title: Enhanced platelet activation by prolactin in patients with ischemic stroke.
abstract: 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 detected a 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.
authors.affiliation: Department of Gastroenterology, Endocrinology and Nutrition, University of Greifswald, Friedrich-Loeffler-Strasse 23a, 17487 Greifswald, Germany. henri.wallaschofski@uni-greifswald.de
authors.forename: Henri
authors.initials: H
authors.lastname: Wallaschofski
authors.forename: Tobias
authors.initials: T
authors.lastname: Lohmann
authors.forename: Eva
authors.initials: E
authors.lastname: Hild
authors.forename: Anna
authors.initials: A
authors.lastname: Kobsar
authors.forename: Annelie
authors.initials: A
authors.lastname: Siegemund
authors.forename: E
authors.initials: E
authors.lastname: Spilcke-Liss
authors.forename: Betina
authors.initials: B
authors.lastname: Hentschel
authors.forename: Christian
authors.initials: C
authors.lastname: Stumpf
authors.forename: Werner G
authors.initials: WG
authors.lastname: Daniel
authors.forename: Christian D
authors.initials: CD
authors.lastname: Garlichs
authors.forename: Martin
authors.initials: M
authors.lastname: Eigenthaler
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D001241:Aspirin / Q000494:pharmacology; D002545:Brain Ischemia; D000077144:Clopidogrel; D005260:Female; D006801:Humans; D002546:Ischemic Attack, Transient; D020738:Leptin / Q000097:blood; D008297:Male; D008875:Middle Aged; D019007:P-Selectin / Q000032:analysis; D015539:Platelet Activation / Q000187:drug effects*; D011388:Prolactin / Q000097:blood* / Q000494:pharmacology; D012189:Retrospective Studies; D012307:Risk Factors; D020521:Stroke / Q000097:blood / Q000188:drug therapy* / Q000209:etiology*; D019851:Thrombophilia; D013988:Ticlopidine / Q000031:analogs & derivatives / Q000494:pharmacology
chemical_list: D020738:Leptin; D019007:P-Selectin; D011388:Prolactin; D000077144:Clopidogrel; D013988:Ticlopidine; D001241:Aspirin