Platelet-activating anti–platelet factor 4 disorders (Registro nro. 22754)

000 -Cabecera
Campo de control interno 02385nam a2200253 4500
001 - Número de control
control field ESSALUD
007 - Tipo material - Descripcion fisica - info general
Tipo material - Descripcion fisica - info general ta
008 - Elementos de Longitud Fija - Información General
Elementos de Longitud Fija - Información t pe ||||| |||| 00| 0 spa d
040 ## - Origen de la Catalogación
Origen de la Catalogación BMG
041 ## - Idioma
Idioma spa
100 ## - Autor
Autor Warkentin, Theodore E.
Rol del Autor Autor
9 (RLIN) 53833
245 ## - Titulo
Titulo Platelet-activating anti–platelet factor 4 disorders
300 ## - Páginas
Paginación páginas: 478-491
520 ## - Resumen
Resumen Platelet-activating antibodies against platelet factor 4 (PF4) cause highly prothrombotic disorders with reduced platelet counts. In heparin-induced thrombocytopenia (HIT), these antibodies bind PF4–heparin complexes, causing heparin-dependent platelet activation. Less common autoimmune and spontaneous HIT variants that are triggered by heparin and nonpharmacologic polyanions, respectively, have atypical clinical features and antibodies with additional heparin-independent platelet-activating properties. Vaccine-induced immune thrombocytopenia and thrombosis (VITT) antibodies directly target PF4. Initially, VITT was linked to adenoviral vector–based coronavirus disease 2019 vaccines, but in rare cases, an immune thrombocytopenia and thrombosis disorder that is clinically nearly identical to VITT can be caused by infection resulting from natural exposure to viruses, especially adenovirus. In persons with the IGLV3-21*02/*03 gene, anti–adenovirus protein VII antibody specificity shifts to PF4 by way of a specific somatic hypermutation (K31E) that creates VITT antibodies. In VITT-like monoclonal gammopathy of thrombotic significance, monoclonal anti-PF4 antibodies cause chronic prothrombotic conditions. Accurate diagnosis relies on distinct assays for HIT and VITT antibodies. Beyond anticoagulation, inhibition of FcγIIa receptor–mediated platelet activation may be needed for anti-PF4 disorders with heparin-independent reactivity (e.g., high-dose immune globulin in acute disease manifestations and Bruton’s tyrosine kinase inhibitors in chronic manifestations).
650 ## - Temas - Descriptores
Temas - Descriptores ANTICOAGULACION
9 (RLIN) 53834
650 ## - Temas - Descriptores
Temas - Descriptores TROMBOEMBOLISMO
9 (RLIN) 32218
650 ## - Temas - Descriptores
Temas - Descriptores ANTICOAGULACION
9 (RLIN) 53834
650 ## - Temas - Descriptores
Temas - Descriptores VACUNAS
9 (RLIN) 8158
650 ## - Temas - Descriptores
Temas - Descriptores CORONAVIRUS
9 (RLIN) 39659
650 ## - Temas - Descriptores
Temas - Descriptores INFECCIONES VIRALES
9 (RLIN) 53766
700 ## - Autor Personal
Autor Personal Greinacher, Andreas
9 (RLIN) 53835
773 0# - Revista (Relacion con el numero)
Host Biblionumber 22717
Host Itemnumber 22638
Ciudad, Editorial Massachusetts NEJM Group
Codigo barras item/ejemplar NEJM005
Titulo de la Revista The New England Journal of Medicine
Número de control de registro ESSALUD
ISSN 0028-4793
942 ## - Elementos de Koha
Tipo de Documento Artículos
Fecha procesamiento 2026-07-31
Catalogador SQB

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