Semin Thromb Hemost 2002; 28(6): 515-518
DOI: 10.1055/s-2002-36693
Copyright © 2002 by Thieme Medical Publishers, Inc., 333 Seventh Avenue, New York, NY 10001, USA. Tel.: +1(212) 584-4662

Gestational Thrombocytopenia and Pregnancy-Induced Antithrombin Deficiency: Progenitors to the Development of the HELLP Syndrome and Acute Fatty Liver of Pregnancy

Hisanori Minakami1 , Hideto Yamada1 , Shigenori Suzuki2
  • 1Department of Reproductive and Developmental Medicine, Hokkaido University Graduate School of Medicine, Sapporo
  • 2College of Medical Technology, Hokkaido University, Sapporo, Japan
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Publikationsverlauf

Publikationsdatum:
21. Januar 2003 (online)

ABSTRACT

The syndrome of hemolysis, elevated liver enzymes, and low platelet count (HELLP syndrome) and of acute fatty liver of pregnancy (AFLP) do not have an abrupt onset. Thrombocytopenia or reduced antithrombin activity, or both, seen at presentation do not result from these complications. There are a small number of pregnant women who exhibit a gradual antenatal decline in platelet counts or antithrombin activity, or both, irrespective of the presence or absence of preeclampsia. Those who develop a profound decrease in either platelet counts or antithrombin activity are at an increased risk for developing perinatal aspartate aminotransferase (AST) elevation. Thrombocytopenia or reduced antithrombin activity, or both, precede the onset of these diseases. Therefore, monitoring of platelet counts and antithrombin activity during pregnancy is clinically useful for identifying women at an increased risk of the HELLP syndrome and AFLP. Because women with twin pregnancies are likely to exhibit a decrease in platelet counts or antithrombin activity, or both, compared with women with singleton pregnancies, HELLP syndrome and AFLP are more likely to occur in women with twin pregnancies.

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