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題名 | 敗血症發炎反應與凝血系統的交互作用=Interaction between Iinflammation and Coagulation |
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作者姓名(中文) | 陽光耀; 李毓芹; 彭瑞鵬; | 書刊名 | 中華民國重症醫學雜誌 |
卷期 | 6:3 民93 |
頁次 | 頁211-219 |
分類號 | 415.27 |
關鍵詞 | 敗血症; 發炎反應; 凝血系統; 活性蛋白C; 抗凝血Ⅲ; 組織因子路徑抑制劑; Sepsis; Inflammation; Coagulation; Activated protein C; Antithrombin Ⅲ; Tissue factor pathway inhibitor; TFPI; |
語文 | 中文(Chinese) |
中文摘要 | 在敗血症中,發炎反應與凝血系統之間存有許多相互影響的機制,其中最典型的例子就是瀰漫性血管內凝血及多重器官衰竭的發生。最近有愈來愈多的研究證據顯示,此兩種系統是密切相關的,不僅是發炎反應可以啟動活化凝血系統,凝血系統也會參與調節發炎反應的嚴重程度。目前已知全身性的發炎反應影響凝血系統之機轉,可經由促進組織因子中介參與活化凝血因子的生成、降低內生性抗凝血分子的作用與合成,如:抗凝血III(antithrombin III)、活性蛋白C(APC)及組織因子路徑抑制劑(TFPI)、或是經由抑制抗凝血之纖維素溶解作用,例如:PAI-1或TAFI,來產生過度凝血的現象。至於發炎前趨細胞激素,在調節凝血作用及纖維素溶解作用上,亦扮演了重要的角色;可是,雖然早期的研究顯示抗發炎反應治療藥物,理論上應有相當的療效,但是在最近的臨床研究中,卻發現其並無法改善敗血症患者的嚴重度及死亡率。因為,發炎反應與凝血機轉是相互影響的,而且在大多數的敗血症患者身上,都可以發現凝血系統過度活化的情形;因此,針對抗凝血系統的藥物似乎是治療敗血症的另一個重要的方向。在初期的臨床試驗已知,以抗凝血機制為標靶的治療,似乎可以降低敗血症的疾病嚴重度與死亡率;而且直到最近,由於對發炎反應與凝血機轉相互作用的病理機轉之進一步瞭解,發展出人工合成的人類活性蛋白C(drotrecogin α),其為第一個被臨床證實有效的抗敗血症藥物,可以積極降低敗血症及多重器官衰竭患者28天的死亡率。本文將會詳述發炎反應與凝血系統交互作用的機轉,並闡述這類抗凝血藥物如何參與兩者間的交互作用,並簡要分析這些藥物最近臨床試驗的結果。 |
英文摘要 | The relevance of the interaction between coagulation and inflammation as a response to severe infection, in its most extreme form manifesting as disseminated intravascular coagulation (DIC) and multiple organ dysfunction syndrome (MODS). Increasing evidence points to extensive cross-talk between these two systems, whereby inflammation leads not only to activation of coagulation, but coagulation also considerably affects inflammatory activity. Systemic inflammation results in activation of coagulation, due to tissue factor-mediated thrombin generation, downregulation of physiological anticoagulant mechanisms, e.g. antithrombin III, activated protein C, or tissue factor pathway inhibitor (TFPI), and inhibition of fibrinolysis, such as plasminogen activator inhibitor 1 (PAI-1) or thrombin activatable fibrinolysis inhibitor (TAFI). Proinflammatory cytokines play a central role in the differential effects on the coagulation and fibrinolysis pathways. However, despite promising preclinical results, interventions directed at the inflammatory elements have not reduced the morbidity and mortality associated with severe sepsis. In fact, inflammation and coagulation are tightly linked. Sepsis-associated coagulopathy is almost universal in patients with severe sepsis and septic shock. Preclinical observations indicate that antithrombotic-targeted therapy has the potential to reduce morbidity and mortality in this disease. Advances in the understanding of the molecular mechanisms that control clotting and inflammation have led to the successful development of recombinant human activated protein C (drotrecogin α) as the first antithrombotic-targeted therapy to significantly reduce 28-day mortality in patients with severe sepsis and multiple organ failure. Optimal use of this and other anticoagulant agents in sepsis will necessitate further basic research into the critical linkage between coagulation and inflammation. The pathophysiological and clinical significance of these anticoagulant agents and the relationship of coagulation to inflammation are discussed, as are results of clinical trials of antithrombotic therapy. |
本系統之摘要資訊系依該期刊論文摘要之資訊為主。