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Am J Perinatol 2017; 34(4): 415-418
DOI: 10.1055/s-0036-1586751
Commentary
Thieme Medical Publishers 333 Seventh Avenue, New York, NY 10001, USA.

Biomarkers for Prediction, Risk Stratification, and Ruling Out Preeclampsia: What Are the Appropriate Goals and Objectives?

Authors

  • John R. Barton

    1   Department of Obstetrics/Gynecology, Baptist Health Lexington, Lexington, Kentucky

  • Baha M. Sibai

    2   Department of Obstetrics and Gynecology, University of Texas Health Sciences Center at Houston, Houston, Texas
Further Information

Publication History

24 April 2016

29 June 2016

Publication Date:
29 August 2016 (online)

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The reported incidence of gestational hypertension and preeclampsia ranges from 5 to 10% of all pregnancies. The incidence is increasing because of the trend toward advanced maternal age and/or increased body mass index (BMI) at the time of pregnancy. Hypertensive disorders of pregnancy can develop at < 34 weeks (0.2%), 34 to 37 weeks, ≥ 37 weeks, during labor, or even for the first time in the postpartum period. The majority of cases, however, occur in women in their first pregnancy and most cases develop at ≥ 37 weeks of gestation. Numerous pathophysiologic abnormalities have been suggested to explain the mechanisms leading to the development of preeclampsia. Some of these mechanisms have included impaired trophoblast differentiation and invasion, placental and endothelial dysfunction, immune maladaptation to paternal antigens, an imbalance in angiogenic and antiangiogenic factors, and exaggerated systemic inflammatory response.[1]

During the past decade, several prospective and nested case–control studies have found that certain maternal risk factors, biophysical clinical factors, and serum biomarkers were associated with subsequent development of preeclampsia. Maternal risk factors associated with an increased risk for preeclampsia include chronic hypertension, pregestational diabetes, obesity, family history of preeclampsia, and a history of an adverse outcome in a previous pregnancy.[2] An excess of the antiangiogenic proteins, soluble fms-like tyrosine kinase 1 (sFlt1) and soluble endoglin released from the placenta appears to play an important role in the pathogenesis of preeclampsia. Further, blood concentrations of placental growth factor (PlGF) were reduced throughout pregnancy among women who subsequently develop preeclampsia.[3]

Note

Dr. Barton was an investigator for the Preeclampsia Triage by Rapid Assay trial sponsored by Alere and serves on the Data Monitoring Committee for the Preserve-1 trial which is evaluating a therapeutic agent for preeclampsia and is sponsored by rEVO Biologics. Dr. Sibai is an investigator for the Preserve-1 trial (rEVO Biologics) and served on the Adjudication Committee of the Preeclampsia Triage by Rapid Assay trial (Alere).