Journal of Reproductive Immunology
Volume 84, Issue 1 , Pages 95-99, January 2010

Anti-β2 glycoprotein-I antibody increases the risk of pregnancy-induced hypertension: a case-controlled study

  • Hideto Yamada

      Affiliations

    • Department of Obstetrics and Gynecology, Kobe University Graduate School of Medicine, 7-5-1 Kusunoki-cho Chuo-ku, Kobe 650-0017, Japan
    • Corresponding Author InformationCorresponding author. Tel.: +81 78 382 6000; fax: +81 78 382 5756.
  • ,
  • Tatsuya Atsumi

      Affiliations

    • Department of Medicine II, Hokkaido University Graduate School of Medicine, Sapporo, Japan
  • ,
  • Olga Amengual

      Affiliations

    • Department of Medicine II, Hokkaido University Graduate School of Medicine, Sapporo, Japan
  • ,
  • Takao Koike

      Affiliations

    • Department of Medicine II, Hokkaido University Graduate School of Medicine, Sapporo, Japan
  • ,
  • Itsuko Furuta

      Affiliations

    • Department of Obstetrics and Gynecology, Hokkaido University Graduate School of Medicine, Sapporo, Japan
  • ,
  • Kaori Ohta

      Affiliations

    • Molecular Biostatistics Research Team, Research Center for Charged Particle Therapy, National Institute of Radiological Science, Chiba, Japan
  • ,
  • Gen Kobashi

      Affiliations

    • Molecular Biostatistics Research Team, Research Center for Charged Particle Therapy, National Institute of Radiological Science, Chiba, Japan

Received 1 May 2009; received in revised form 25 September 2009; accepted 1 October 2009. published online 23 November 2009.

Abstract 

The aim of this study was to evaluate whether anti-β2 glycoprotein-I antibody (anti-β2GPI) of the IgG or IgM classes is associated with the development of pregnancy-induced hypertension (PIH) or preeclampsia in the Japanese population. In a case-controlled cohort study, peripheral blood was obtained at 8–14 weeks of gestation from a consecutive series of 1155 women. The case group comprised 36 patients who later developed PIH during the pregnancy. Of the 36 PIH patients, 13 had severe PIH, 18 had preeclampsia and 11 had severe preeclampsia. One hundred and eleven age- and parity-matched women whose pregnancies ended in normal delivery without obstetric complications were selected as controls. We found that a titer of anti-β2GPI IgG1.0U/ml was a risk factor for severe PIH (P=0.023, OR 5.7 95%CI 1.4–22.8). In addition, titers of anti-β2GPI IgM1.2U/ml was found to be a risk factor for PIH (P=0.001, OR 8.8 95%CI 1.6–47.5). In women positive for anti-β2GPI but negative for lupus anticoagulant, anti-cardiolipin, phosphatidylserine-dependent anti-prothrombin, or kininogen-dependent anti-phosphatidylethanolamine antibodies, the presence of anti-β2GPI was not a significant risk factor for development of PIH or preeclampsia. In conclusion, the presence of anti-β2GPI antibody represents a risk factor for developing PIH and severe PIH. This finding supports the utility of anti-β2GPI determination as one of the laboratory criteria for anti-phospholipid syndrome classification. The usefulness of anti-β2GPI measurement among women without other anti-phospholipid antibodies requires further study.

Keywords: Anti-phospholipid antibody, Anti-β2 glycoprotein-I antibody, Preeclampsia, Pregnancy-induced hypertension

 

PII: S0165-0378(09)00522-1

doi:10.1016/j.jri.2009.10.005

Journal of Reproductive Immunology
Volume 84, Issue 1 , Pages 95-99, January 2010