Thromb Haemost 2012; 108(01): 107-118
DOI: 10.1160/TH11-12-0860
Platelets and Blood Cells
Schattauer GmbH

Reactive leptin resistance and the profile of platelet activation in acute ischaemic stroke patients

Maria Lukasik
1   Department of Neurology, Poznan University of Medical Sciences, Poznan, Poland
,
Slawomir Michalak
1   Department of Neurology, Poznan University of Medical Sciences, Poznan, Poland
2   Department of Neurochemistry and Neuropathology, Poznan University of Medical Sciences, Poznan, Poland
3   Neuroimmunological Unit, Polish Academy of Sciences, Poznan, Poland
,
Grzegorz Dworacki
4   Department of Clinical Immunology, Poznan University of Medical Sciences, Poznan, Poland
,
Karolina Siewiera
5   Department of Haemostasis and Haemostatic Disorders, Medical University, Lodz, Poland
,
Mariusz Kaczmarek
4   Department of Clinical Immunology, Poznan University of Medical Sciences, Poznan, Poland
,
Cezary Watala
5   Department of Haemostasis and Haemostatic Disorders, Medical University, Lodz, Poland
,
Wojciech Kozubski
1   Department of Neurology, Poznan University of Medical Sciences, Poznan, Poland
› Author Affiliations
Further Information

Publication History

Received: 13 December 2011

Accepted after major revision: 05 April 2012

Publication Date:
22 November 2017 (online)

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Summary

Leptin is an adipokine that in vitro enhances agonist-induced platelet aggregation and adipokine expression. Hyperleptinaemia represents a risk factor for cardiovascular disease. We conducted a prospective evaluation of the potential link between blood platelet activation and plasma leptin levels in post-stroke patients. Using five-colour flow cyto-metry, the platelet surface expression of CD40L, CD62P, the subpopulations of monocyte-platelet aggregates and platelet-derived microparticles (PMPs) as well as the plasma leptin, soluble leptin receptor (sOb-R), leptin/sOb-R ratio, the plasma adiponectin, and leptin/adiponectin ratio were assessed in 98 stroke patients on the first (V0), 10th (V1) and 90th (V2) day after stroke and once in 78 age-, gender- and vascular risk factor-matched disease controls. We demonstrated that at V0 leptin resistance, defined as leptin/sOb-R ratio, was higher than in the controls [1.1 (0.5–1.8 vs. 0.5 (0.2–1.1); p=0.02]. After adjustment according to the factors which influence platelet activation, we confirmed the relationship between percentage of circulating PMPs and plasma leptin level (B=0.18; p=0.02) or the leptin/sOb-R ratio (B=0.23; p=0.02) in normal-weight subjects in the acute phase of stroke. No correlation could be demonstrated between the adipokine parameters and the percentage of monocyte-platelet aggregates or expression of platelet pro-inflammatory glycoproteins. In conclusion, formation of PMPs on the first day following an ischaemic stroke shows a positive correlation with leptin levels and with resistance to leptin. Leptin level does not seem to affect the expression of platelet surface proinflammatory glycoproteins.