Exp Clin Endocrinol Diabetes 2006; 114(4): 188-191
DOI: 10.1055/s-2006-924064
Article

J. A. Barth Verlag in Georg Thieme Verlag KG Stuttgart · New York

Hyperprolactinemia of Pregnancy is Not Associated with Increased In Vivo Platelet Activity and Shortened In Vitro Bleeding Times

A. Atmaca1 , A. Gurlek1 , S. Dagdelen1 , N. Erarslan2 , Y. Buyukasik2 , M. Gultekin3 , B. S. Karamursel3 , L. Onderoglu3
  • 1Hacettepe University School of Medicine, Department of Internal Medicine, Division of Endocrinology and Metabolism, Ankara, Turkey
  • 2Hacettepe University School of Medicine, Department of Internal Medicine, Division of Hematology, Ankara, Turkey
  • 3Hacettepe University School of Medicine, Department of Obstetrics and Gynecology, Ankara, Turkey
Further Information

Publication History

Received: September 22, 2005 First decision: November 17, 2005

Accepted: December 23, 2005

Publication Date:
17 May 2006 (online)

Introduction

Pregnancy is a major independent risk factor for venous thromboembolism (VTE). However, the underlying mechanism for increased risk of hypercoagulable state in pregnancy is still not clear. It has been proposed that increases in the procoagulant factors (von Willebrand factor, factors V and VIII, and fibrinogen), decreases in protein S, increases in plasminogen activator inhibitors 1 and 2, and acquired resistance to protein C might be operative in predispositon to VTE during pregnancy ([Toglia and Weg, 1996]; [Bates and Ginsberg, 1997]; [Rosendaal, 1999]). The changes in endocrine factors during pregnancy may also contribute to the increased risk of VTE ([Wallaschofski et al., 2001]). It is well known that prolactin (PRL) is markedly increased during pregnancy ([Boyar et al., 1975]). Expression of both PRL and PRL receptors have recently been identified in hematopoietic tissue ([Dardenne et al., 1994]; [Bresson et al., 1999]). Recently, it has been shown that PRL is a novel cofactor for platelet activation because it increases platelet aggregation via ADP stimulation in vitro ([Wallaschofski et al., 2001]). However, it should be noted that in vitro studies for the assessment of platelet aggregation does not necessarily correlate with in vivo activity of platelets.

β-thromboglobulin (β‐TG), molecular weight of 35 800, is a specific protein component of platelets composed of four identical subunits ([Begg et al., 1978]). It makes up 10 % of the contents of the α-granules. β‐TG is released under the influence of some stimuli that activate platelets, such as ADP and collagen. In view of the involvement of platelets in the thrombogenic processes, the determination of β‐TG is a noninvasive method for evaluating platelet activation in vivo, and allows a better approach to the prethrombotic states and thromboses ([Zahavi and Kakkar, 1980]; [Kaplan and Owen, 1981]; [Walz, 1984]).

In this cross-sectional study, we assessed the plasma β‐TG level to determine in vivo platelet activity during pregnancy. We also investigated PFA-100 closure times, namely in vitro bleeding times, using collagen/ADP (CADP) and collagen/epinephrine (CEPI) cartridges. PFA-100 device is used to screen for platelet-related hemostatic disorders in clinical medicine ([Buyukasik et al., 2002]). We also analyzed the correlations between the prolactin level, β‐TG and in vitro bleeding time in order to verify the relevance of the previous observations assigning a role for hyperprolactinemia on increased platelet activity during pregnancy.

References

M.D. Aysegul Atmaca

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Email: aysegulakin@yahoo.com