Horm Metab Res 2004; 36(1): 1-6
DOI: 10.1055/s-2004-814200
Review
© Georg Thieme Verlag Stuttgart · New York

Co-activation of Platelets by Prolactin or Leptin - Pathophysiological Findings and Clinical Implications

H.  Wallaschofski1 , A.  Kobsar2 , O.  Sokolova2 , M.  Eigenthaler2 , T.  Lohmann1
  • 1Department of Internal Medicine I, University of Erlangen
  • 2Institute of Clinical Biochemistry, University of Wuerzburg, Germany
Further Information

Publication History

Received 8 May 2003

Accepted after revision 18 August 2003

Publication Date:
25 February 2004 (online)

Abstract

Platelet activation is involved in the pathogenesis of atherosclerosis and venous thromboembolism, and might therefore be a possible link between the two entities. Prolactin and leptin have recently been recognized as potent co-activators of ADP-dependent platelet aggregation or P-selectin expression, and are therefore suspected as additional risk factors for both arterial and venous thrombosis. There are clinical situations that have a known association with higher prolactin or leptin levels (pregnancy, obesity or anti-psychotic therapy) and increased risk of thromboembolic events. We compared the impact of both hormones on platelet activation in vitro and in vivo, indicating that prolactin has a stronger effect on platelet activation as leptin in vitro and in vivo. We have also demonstrated that prolactin levels are increased in so called idiopathic thrombosis, and that conversely, patients with prolactinoma have an increased frequency of thrombosis during the hyperprolactinemic state, in a retrospective analysis. Moreover, we have demonstrated increased prolactin values in stroke and myocardial infarction. Prospective studies have yet to be performed to give this theory its final confirmation. The involvement of hormonal factors in platelet aggregation and venous or arterial thrombosis may have important clinical implications such as for risk stratification of patients with venous and arterial thrombosis or new therapeutic options such as decreasing pro-coagulant hormone levels in certain risk situations.

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H. Wallaschofski,M. D. 

Dept. of Internal Medicine I · University of Erlangen

Ulmenweg 18 · 91054 Erlangen · Germany

Phone: + 49 (9131) 85 35230

Fax: + 49 (9131) 85 35231 ·

Email: Henri.Wallaschofski@med1.imed.uni-erlangen.de

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