Serum TSH and hCG levels vary with gestational age (Fig. 4-16). As discussed in Chapter 5 (p. 98), the a-subunits of the two glycoproteins are identical, whereas the 3-subunits, although similar, difer in their amino acid sequence. As a result of this structural similarity, hCG has intrinsic thyrotropic activity, and thus, high serum hCG levels cause thyroid stimulation. Indeed, TSH levels in the irst trimester decline in more than 80 percent of pregnant women, however, they still remain in the normal range for nonpregnant women
The thyroid gland boosts production of thyroid hormones by 40 to 100 percent to meet maternal and fetal needs (Moleti, 2014). To accomplish this, the thyroid gland undergoes moderate enlargement during pregnancy caused by glandular hyperplasia and greater vascularity. Mean thyroid volume increases from 12 mL in the first trimester to 15 mL at term (Glinoer,
Week of pregnancy
FIGURE 4-16 Relative changes in maternal and fetal thyroid function across pregnancy. Maternal changes include a marked and early increase in hepatic production of thyroxine-binding globulin (TBG) and placental production of human chorionic gonadotropin (hCG). Increased TBG increases serum thyroxine (T4) concentrations. hCG has thyrotropin-like activity and stimulates maternal free T4 secretion. This transient hCG-induced increase in serum T4 levels inhibits maternal secretion of thyrotropin. Except for minimally increased free T4 levels when hCG peaks, these levels are essentially unchanged. Fetal levels of all serum thyroid analytes increase incrementally across pregnancy. Fetal triiodothyronine (T3) does not increase until late pregnancy. (Modified from Burrow, 1994.) 1990). That said, normal pregnancy does not typically cause significant thyromegaly, and thus any goiter warrants evaluation.
Early in the first trimester, levels of the principal carrier protein-thyroid-binding globulin (TBG)-rise, reach their zenith at about 20 weeks, and stabilize at approximately double baseline values for the remainder of pregnancy (see Fig. 4-16). he greater TBG concentrations result from both higher hepatic synthesis rates-due to estrogen stimulation-and lower metabolism rates due to greater TBG sialylation and glycosylation. These elevated TBG levels increase total serum thyroxine (T 4) and triiodothyronine (T 3) concentrations, but do not afect the physiologically important serum ree T4 and ree T3 levels. Specifically, total serum T4 levels rise sharply beginning between 6 and 9 weeks' gestation and reach a plateau at 18 weeks. Serum free T 4 levels rise only slightly and peak along with hCG levels, and then they return to normal.
Interestingly, T 4 and T 3 secretion is not similar for all pregnant women (G linoer, 1990). Approximately a third of women experience relative hypothyroxinemia, preferential T3 secretion, and higher, albeit normal, serum TSH levels. hus, thyroidal adjustments during normal pregnancy may vary considerably.
The fetus relies on maternal T 4, which crosses the placenta in small quantities to maintain normal fetal thyroid function (Chap. 58, p. 1118). Recall that the fetal thyroid does not begin to concentrate iodine until 10 to 12 weeks' gestation. he synthesis and secretion of thyroid hormone by fetal pituitary TSH ensues at approximately 20 weeks. At birth, approximately 30 percent of the T 4 in umbilical cord blood is of maternal origin (Leung,i2012).