To estimate the prevalence of antithyroid peroxidase antibodies in the general obstetric population and to compare pregnancy outcomes in women who are antithyroid peroxidase-antibody positive with those who are antithyroid peroxidase-antibody negative.
Between November 2000 and April 2003, all women who presented for prenatal care underwent thyroid screening. Serum samples from women without clinical hypothyroidism who had been screened in the first 20 weeks of gestation and delivered a singleton newborn weighing 500 g or more were analyzed for concentrations of antithyroid peroxidase antibodies. Serum thyroid peroxidase antibody levels were determined using a chemiluminescent immunoassay. Pregnancy outcomes in women with positive antithyroid peroxidase antibodies (more than 50 international units/mL) were compared with those with negative levels.
Serum samples from 17,298 women were tested. Of these, 1,012 (6%) women were identified with positive antithyroid peroxidase antibodies. Women who were antithyroid peroxidase-antibody positive were older, heavier, and more often parous than women with negative antithyroid peroxidase antibodies. Rate of placental abruption was threefold higher in women with antithyroid peroxidase antibodies (1.0% compared with 0.3%, odds ratio 3.4, 95% confidence interval 1.7–6.7) after adjustment for differences in maternal demographics. Seven of the 10 abruptions associated with antithyroid peroxidase antibody occurred in women with normal thyroid-stimulating hormone and free thyroxine levels.
Antithyroid peroxidase antibodies are present in 6% of the general obstetric population and are associated with a threefold increase in the rate of placental abruption. However, this increase in placental abruption does not currently warrant routine antithyroid antibody screening during pregnancy.
The presence of elevated antithyroid peroxidase antibodies is associated with an increased risk of placental abruption in euthyroid pregnant women.
From the Department of Obstetrics and Gynecology, University of Texas Southwestern Medical Center, Dallas, Texas; and the Eunice Kennedy Shriver National Institute of Child Health and Human Development, Bethesda, Maryland.
Supported by NIH grant no. HD-04-023 to University of Texas Southwestern Medical Center.
Dr. Spong, Associate Editor of Obstetrics & Gynecology, was not involved in the review or decision to publish this article.
Corresponding author: Brian M. Casey, MD, Department of Obstetrics and Gynecology, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX 75390-9032; e-mail: email@example.com.
Financial Disclosure Dr. Cunningham received money from McGraw Hill for being the editor of Williams Obstetrics, Williams Gynecology, and “derivative” publications (eg, online, study guides). The other authors did not report any potential conflicts of interest.