Normal suppression of TSH during pregnancy may lead to a misdiagnosis of subclinical hyperthyroidism. Of greater concern is the potential failure to identiy women with early hypothyroidism because of suppressed TSH concentrations. To mitigate the likelihood of such misdiagnoses, Dashe and coworkers (2005) conducted a population-based study at Parkland Hospital to develop gestational-age-specific TSH normal curves for both singleton and twin pregnancies (Fig. 4-17). Similarly, Ashoor and associates (2010) established normal ranges for maternal TSH, free T4, and free T3 at 11 to 13 weeks' gestation.
hese complex alterations of thyroid regulation do not appear to alter maternal thyroid status as measured by metabolic studies. lthough basal metabolic rate increases progressively by as much as 25 percent during normal pregnancy, most 4.0 0.4
FIGURE 4-17 Gestational age-specific thyroid-stimulating hormone (TSH) nomogram derived from 13,599 singleton pregnancies. The nonpregnant reference values of 4.0 and 0.4 mUll are represented as solid black lines. Upper shaded area represents the 28 percent of singleton pregnancies with TSH values above the 97.5th percentile threshold that would not have been identified as abnormal based on the assay reference value of 4.0 mUll. lower shaded area represents singleton pregnancies that would have been (falsely) identified as having TSH suppression based on the assay reference value of 0.4 mUll. (Data from Dashe, 2005.) of this greater oxygen consumption can be attributed to fetal metabolic activity. If fetal body surface area is considered along with that of the mother, the predicted and observed basal metabolic rates are similar to those in nonpregnant women.
Iodine requirements increase during normal pregnancy (Chap. 58, p. 1127). In women with low or marginal intake, deiciency may manifest as low T4 and higher TSH levels. Importantly, more than a third of the world population lives in areas where iodine intake is marginal. For the fetus, early exposure to thyroid hormone is essential for the nervous system, and despite public health programs to supplement iodine, severe iodine deiciency resulting in cretinism afects more than 2 million people globally (Syed, 2015).
In one longitudinal investigation of 20 women, all markers of bone turnover rose during normal pregnancy and failed to reach baseline levels by 12 months postpartum (More, 2003). Investigators concluded that the calcium needed for fetal growth and lactation may be drawn at least in part from the maternal skeleton. he factors afecting bone turnover yield a net result favoring fetal skeletal formation at the expense of the mother, such that pregnancy is a vulnerable period for osteoporosis (Sanz-Salvador, 2015). hat said, prevention is diicult due to a paucity of identiiable risk factors.
Acute or chronic declines in plasma calcium or acute drops in magnesium levels stimulate parathyroid hormone (PTH) release. Conversely, greater calcium and magnesium levels suppress PTH levels. he action of this hormone on bone resorption, intestinal absorption, and kidney reabsorption is to raise extracellular luid calcium concentrations and lower phosphate levels.