Schmidt K G, Rasmussen J W, Bekker C, Madsen P E
Scand J Haematol. 1985 Jan;34(1):39-46. doi: 10.1111/j.1600-0609.1985.tb00742.x.
The kinetics and distribution in vivo of autologous 111-In-labelled platelets were studied in 20 patients with chronic hepatic disease. The patients, 16 of whom were thrombocytopenic, exhibited a shortened platelet mean life time, a reduced platelet recovery and a normal platelet turnover, the latter 2 of which were positively correlated to the platelet count. Platelet in vivo recovery was negatively correlated to the spleen volume. In accordance with this, scintigraphic studies revealed that the spleen was the major organ of platelet sequestration and destruction, the role of the liver being almost negligible. Signs of platelet destruction in the bone marrow were also found. Our results indicate that splenic platelet pooling and accelerated platelet destruction, accompanied by inability of the bone marrow to compensate for the thrombocytopenia are the main causes of the thrombocytopenia accompanying chronic hepatic disease.
对20例慢性肝病患者进行了自体111铟标记血小板的体内动力学和分布研究。患者中有16例血小板减少，其血小板平均寿命缩短，血小板回收率降低，血小板周转率正常，后两者与血小板计数呈正相关。血小板体内回收率与脾脏体积呈负相关。据此，闪烁扫描研究显示脾脏是血小板扣押和破坏的主要器官，肝脏的作用几乎可以忽略不计。还发现了骨髓中血小板破坏的迹象。我们的结果表明，脾脏血小板蓄积和血小板破坏加速，伴有骨髓无法代偿血小板减少，是慢性肝病伴发血小板减少的主要原因。
