knowledge, only one case has been reported. We report on a patient who showed rapid resolution of ASDH with coagulopathy and also discuss such a rare case with speculation of the coagulopathy as a factor to promote this phenomenon.
7 citations
Patent•
30 Jul 2014
TL;DR: In this paper, a novel class of compounds for stopping, avoiding and preventing bleeding or for strengthening the hemostatic system was proposed. But, their use was limited to the prevention of bleeding in humans and other mammals which may be the result of hypocoagulation of the blood coagulation system.
Abstract: The present invention relates to a novel class of compounds for stopping, avoiding and preventing bleeding or for strengthening the hemostatic system. The novel compounds described in the invention, pharmaceutically acceptable salts thereof and/or pharmaceutically acceptable compositions thereof can be used for stopping, avoiding and preventing bleeding in humans and other mammals which may be the result of a state of hypocoagulation of the blood coagulation system, a blood coagulation disorder, hematologic disorders, hemorrhagic disorders, hemophilia, factor VII deficiency, pharmacological treatment, injury, disease, disorders associated with bleeding, surgical intervention, hypothermia, menstruation and pregnancy, and a variety of other human and mammalian diseases associated with blood clotting.
1 citations
TL;DR: Two relatively rare cases involving factor XIII subunit deficiency and antiphospholipid syndrome (APS) with concomitant systemic lupus erythematosus (SLE) in two patients undergoing flap reconstructions after tumor excision are evaluated.
Abstract: Coagulation disorders can be classified into two types: excessive bleeding and excessive clotting. Furthermore, the severity of the coagulation disorders can vary significantly among patients. We evaluated two relatively rare cases involving factor XIII subunit deficiency and antiphospholipid syndrome (APS) with concomitant systemic lupus erythematosus (SLE) in two patients undergoing flap reconstructions after tumor excision. In the patient with excessive bleeding as a result of a factor XIII subunit deficiency, flap necrosis occurred from a large subcutaneous hematoma that pressed on the perforator pedicle. Normal clotting function was restored during the surgery by administering a factor XIII preparation (Fibrogammin® P). The patient with excessive clotting as a result of APS and SLE suffered necrosis of the flaps after undergoing radial forearm free flap (RFFF) and pedicled pectoralis major musculocutaneous (PMMC) flap operations. With clotting factor deficiencies, there are patients in whom no evidence of a coagulation disorder exists preoperatively. It is important for surgeons to pay close attention to the potential for coagulation disorders patients and to consult with specialists promptly when indicated.