Thromb Haemost 1987; 58(03): 811-816
DOI: 10.1055/s-0038-1645995
Original Article
Schattauer GmbH Stuttgart

Kinetics and In Vivo Distribution of In-111-Labelled Platelets and Platelet Function in Familial Hypercholesterolaemia

P Wessels
The MRC Blood Platelet Research Unit, University of the Orange Free State, Bloemfontein, South Africa
,
A du P Heyns
The MRC Blood Platelet Research Unit, University of the Orange Free State, Bloemfontein, South Africa
,
A J Esterhuysen
The MRC Blood Platelet Research Unit, University of the Orange Free State, Bloemfontein, South Africa
,
P N Badenhorst
The MRC Blood Platelet Research Unit, University of the Orange Free State, Bloemfontein, South Africa
,
M G Lötter
The MRC Blood Platelet Research Unit, University of the Orange Free State, Bloemfontein, South Africa
,
H Pieters
The MRC Blood Platelet Research Unit, University of the Orange Free State, Bloemfontein, South Africa
,
H F Kotzè
The MRC Blood Platelet Research Unit, University of the Orange Free State, Bloemfontein, South Africa
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Publikationsverlauf

Received 22. Januar 1987

Accepted after revision 07. Mai 1987

Publikationsdatum:
28. Juni 2018 (online)

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Summary

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/μl/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.