Undiagnosed hypothyroidism in pregnant women may adversely affect their fetuses; therefore, screening for thyroid deficiency during pregnancy may be warranted.

Objective-To examine the relation between certain pregnancy complications and thyroid stimulating hormone (TSH) measurements in a cohort of pregnant women. Methods-TSH was measured in sera obtained from women during the second trimester as part of routine prenatal care. Information was then collected about vaginal bleeding, premature delivery, low birthweight, abruptio placentae, pregnancy induced hypertension, need for cesarean section, low Apgar scores, and fetal and neonatal death. Results-Among 9403 women with singleton pregnancies, TSH measurements were 6 mU/l or greater in 209 (2.2%). The rate of fetal death was significantly higher in those pregnancies (3.8%) than in the women with TSH less than 6 mU/l (0.9%, odds ratio 4.4, 95% confidence interval 1.9-9.5). Other pregnancy complications did not occur more frequently Conclusion-From the second trimester onward, the major adverse obstetrical outcome associated with raised TSH in the general population is an increased rate of fetal death. If thyroid replacement treatment avoided this problem this would be another reason to consider population screening. (J Med Screen 2000;7:127-130) Keywords: thyroid stimulating hormone; pregnancy; fetal death Although clinically apparent maternal hypothyroidism during pregnancy has long been known to be associated with both maternal and fetal complications, most of the studies documenting those problems have focused on patients in specialty or high risk clinics. The present study assesses the impact of maternal hypothyroidism in a cohort of pregnant women being managed in primary care settings. In 1991, our group reported thyroid stimulating hormone (TSH) measurements in a cohort of 2000 pregnant women whose sera were being obtained for -fetoprotein measurements at 15-18 weeks' gestation as part of routine care. 1 TSH measurements were at, or above, 6 mU/l in 49 of the women (2.4%). In six of these 49 women the thyroxine (T 4 ) and/or free T 4 measurements were suYciently abnormal (more than two standard deviations below the average) for clinical manifestations to be anticipated. It was not possible to gather individual information about health status in this cohort, because all identifiers were removed from the serum samples before the thyroid measurements were performed. Given the frequency of thyroid deficiency identified in this pregnancy population, it was decided that its possible impact on late pregnancy and delivery should be evaluated. To accomplish this, it was necessary to study a second, larger cohort of pregnant women. Materials and methodsThe Foundation for Blood Research oVers prenatal serum screening services for open neural tube defects and Down's syndrome to all primary care prenatal practices in Maine. The testing is generally performed between 15 and 18 weeks' gestation. Approximately two thirds of the women receiving prenatal care in Maine opt for those services.Between July 1990 and June 1992 the order form for the prenatal screening test contained a supplementary consent form, asking women...

Although it is not known what severity of maternal thyroid deficiency is necessary to cause fetal brain damage, the present data indicate a sufficiently high prevalence of thyroid dysfunction to demand investigation of the mental development of the offspring of women with thyroid dysfunction and of the effect of replacement therapy.

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The fetus is totally dependent in early pregnancy on maternal thyroxine for normal brain development. Adequate maternal dietary intake of iodine during pregnancy is essential for maternal thyroxine production and later for thyroid function in the fetus. If iodine insufficiency leads to inadequate production of thyroid hormones and hypothyroidism during pregnancy, then irreversible fetal brain damage can result. In the United States, the median urinary iodine (UI) was 168 microg/L in 2001-2002, well within the range of normal established by the World Health Organization (WHO), but whereas the UI of pregnant women (173 microg/L; 95% CI 75-229 microg/L) was within the range recommended by WHO (150-249 microg/L), the lower 95% CI was less than 150 microg/L. Therefore, until additional physiologic data are available to make a better judgment, the American Thyroid Association recommends that women receive 150 microg iodine supplements daily during pregnancy and lactation and that all prenatal vitamin/mineral preparations contain 150 microg of iodine.

Newborn T4 concentrations within a normal physiological reference range are not associated with maternal thyroid function and do not predict cognitive outcome in a population living in an iodine-sufficient area.

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