Ohsato K, Okamoto K
Department of Surgery I, University of Occupational and Environmental Health.
Nihon Rinsho. 1993 Jan;51(1):50-5.
A brief explanation of the molecular markers of coagulation, fibrinolysis and endothelial cell activation was done. The clinical significance of markers, such as, soluble fibrin monomer complex, FDP D-dimer, prothrombin fragment 1 + 2, thrombin-antithrombin III complex, plasmin-alpha 2 plasmin inhibitor complex and plasma thrombomodulin in our patients with disseminated intravascular coagulation (DIC) due to abdominal sepsis and malignancy is discussed. The coagulopathy in the DIC patients due to abdominal sepsis had a different aspect from that in the DIC patients due to malignancy. Activation of the coagulation and fibrinolytic systems in sepsis was milder than that in malignancy, despite the decrease of antithrombin III activity in the patients with sepsis. In the patients with sepsis, granulocyte elastase was increased. It was proposed that the coagulopathy was caused not only thrombin formation but also by granulocyte proteinase. It could be expected that the pathophysiology of disseminated intravascular coagulation should be clarified, because of the high sensitivity.
对凝血、纤维蛋白溶解和内皮细胞活化的分子标志物进行了简要解释。讨论了可溶性纤维蛋白单体复合物、FDP D-二聚体、凝血酶原片段1+2、凝血酶-抗凝血酶III复合物、纤溶酶-α2纤溶酶抑制剂复合物和血浆血栓调节蛋白等标志物在我们因腹部脓毒症和恶性肿瘤导致弥散性血管内凝血(DIC)患者中的临床意义。因腹部脓毒症导致的DIC患者的凝血病与因恶性肿瘤导致的DIC患者有所不同。尽管脓毒症患者抗凝血酶III活性降低,但脓毒症中凝血和纤维蛋白溶解系统的激活比恶性肿瘤中更轻。在脓毒症患者中,粒细胞弹性蛋白酶增加。有人提出凝血病不仅由凝血酶形成引起,还由粒细胞蛋白酶引起。由于高敏感性,可以预期弥散性血管内凝血的病理生理学将得到阐明。