Institut für Klinische Molekularbiologie, Christian-Albrechts-Universität, Schittenhelmstr. 12, 24105 Kiel, Germany.
Hamostaseologie. 2011 May 2;31(2):94-102, 104. doi: 10.5482/ha-1134. Epub 2010 Dec 9.
Overwhelming evidence has linked inflammatory disorders to a hypercoagulable state. In fact, thromboembolic complications are among the leading causes of disability and death in many acute and chronic inflammatory diseases. Despite this clinical knowledge, coagulation and immunity were long regarded as separate entities. Recent studies have unveiled molecular underpinnings of the intimate interconnection between both systems. The studies have clearly shown that distinct pro-inflammatory stimuli also activate the clotting cascade and that coagulation in turn modulates inflammatory signaling pathways. In this review, we use evidence from sepsis and inflammatory bowel diseases as a paradigm for acute and chronic inflammatory states in general and rise hypotheses how a systematic molecular understanding of the "inflammation-coagulation" crosstalk may result in novel diagnostic and therapeutic strategies that target the inflammation-induced hypercoagulable state.
大量证据表明炎症性疾病与高凝状态有关。事实上，血栓栓塞并发症是许多急性和慢性炎症性疾病导致残疾和死亡的主要原因之一。尽管有这种临床认识，但长期以来，凝血和免疫被视为两个独立的实体。最近的研究揭示了这两个系统之间密切联系的分子基础。这些研究清楚地表明，不同的促炎刺激也会激活凝血级联反应，而凝血反过来又会调节炎症信号通路。在这篇综述中，我们使用脓毒症和炎症性肠病的证据作为一般急性和慢性炎症状态的范例，并提出假设，即系统地理解“炎症-凝血”相互作用如何可能产生针对炎症引起的高凝状态的新的诊断和治疗策略。
