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EL PAPEL TROMBOGENICO DE UN SISTEMA FIBRINOLITICO ANORMAL

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EL PAPEL TROMBOGENICO DE UN SISTEMA FIBRINOLITICO ANORMAL

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El sistema fibrinolítico se encuentra expuesto a numerosos factores que pueden alterar el equilibrio que mantienen la plasmina, sus precursores, los activadores e inhibidores del sistema. Se plantean los conocimientos actuales y el objetivo de las investigaciones en el futuro.
kwaan9.jpg Autor:
Hau C. Kwaan
Columnista Experto de SIIC

Institución:
Division of Hematology/Oncology School of Medicine Northwestern University of Feinberg IL, USA

Artículos publicados por Hau C. Kwaan
Coautores
Lisa N. Boggio, MD.*  Chadi Nabhan, MD* 
Division of Hematology and Oncology, Department of Medicine, Northwestern University Feinberg School of Medicine and Robert H. Lurie Comprehensive Cancer Center of Northwestern University, Chicago, IL*
Recepción del artículo
6 de Julio, 2004 		Primera edición
7 de Junio, 2005 		Segunda edición, ampliada y corregida
7 de Junio, 2021

EL PAPEL TROMBOGENICO DE UN SISTEMA FIBRINOLITICO ANORMAL

Resumen
Cuando hay un desequilibrio en el sistema fibrinolítico, ya sea adquirido o hereditario, se encuentra aumentado el riesgo de sangrado o de trombosis. Este artículo describe las características de la fibrinólisis anormal que llevan a la trombosis. Los trastornos hereditarios son infrecuentes y pueden afectar la síntesis de plasminógeno, sus activadores y sus inhibidores. Estas anormalidades en la síntesis de plasminógeno y el polimorfismo en el inhibidor de los activadores del plasminógeno tipo 1 (IAP-1) pueden desembocar en eventos tromboembólicos. Los trastornos adquiridos se encuentran en una variedad de enfermedades, principalmente diabetes, cáncer y enfermedades inflamatorias. Los medicamentos también pueden elevar el riesgo de trombosis a través de un aumento en la producción de los inhibidores del plasminógeno o una disminución en la producción de la proteína S. Factores trombofílicos adicionales como deficiencias de la proteína C, de la proteína S y de antitrombina; mutaciones del factor V y la protrombina, y la producción excesiva de factores de la coagulación como los factores VII y II, deben considerarse parte del desarrollo de las condiciones tromboembólicas. El manejo continúa siendo problemático al no haber terapias a largo plazo que restituyan el equilibrio del sistema fibrinolítico.

Palabras clave
Plasminógeno, fibrinólisis, trombosis, cáncer, estados de hipercoagulabilidad


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THE THROMBOGENIC ROLE OF AN ABNORMAL FIBRINOLYTIC SYSTEM

Abstract
When there is an imbalance of the fibrinolytic system, either acquired or hereditary, the risk of bleeding or thrombosis increases. This article describes the characteristics of abnormal fibrinolysis that leads to thrombosis. Hereditary disorders are uncommon and can affect the synthesis of plasminogen, its activators, and its inhibitors. These abnormalities of plasminogen synthesis and polymorphisms in plasminogen activator inhibitor 1 (PAI-1) can lead to thromboembolic events. Acquired disorders are found in a variety of diseases, especially in diabetes, cancer, and inflammatory states. Medications can also increase the risk of thrombosis through increased production of plasminogen inhibitors or decreased production of protein S. Additional thrombophilic factors such as deficiencies of protein C, protein S, and antithrombin; mutations of factor V and prothrombin; and excessive production of clotting factors such as factor VIII and II must be considered in the development of thromboembolic conditions. Management continues to be problematic with no long-acting therapy to counteract an imbalance of the fibrinolytic system.

Key words
Plasminogen, fibrinolysis, thrombosis, cancer, hypercoagulable states


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Especialidades
Principal: Hematología
Relacionadas: Bioquímica, Diagnóstico por Laboratorio, Medicina Interna



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