The cytokine‐mediated imbalance between coagulant and anticoagulant mechanisms in sepsis and endotoxaemia

Abstract

Abstract. Disseminated intravascular coagulation (DIC)is a frequently occurring complication of sepsis and may contribute to multiple organ failure. More insight into the pathogenesis of this derangement of the coagulation system is necessary to develop more effective therapeutic strategies for this condition. Recently, more detailed knowledge on the pathogenetic pathways involved in DIC has been obtained by the study of models of experimental bacteraemia and endotoxaemia in human subjects and non-human primates. The mechanisms that lead to activation of coagulation, potentiated by the simultaneous depression of physiological inhibitory systems and to impaired function of the fibrinolytic system, are outlined in this review. In addition, the mediatory role of various cytokines in the derangement of coagulation is discussed.

Candidate inhibitors of porcine complement

“…They can act in autokrine, paracrine or endocrine manner, inducing their effects on the cells who released the cytokine, on adjacent cells or on distant cells respectively (2). The cytokines induce a range of effects like chemotaxis, upregulation of receptors on cells, trigger blood clotting, and capillary leak (15)(16)(17). Effects of the cytokines along with effects of a range of other mediators like lipid-metabolites and reactive-oxygen species "create" the state of inflammation (14).…”

Tissue factor and tissue factor pathway inhibitor

“…This 'cross talk' between the coagulation and inflammatory systems is increasingly recognised. The central role of tissue factor as the sole activator of coagulation in sepsis has been confirmed by laboratory studies [59,64]. Animal models of sepsis are broadly divided into those where a septic insult is administered systemically (intravenous injection of endotoxin) or as a local phenomenon (caecal ligation and puncture).…”

A case of thyroid storm with a markedly elevated level of circulating soluble interleukin-2 receptor complicated by multiple organ failure and disseminated intravascular coagulation syndrome

“…TS can readily fulfill two of the four items in the diagnostic criteria for SIRS [15], fever (>38.0°C) and tachycardia (>90/min), because these symptoms are also diagnostic items for TS [1,2]. Thus, TS may be to be complicated by DIC via pathophysiological mechanisms similar to those in SIRS, which include a cytokine-mediated imbalance between coagulant and anticoagulant pathways [17]. Nevertheless, it is important to note that sIL2-R levels were indistinguishable in the presence or absence of SIRS, severe sepsis, or septic shock in nonstorm patients with acute onset medical conditions in an Emergency Department [18].…”