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111铟标记血小板的动力学、体内分布及家族性高胆固醇血症患者的血小板功能

Kinetics and in vivo distribution of in-111-labelled platelets and platelet function in familial hypercholesterolaemia.

作者信息

Wessels P, Heyns A D, Esterhuysen A J, Badenhorst P N, Lötter M G, Pieters H, Kotzè H F

机构信息

MRC Blood Platelet Research Unit, University of the Orange Free State, Bloemfontein, South Africa.

出版信息

Thromb Haemost. 1987 Oct 28;58(3):811-6.

PMID:3433247
Abstract

The kinetics, in vivo distribution and sites of sequestration of autologous In-111-labelled platelets and other platelet function parameters were studied in ten patients with type IIa or IIb familial hypercholesterolaemia and thrombotic complications of atherosclerosis. The in vitro platelet aggregation response to ADP (P = 0.50) and collagen (P = 0.46); binding of fibrinogen to platelets (P = 0.61); and plasma beta-thromboglobulin levels (P = 0.42) of the patients and normal reference subjects did not differ significantly. The in vivo distribution of In-111-labelled platelets at equilibrium was within normal limits, and at the end of platelet life-span the sequestration pattern of labelled platelets in the reticuloendothelial system was also normal (spleen P = 0.31; liver P = 0.54). There was minimal evidence of in vivo platelet activation: only mean platelet lifespan (MPLS), 195 +/- 57 hours (difference between mean MPLS of patients and controls was 25 hours, with a 95% confidence interval from 23 to 31 hours; P = 0.02); mean platelet platelet turnover, 2298 +/- 824 platelets/microliter/hour (P = 0.005); plasma platelet factor 4 (P = 0.02); and the mean circulating platelet aggregate ratio, 0.8 +/- 0.1 (P = 0.02); differed significantly from normal. These results suggest that abnormalities of platelet function and kinetics observed in type II hyperlipoproteinaemia cannot be ascribed wholly to the hyperlipidaemia, but may be induced by the associated atherosclerosis.

摘要

对10例患有IIa型或IIb型家族性高胆固醇血症及动脉粥样硬化血栓并发症的患者,研究了自体铟 - 111标记血小板的动力学、体内分布、潴留部位及其他血小板功能参数。患者和正常对照者的体外血小板对ADP的聚集反应(P = 0.50)和对胶原的聚集反应(P = 0.46);纤维蛋白原与血小板的结合(P = 0.61);以及血浆β - 血小板球蛋白水平(P = 0.42),差异均无统计学意义。铟 - 111标记血小板在平衡时的体内分布在正常范围内,在血小板寿命末期,标记血小板在网状内皮系统中的潴留模式也正常(脾脏P = 0.31;肝脏P = 0.54)。体内血小板活化的证据极少:仅平均血小板寿命(MPLS),195±57小时(患者与对照组平均MPLS的差异为25小时,95%置信区间为23至31小时;P = 0.02);平均血小板周转率,2298±824个血小板/微升/小时(P = 0.005);血浆血小板因子4(P = 0.02);以及平均循环血小板聚集率,0.8±0.1(P = 0.02),与正常情况有显著差异。这些结果表明,II型高脂蛋白血症中观察到的血小板功能和动力学异常不能完全归因于高脂血症,而可能是由相关的动脉粥样硬化引起的。

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