Abstract
Coagulation is a constant attendant of inflammation and is fundamental to confine infection and/or the inflammatory response to a limited area. Coagulation is tightly controlled by various factors, such as tissue factor (TF), finally activating thrombin, which cleaves fibrinogen to initiate fibrin clot formation. Systemic inflammatory response syndrome (SIRS) and sepsis remain a major health concern on intensive care units (ICUs) in the western world often ending in multiple organ dysfunction and death. The pathogenesis of both systemic disorders are attributed to an uncontrolled inflammatory response and dysregulated coagulation, the latter often causing disseminated intravascular coagulation (DIC), microvascular failure and multiple organ dysfunction [1, 2]. Fibrin(ogen) degradation products, D-dimers, Bβ15-42 and soluble fibrin are increased in septic patients with organ dysfunction [3, 4], but the contribution of these fragments to the pathogenesis of sepsis remains unclear.
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Jennewein, C., Tran, N., Zacharowski, K. (2011). The Inflammatory Potential of Fibrin(ogen) and its Degradation Products. In: Vincent, JL. (eds) Annual Update in Intensive Care and Emergency Medicine 2011. Annual Update in Intensive Care and Emergency Medicine 2011, vol 1. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-18081-1_6
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DOI: https://doi.org/10.1007/978-3-642-18081-1_6
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