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

Identifieur interne : 005F60 ( Main/Exploration ); précédent : 005F59; suivant : 005F61

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

Auteurs : RBID : pubmed:3433247

English descriptors

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.

PubMed: 3433247

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Le document en format XML

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<title xml:lang="en">Kinetics and in vivo distribution of in-111-labelled platelets and platelet function in familial hypercholesterolaemia.</title>
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<name sortKey="Wessels, P" uniqKey="Wessels P">P Wessels</name>
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<nlm:affiliation>MRC Blood Platelet Research Unit, University of the Orange Free State, Bloemfontein, South Africa.</nlm:affiliation>
<country xml:lang="fr">Afrique du Sud</country>
<wicri:regionArea>MRC Blood Platelet Research Unit, University of the Orange Free State, Bloemfontein</wicri:regionArea>
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<name sortKey="Heyns, A D" uniqKey="Heyns A">A D Heyns</name>
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<name sortKey="Esterhuysen, A J" uniqKey="Esterhuysen A">A J Esterhuysen</name>
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<name sortKey="Badenhorst, P N" uniqKey="Badenhorst P">P N Badenhorst</name>
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<name sortKey="L Tter, M G" uniqKey="L Tter M">M G Lötter</name>
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<name sortKey="Pieters, H" uniqKey="Pieters H">H Pieters</name>
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<name sortKey="Kotze, H F" uniqKey="Kotze H">H F Kotzè</name>
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<term>Humans</term>
<term>Hyperlipoproteinemia Type II (blood)</term>
<term>Hyperlipoproteinemia Type II (complications)</term>
<term>Indium Radioisotopes</term>
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<div type="abstract" xml:lang="en">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.</div>
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<Year>1987</Year>
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<Title>Thrombosis and haemostasis</Title>
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<AbstractText>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.</AbstractText>
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