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Nonspecific Removal of Sepsis Mediators

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Sepsis

Sepsis is a growing clinical problem in our society, with an estimated annual incidence rate of above 300 cases per 100,000 people and mortality that exceeds 30% in those individuals suffering the disease (Esteban et al. 2007; Angus et al. 2001). Despite apparent recent successes in the treatment (Bernard et al. 2001), sepsis morbidity and mortality remain very high. This implies that new efforts are needed to translate to the clinical practice the huge information that preclinical research has generated in the past decade about the mechanisms of sepsis.

One of the problems is that sepsis entails multiple disorders in different organs and systems, the individual contribution of each one, or the dominance of a particular one, in the disease process being unclear. Initially, sepsis was considered a disorder due to an uncontrolled inflammatory response (Hotchkiss and Karl 2003). However, clinical interventions directed to the inflammatory elements did not reduce morbidity and mortality associated with the disease (Hotchkiss and Karl 2003). Since inflammation and coagulation are tightly linked, and sepsis-associated coagulopathy is almost universal in patients with severe sepsis, antithrombotic-targeted therapy has been clinically investigated with an apparent success, though controversial and limited (Costa et al. 2007; Nadel et al. 2007). Recent data also suggests that most deaths from sepsis are due to an extensive death of immune mediator cells (Hotchkiss and Nicholson 2006). Therefore, in 15 years we have moved from immunostimulation to immunosuppression as cause of sepsis, with one stop in coagulation disorders.

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Pérez-Fernandez, X.L., Riera, J.S., Mañez, R. (2008). Nonspecific Removal of Sepsis Mediators. In: Rello, J., Restrepo, M.I. (eds) Sepsis. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-540-79001-3_6

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