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DOI: 10.1055/s-0037-1619502
Sexualsteroide und Hämostase
Sexual steroids and hemostasisPublication History
Publication Date:
27 December 2017 (online)
Zusammenfassung
Der Einfluß von Sexualsteroiden auf die Hämostase wurde vor allem bei Anwenderinnen von oralen Kontrazeptiva (OCs) und Präparaten für die Hormonersatztherapie (HRT) intensiv untersucht. Es kommt bei beiden Anwendungsformen zu einer östrogenbedingten Aktivierung prokoagulatorischer Prozesse, die dosisabhängig und für das synthetische Ethinylestradiol der »Pille« stärker ausgeprägt ist als für die natürlichen Östrogenkomponenten der HRT-Präparate. Zugleich werden antikoagulatorische und fibrinolytische Prozesse aktiviert, so daß ein Gleichgewicht zwischen Blutgerinnung und Fibrinolyse auf höherem Niveau resultiert. Ungeachtet dessen ist die exogene Anwendung von Sexualsteroiden mit einem erhöhten Risiko für venöse Thrombosen verbunden, das wahrscheinlich durch genetisch bedingte Veranlagung zu Gerinnungsstörungen bedingt zu sein scheint bzw. durch zusätzliche Risikofaktoren wie Rauchen. In früheren epidemiologischen Studien wurde zunächst eine Risikoerhöhung für thromboembolische Ereignisse bei Anwenderinnen von OCs mit Gestagenen der »3. Generation« im Vergleich zu Präparaten der »2. Generation« gefunden, die mit einer Resistenz gegenüber aktiviertem Protein C als biologischem Korrelat erklärt wurde. Neuere Studien konnten diese Ergebnisse jedoch nicht bestätigen, wobei Studieneinflüsse wie Anwendungsdauer, Alter der Anwenderinnen und besonderes Verschreibungsverhalten für diese Unterschiede verantwortlich gemacht werden. Arterielle Gefäßverschlüsse werden durch Sexualsteroide offensichtlich nicht induziert, da die direkte gefäßerweiternde Wirkung dieser Substanzgruppe diesen Komplikationen eher vorbeugt. Bei Vorliegen von Risikofaktoren und/oder einer erblichen bzw. erworbenen Prädisposition für Gerinnungsstörungen sollte die exogene Gabe von Sexualsteroiden vermieden oder eine engmaschige Kontrolle des Gerinnungsstatus vorgenommen werden.
Summary
The influence of sexual steroids on hemostasis was intensively studied in users of oral contraceptives (OCs) and hormone replacement therapy (HRT). Both forms of exogenous use of hormones are connected with an estrogen-derived activation of procoagulatory processes. This activation is dose-dependent and more pronounced for the synthetic derivative of the “pill”, ethinyl estradiol, than for the natural estradiol of HRT regimens. At the same time, anticoagulatory and fibrinolytic mechanisms will be activated as well, so that the balance between coagulation and fibrinolysis is moved towards a higher level. Nevertheless, there is an increased risk of venous thromboembolism in connection with the exogenous administration of sexual steroids, which is probably due to genetic predisposition for clotting abnormalities or additional risk factors like smoking. In earlier epidemiological studies a higher risk of venous thrombotic events was found in users of 3rd generation OCs than in users of 2nd generation pills. This effect was initially explained by an acquired resistance to activated protein C being the biological correlate. Recent studies did not confirm these earlier findings, but explained the differences by confounders, such as age of OC users, duration of intake or prescription biases. Exogenous sexual steroids do obviously not induce arterial thrombosis, but rather prevent these processes due to their direct vasodilator action. In users with additional risk factors and/or known thrombophilic predisposition the administration of exogenous sexual hormones should be avoided or the clotting status should be controlled at reasonable intervals.
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