Jackson C A, Greaves M, Patterson A D, Brown C B, Preston F E
Br J Haematol. 1982 Sep;52(1):69-77. doi: 10.1111/j.1365-2141.1982.tb03862.x.
Increased platelet aggregability on stimulation with sodium arachidonate (NaAA), collagen and ADP was found in a group of 14 patients with nephrotic syndrome when compared with age and sex matched controls. Five of the group also exhibited spontaneous platelet aggregation (SPA), associated with synthesis of thromboxane B2 (TxB2), and which appeared to correlate with a markedly increased serum triglyceride concentration. Thromboxane B2 generation in response to NaAA was increased and reflected both the low serum albumin concentration and the platelet aggregation response to this agent. Addition of albumin in vitro decreased the amount of TxB2 generated for a given dose of NaAA and increased NaAA and collagen-induced platelet aggregation thresholds. However, albumin had no significant effect on collagen-induced TxB2 production. The results suggest that the hypoalbuminaemia and associated reduced binding of arachidonic acid and increased synthesis of TxA2 account in part for the increased platelet aggregability seen in the nephrotic syndrome but that other mechanisms are also involved.
与年龄和性别匹配的对照组相比,在一组14例肾病综合征患者中发现,用花生四烯酸钠(NaAA)、胶原和二磷酸腺苷(ADP)刺激时血小板聚集性增加。该组中有5例还表现出自发性血小板聚集(SPA),与血栓素B2(TxB2)的合成有关,且似乎与血清甘油三酯浓度显著升高相关。对NaAA的反应中血栓素B2生成增加,反映了低血清白蛋白浓度以及血小板对该试剂的聚集反应。体外添加白蛋白可降低给定剂量NaAA产生的TxB2量,并提高NaAA和胶原诱导的血小板聚集阈值。然而,白蛋白对胶原诱导的TxB2产生没有显著影响。结果表明,低白蛋白血症以及花生四烯酸结合减少和TxA2合成增加部分解释了肾病综合征中血小板聚集性增加的现象,但其他机制也参与其中。