Ballard H S, Marcus A J
Arch Intern Med. 1976 Mar;136(3):316-9.
Primary and secondary platelet aggregation in response to adenosine diphosphate was studied in 24 patients with portal (Laënnec) cirrhosis and compared with platelet aggregation in 14 normal subjects. In 12 patients with cirrhosis, platelet aggregation was diminished when compared to controls. Of the 12 patients with impaired aggregation, 6 had elevated levels of fibrinogen-fibrin degradation products (FDPs), 11 had thrombocytopenia, 10 had shortened euglobulin lysis times, 11 had prolonged bleeding times, 4 had hypofibrinogenemia, and all had prolonged thrombin clotting times. The data suggest that elevated levels of serum FDPs do not explain fully the impairment of platelet aggregation or the prolongation of the thrombin clotting time that was noted in patients with advanced liver disease. A possible explanation for the prolongation of the thrombin clotting time is the presence of "altered" plasma fibrinogen.
研究了24例门脉(Laënnec)肝硬化患者对二磷酸腺苷的原发性和继发性血小板聚集情况,并与14名正常受试者的血小板聚集情况进行了比较。在12例肝硬化患者中,与对照组相比血小板聚集减少。在12例聚集功能受损的患者中,6例纤维蛋白原-纤维蛋白降解产物(FDPs)水平升高,11例血小板减少,10例优球蛋白溶解时间缩短,11例出血时间延长,4例纤维蛋白原血症,所有患者凝血酶凝血时间均延长。数据表明,血清FDPs水平升高并不能完全解释晚期肝病患者血小板聚集功能受损或凝血酶凝血时间延长的原因。凝血酶凝血时间延长的一个可能解释是存在“改变的”血浆纤维蛋白原。