Thromb Haemost 2006; 96(01): 38-44
DOI: 10.1160/TH05-09-0634
Platelets and Blood Cells
Schattauer GmbH

Enhanced platelet activation by prolactin in patients with ischemic stroke

Henri Wallaschofski
1   Department of Gastroenterology, Endocrinology and Nutrition, University of Greifswald
,
Tobias Lohmann
2   City Hospital Dresden-Neustadt
,
Eva Hild
3   Institute of Clinical Biochemistry and Pathobiochemistry, University of Würzburg
,
Anna Kobsar
3   Institute of Clinical Biochemistry and Pathobiochemistry, University of Würzburg
,
Annelie Siegemund
4   Laborgemeinschaft Reisig Ackermann Leipzig
,
E. Spilcke-Liss
1   Department of Gastroenterology, Endocrinology and Nutrition, University of Greifswald
,
Betina Hentschel
5   Institute for Medical Informatics, Statistics and Epidemiology, University of Leipzig
,
Christian Stumpf
6   Department of Internal Medicine II, University of Erlangen, Germany
,
Werner G. Daniel
6   Department of Internal Medicine II, University of Erlangen, Germany
,
Christian D. Garlichs
6   Department of Internal Medicine II, University of Erlangen, Germany
,
Martin Eigenthaler
3   Institute of Clinical Biochemistry and Pathobiochemistry, University of Würzburg
› Author Affiliations
Further Information

Publication History

Received 23 September 2005

Accepted after resubmission 07 June 2006

Publication Date:
29 November 2017 (online)

Summary

Prolactin and leptin are newly recognised platelet co-stimulators due to potentiation of ADP-induced platelet aggregation. Elevated leptin levels have recently been found to be a risk factor for ischemic stroke in both men and women, and especially in combination with increased blood pressure for hemorrhagic stroke in men. Until now an association between hyperprolactinemia and ischemic stroke has not been investigated systematically.We determined plasma prolactin and leptin levels as well as platelet P-selectin expression in 36 patients with ischemic stroke or transient ischemic attack and detecteda significant correlation between increased prolactin values and enhanced ADP stimulated P-selectin expression on platelets. In contrast, no correlation of leptin values with platelet P-selectin expression was found. Next we determined plasma prolactin and leptin as well as acquired and congenital risk factors of thrombophilia in patients with first-ever non-hemorrhagic stroke with or without atrial fibrillation. Excluding patients with such preexisting risk factors,21 patients with and 59 patients without atrial fibrillation were identified. Patients without atrial fibrillation revealed significantly higher plasma prolactin levels than patients with atrial fibrillation. Furthermore, the influence of aspirin or clopidogrel on prolactin stimulated P-selectin expression in vitro was tested, showing that aspirin was without effect,whereas clopidogrel significantly inhibited platelet P-selectin expression. In conclusion, hyperprolactinemia might be a novel risk factor for stroke mediating its thrombogenic effect through enhanced platelet reactivity, and this might correspond to a higher efficacy of antiplatelet combination therapy with clopidogrel compared to aspirin therapy alone.

 
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