Cerebral Venous Thrombosis in Paroxysmal Nocturnal Hemoglobinuria
نویسندگان
چکیده
منابع مشابه
Cerebral Venous Thrombosis in Paroxysmal Nocturnal Hemoglobinuria
Dural sinus thrombosis developed in two young women with paroxysmal nocturnal haemoglobinuria (PNH). The incidence, the clinical presentation, the radiologic findings, the therapy and the pathophysiology of haemolysis and thrombosis are discussed.
متن کاملThrombosis in paroxysmal nocturnal hemoglobinuria.
The most frequent and feared complication of paroxysmal nocturnal hemoglobinuria (PNH) is thrombosis. Recent research has demonstrated that the complement and coagulation systems are closely integrated with each influencing the activity of the other to the extent that thrombin itself has recently been shown to activate the alternative pathway of complement. This may explain some of the complexi...
متن کاملAn unusual cause of cerebral venous sinus thrombosis. Paroxysmal nocturnal hemoglobinuria.
Cerebral venous sinus thrombosis caused by paroxysmal nocturnal hemoglobinuria is uncommon. Our case is a 44-year-old woman who presented with a 2 day history of headaches, nausea, and seizures followed by a Todd`s paresis; she had been diagnosed as paroxysmal nocturnal hemoglobinuria for 4 years. A magnetic resonance venography revealed extensive thrombosis of the cerebral venous sinus. She re...
متن کاملParoxysmal nocturnal hemoglobinuria presenting as cerebral venous sinus thrombosis: a case report
Paroxysmal Nocturnal Hemoglobinuria (PNH) is a rare type of acquired hemolytic anemia that is frequently associated with thrombophilia. It may rarely present with cerebral venous sinus thrombosis, which manifests clinically with signs of raised intracranial pressure and requires lifelong anticoagulation therapy. One such rare presentation was seen in a 28 years old male who had history of recur...
متن کاملMechanisms and clinical implications of thrombosis in paroxysmal nocturnal hemoglobinuria.
Paroxysmal nocturnal hemoglobinuria (PNH) is a rare acquired disease characterized by a clone of blood cells lacking glycosyl phosphatidylinositol (GPI)-anchored proteins at the cell membrane. Deficiency of the GPI-anchored complement inhibitors CD55 and CD59 on erythrocytes leads to intravascular hemolysis upon complement activation. Apart from hemolysis, another prominent feature is a highly ...
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ژورنال
عنوان ژورنال: Medicine
سال: 2015
ISSN: 0025-7974
DOI: 10.1097/md.0000000000000362