Agrenius V, Chmielewska J, Widström O, Blombäck M
Dept of Thoracic Medicine, Karolinska Institute, Karolinska Hospital, Stockholm, Sweden.
Eur Respir J. 1991 Oct;4(9):1135-9.
Chronic malignant pleural effusions are usually treated with an intrapleurally administered irritant that creates an inflammatory reaction. The induced inflammation results in fibrin deposition and termination of fluid exudation. In the present study several factors in the coagulation system in the pleural fluid were followed during treatment with tube drainage and quinacrine instillation into the pleural space. In the chronic exudative phase before treatment, both thrombin activity and fibrinopeptide A (FPA), were present at low levels. During treatment the levels increased markedly. Beta-thromboglobulin, a platelet marker, showed a similar pattern. Prothrombin, antithrombin III, prekallikrein and kallikrein inhibiting activity showed no such variations in activity. The high thrombin activity and FPA level induced by treatment reflect an active process of fibrin formation which seems to play an important role in arresting chronic pleural exudation.
慢性恶性胸腔积液通常采用胸腔内注入刺激性物质进行治疗，该物质会引发炎症反应。诱导产生的炎症会导致纤维蛋白沉积并终止液体渗出。在本研究中，在进行胸腔置管引流和向胸腔内滴注喹吖因治疗期间，对胸腔积液中凝血系统的几个因素进行了跟踪监测。在治疗前的慢性渗出期，凝血酶活性和纤维蛋白肽A（FPA）水平均较低。治疗期间，这些水平显著升高。血小板标志物β-血小板球蛋白呈现出类似的模式。凝血酶原、抗凝血酶III、前激肽释放酶和激肽释放酶抑制活性在活性方面未表现出此类变化。治疗诱导产生的高凝血酶活性和FPA水平反映了纤维蛋白形成的活跃过程，这似乎在阻止慢性胸腔渗出中发挥着重要作用。
