Current view on alveolar coagulation and fibrinolysis in acute inflammatory and chronic interstitial lung diseases
Review published in Thrombosis and haemostasis (2008)
Abstract
Acute inflammatory and chronic interstitial lung diseases are characterized by excessive and persistent fibrin deposition in the lung. Intraalveolar fibrin accumulation, observed under these conditions, arises from a leakage of plasma proteins (including fibrinogen) into the alveolar space in combination with a disbalance of alveolar haemostasis. Tissue factor in association with factor VIIa and inhibition of urokinase by plasminogen activator inhibitor-1 are major factors that are responsible for the procoagulant and antifibrinolytic state. In addition, in acute respiratory distress syndrome (ARDS) patients, factor VII-activating protease and extracellular RNA, which may be released into the extracellular milieu from damaged cells during lung injury, may contribute to fibrin formation as well. Fibrin itself can increase vascular permeability, influence the expression of inflammatory mediators and alter the migration and proliferation of various cell types. Additionally, fibrin may inactivate pulmonary surfactant and provide a matrix on which fibroblasts can migrate and produce collagen. Furthermore, cellular activities of haemostatic proteases may also contribute to proinflammatory and fibrotic processes in the lung. The application of coagulation inhibitors, like tissue factor pathway inhibitor, active site-inactivated factor VIIa, activated protein C, antithrombin, heparin or hirudin turned out to be beneficial in experimental models of acute and chronic lung injury. However, the ability of anticoagulant and profibrinolytic agents to improve clinical outcome remains to be elucidated. In the current article, the role of the alveolar coagulation and fibrinolysis systems in acute inflammatory and chronic interstitial lung diseases is discussed with regard to pathomechanisms and modalities of intervention.
Abstract sourced from PubMed (NCBI) for the cited record. See the original publication for the authoritative version.
Resumen
Acute inflammatory and chronic interstitial lung diseases are characterized by excessive and persistent fibrin deposition in the lung.
Por qué esto importa para la hirudoterapia
Esta revisión examina la coagulación alveolar y la fibrinólisis en enfermedades pulmonares inflamatorias agudas e intersticiales crónicas, describiendo mecanismos procoagulantes y antifibrinolíticos —factor tisular, factor VIIa, inhibidor del activador del plasminógeno-1— y las consecuencias de la deposición intraalveolar de fibrina. Señala que varios inhibidores de la coagulación, incluida la hirudina, fueron beneficiosos en modelos experimentales de lesión pulmonar aguda y crónica, aunque el beneficio clínico de los agentes anticoagulantes/profibrinolíticos sigue sin demostrarse. La mención explícita de la hirudina hace que esto sea relevante para el interés de la ASH en los anticoagulantes derivados de sanguijuelas y sus posibles aplicaciones terapéuticas. Sin embargo, la referencia a la hirudina se limita a modelos experimentales preclínicos dentro de una revisión amplia, sin datos de terapia con sanguijuelas ni de secretoma.
Citación
Current view on alveolar coagulation and fibrinolysis in acute inflammatory and chronic interstitial lung diseases
Wygrecka M et al. · Thrombosis and haemostasis, 2008
Contexto clínico relacionado
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Añadido a la biblioteca ASH: May 27, 2026 · Última actualización del sitio: 18 de junio de 2026