Trombosis cerebral en presencia de un inhibidor especifico contra el factor xii de la coagulación
Archivos
Autores
Martínez Betancur, Octavio
López de Goenaga, Inés
Director
Tipo de contenido
Artículo de revista
Idioma del documento
EspañolFecha de publicación
1998
Título de la revista
ISSN de la revista
Título del volumen
Documentos PDF
Resumen
El presente informe determina la especificidad de un inhibidor de la coagulación dirigido contra el factor XII, activador intrínseco de la fibrinólisis plasmática, en un paciente con un evento oclusivo vascular cerebral agudo de tipo trombótico, sobre un transfondo de múltiples infartos cerebrales antiguos. Se excluyó la presencia de anticoagulante lúpico mediante la prueba de neutralización de plaquetas. Como resultado de la inhibición del factor XII, se demostró la ausencia de actividad fibrinolítica del plasma en presencia de trombosis aguda, al no detectar productos de degradación de la fibrina (dímero-D y gelación del etanol negativos) y por la prolongación anormal del tiempo de lisis de eugloublina.
We report the presence of an specific inhbitor directed against Hageman factor (factor XII) in a male patient who suffered occlusive stroke and showed tomografic evidence of multiple previous brain infarcts. The presence of a lupus anticoagulant was excluded by means of the platelet neutralisation test. The reduction of the fibrinolytic activity in response to thrombosis as a result of factor XII inhibition was demonstrated by the abnormal prolongation of the euglobin lysis time as well as the absence of fibrin degradation products (negative D-dimer assay and ethanol gelation test).
We report the presence of an specific inhbitor directed against Hageman factor (factor XII) in a male patient who suffered occlusive stroke and showed tomografic evidence of multiple previous brain infarcts. The presence of a lupus anticoagulant was excluded by means of the platelet neutralisation test. The reduction of the fibrinolytic activity in response to thrombosis as a result of factor XII inhibition was demonstrated by the abnormal prolongation of the euglobin lysis time as well as the absence of fibrin degradation products (negative D-dimer assay and ethanol gelation test).