Sociedad Americana de Hirudoterapia

The tissue factor pathway in disseminated intravascular coagulation.

Review published in Seminars in thrombosis and hemostasis (2001)

Última actualización: 18 de junio de 2026Revisado por: ASH Editorial Board
Artículo de investigación — revisión de evidenciaReferencia del artículo
Evidence: Narrative reviewDesarrollo de fármacosFarmacología salivalØsterud et al. · Seminars in thrombosis and hemostasis, 2001

Abstract

In most instances, tissue factor (TF) exposed to the circulation is the sole culprit underlying the initiation of disseminated intravascular coagulation (DIC), although notable exceptions because of a more direct activation of the coagulation system, by snake venoms, for example, do occur. Peripheral monocytes and subendothelial structures are the potential sources of such TF; in the former, TF emerges on the cell surface on synthesis induction and in the latter it becomes available subsequent to permeability changes or damage to the endothelium. Subendothelial TF is constitutively present in fibroblasts, pericytes, and macrophages and at a higher than normal level in tumor-associated macrophages. This scenario of coagulation activation probably describes the principal events underlying emerging acute DIC states under pathophysiological conditions such as abruptio placentae, septic abortion, amniotic fluid embolization, and pregnancy toxemia. Under disease conditions associated with DIC, the continuous exposure to excess TF typically exhausts the available tissue factor pathway inhibitor (TFPI), leading to rampant thrombin generation, persistent feedback activation of factor XI (FXI) by the generated thrombin, and hence virtually uncheckable ongoing fibrin generation (DIC). Recently, it was shown that patients subject to meningococcal sepsis had comparatively large amounts of mainly monocyte-derived circulating TF-containing microparticles. Because phosphatidylserine (PS) is exposed on such particles, in addition to TF, they probably contribute crucially to DIC during meningococcal sepsis. Although endothelial cells (EC) have been shown to express large amounts of TF in vitro, this observation hardly relates to the situation in vivo, where, in contrast, synthesis and exposure of EC TF is very limited and not likely to be of any significance in emerging and ongoing DIC.

Abstract sourced from PubMed (NCBI) for the cited record. See the original publication for the authoritative version.

Publication typeJournal ArticleReview
Indexed MeSH termsAnimalsBlood CoagulationDisseminated Intravascular CoagulationFemaleHumansPregnancySignal TransductionThromboplastin

Resumen

In most instances, tissue factor (TF) exposed to the circulation is the sole culprit underlying the initiation of disseminated intravascular coagulation (DIC), although notable exceptions because of a more direct activation of the coagulation system, by snake venoms, for example, do occur....

Por qué esto importa para la hirudoterapia

Esta revisión examina el papel del factor tisular (FT) en el inicio y la propagación de la coagulación intravascular diseminada (CID), destacando cómo el exceso de FT agota el inhibidor de la vía del factor tisular disponible. Explora cómo los monocitos periféricos y las estructuras subendoteliales exponen FT a la circulación en diversas condiciones fisiopatológicas, tales como el desprendimiento prematuro de placenta, la embolia de líquido amniótico y la sepsis meningocócica. Si bien una comprensión profunda de las cascadas de coagulación y la enfermedad trombótica resulta fundamental para la anticoagulación farmacológica, este artículo no tiene relevancia directa para la hirudoterapia. Se centra por completo en la coagulopatía endógena humana sin mencionar las sanguijuelas, la hirudina ni las terapias derivadas de sanguijuela.

Citación

The tissue factor pathway in disseminated intravascular coagulation.

Østerud et al. · Seminars in thrombosis and hemostasis, 2001

Contexto clínico relacionado

Añadido a la biblioteca ASH: May 28, 2026 · Última actualización del sitio: 18 de junio de 2026

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