Correct Answer:

Obtain free thyroxine (T4) level

Educational Objective:

Analyze the differences in normal thyroid laboratory values during and outside of pregnancy.

Key Point:

The American College of Obstetricians and Gynecologists does not support universal thyroid screening in pregnancy, but it is recommended for pregnant women with a current or past history of thyroid disorder, goiter, or in those who are symptomatic. There are serious fetal consequences of poorly controlled thyroid disease and, for this reason, at-risk women should be identified early in pregnancy or, ideally, prior to conception. Physiologic changes in the thyroid during pregnancy are reflected in changes in normal thyroid laboratory values; what is normal outside of pregnancy may be pathologic during gestation.

Explanation:

Fetal complications of hyperthyroidism include spontaneous abortion, premature labor, low birthweight, small for gestational age, intrauterine growth restriction, and still birth. Maternal risks include heart failure and preeclampsia. Fetal complications of hypothyroidism include placental abruption, nonreassuring fetal heart rate tracing, preterm delivery, low birthweight, perinatal morbidity and mortality, and neuropsychological and cognitive impairments. Maternal risks include preeclampsia/gestational hypertension, increased rate of cesarean delivery, and postpartum hemorrhage.

Postpartum thyroiditis is described as the onset of temporary thyroid dysfunction within the first year after delivery or spontaneous delivery in women who were euthyroid and not taking thyroid treatment prior to pregnancy. It occurs in about 16.7% of all postpartum women. Approximately one-half of these women develop permanent hypothyroidism 5 to 10 years later. It is an indication for obtaining a TSH level during pregnancy. Measuring TSH levels is the easiest and most cost-effective method to test for thyroid dysfunction.

A normal range of TSH in the first trimester is 0.1 to 2.5 mIU/L; the normal nonpregnant range is 0.4 to 4.0 mIU/L. In this scenario, the patient’s TSH level would be normal if she were not pregnant. Treatment decisions depend on determining whether this is overt or subclinical hypothyroidism, and this can be ascertained by obtaining a free T4 level. Ranges for normal free T4 levels vary among different laboratories, so the result should be compared against that laboratory’s reference range. Normal T4 levels indicate subclinical hypothyroidism; low indicates overt hypothyroidism. Approximate 90% of hypothyroidism in pregnancy is subclinical, and most cases (overt and subclinical) in iodine-sufficient areas are caused by chronic autoimmune thyroiditis (Hashimoto thyroiditis).

It is premature to begin thyroid hormone replacement based on the TSH level alone. The free T4 level is needed to distinguish overt from subclinical hypothyroidism, as treatment is generally not recommended for the latter. The evidence is insufficient to suggest that treatment improves neurocognitive development and obstetric outcomes versus untreated women with subclinical hypothyroidism.

The fetus depends on maternal thyroxine early in the pregnancy for normal neurologic development. The fetus does not produce its own thyroxine until 12 weeks. Thus, treatment, if indicated, it needs to be started as soon as overt hypothyroidism is recognized. It is inappropriate to wait until the second trimester to repeat testing and potentially delay crucial treatment.

Although 3.0 mIU/L is a normal TSH level in a nonpregnant woman, it is elevated as previously described. A low TSH level (range, 0.1-0.4 mIU/L), however, is physiologic in the first trimester, as β-human chorionic gonadotropin weakly binds thyroid receptors and thyroxine is produced as normal, suppressing TSH secretion from the pituitary. An elevated TSH level requires further evaluation.

References:

American College of Obstetricians and Gynecologists. Practice bulletin 148: thyroid disease in pregnancy. Obstet Gynecol. 2015;125(4):996-1005.

Creasy RK, et al. Creasy and Resnik’s Maternal-Fetal Medicine: Principles and Practice. 7th ed., 2014.

De Groot L, Abalovich M, Alexander EK, et al. Management of thyroid dysfunction during pregnancy and postpartum: an Endocrine Society clinical practice guideline. J Clin Endocr Metab. 2012;97:2543-2565.

Gabbe SG, et al. Obstetrics: Normal and Problem Pregnancies. 7th ed., 2016.

Petraglia F, D’Antona D. Maternal adaptations to pregnancy: endocrine and metabolic changes. Accessed April 26, 2018.