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DOI: 10.5482/HAMO-12-11-0020
Hereditäre Thrombophilien und Plazenta-medierte Schwangerschafts-komplikationen im II./III. Trimenon
Hereditary thrombophilias and placentalmediated pregnancy complications in the II./III. trimesterPublikationsverlauf
Eingegangen:
29. November 2012
Angenommen in revidierter Form:
18. Januar 2013
Publikationsdatum:
28. Dezember 2017 (online)
Zusammenfassung
Plazenta-medierte Schwangerschaftskomplikationen (PmSk) wie Präeklampsie (PE), intra uterine Wachstumsrestriktion (IUGR) und vorzeitige Plazentalösung (VPL) sind häufige Ursachen mütterlicher und kindlicher Morbidität und Mortalität. Die hohe Prä -valenz in Casecontrol-Studien sowie morphologische Untersuchungen der Plazenta bei diesen Frauen legten die Vermutung einer Assoziation zwischen hereditären Thrombo-philien und PmSk nahe. Allerdings ist die Daten lage widersprüchlich, da nachfolgende prospektive Kohortenstudien und aktuelle Metaanalysen keinen signifikanten Zusam-menhang zwischen hereditären Thrombophilien und PmSk nachweisen konnten. Infolge der multifaktoriellen Ätiologie der PmSk dürfte es schwierig sein, zu beweisen, dass here-ditäre Thrombophilien unabhängige Risikofaktoren für PmSk sind.
Aktuelle Leitlinien empfehlen keine Untersuchung auf hereditäre Thrombophilien nach vorangegangenen PmSk. Aktuelle In-vitro-Studien zeigten positive nicht antikoagulatorische Wirkungen von niedermolekularen Heparinen (NMH) auf die frühe Plazentation. Retrospektive Case-control-Studien sowie neue randomisierte und prospektive Studien ergaben, dass durch die Gabe von NMH ab der Frühschwangerschaft eine signifikante Sen-kung des Wiederholungsrisikos für PmSk in nachfolgenden Schwangerschaften bei Frauen mit und ohne hereditäre Thrombophilien zu erreichen ist. Schlussfolgerung: Große randomisierte Multizenterstudien sind notwendig, um die Bedeutung hereditärer Thrombophilien für PmSk und den Nutzen einer Prävention mit NMH zu klären.
Summary
Placental-mediated pregnancy complications (PmC) like preeclampsia, intrauterine growth restriction and placental abruption are common causes of fetal and maternal morbidity and mortality. The high prevalence of hereditary thrombophilias in case-control studies associated with pathological morphological findings of the placenta in these cases gave evidence for the association between hereditary thrombophilias and PmC. However, data from the literature are inconsistent, since subsequent prospective cohort studies could not demonstrate significant associations between inherited thrombophilia and PmC. Because of the multifactorial aetiology of PmC it may be difficult to prove, that hereditary thrombophilias are independent risk factors for PmC.
Current guidelines do not recommend screening for inherited thrombophilias in patients with previous PmC. Evidence from current in vitro studies have shown, that heparin has beneficial non-anticoagulatory effects on trophoblast invasion. Retrospective case-control studies and recently published randomised controlled cohort studies have shown, that prophylactic administration of low-molecular-weight heparin (LWH), started in early pregnancy, may lead to a significant reduction in the incidence of PmC in subsequent pregnancies in patients with and without hereditary thrombophilias and previous PmC. Conclusion: Large, well-designed multicenter studies are needed to elucidate the role of hereditary thrombophilias in cases of PmC and to confirm the benefit of LWH for subsequent pregnancy outcomes.
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