Alternatively, the Endocrine Society’s clinical practice guidelines regarding the management of thyroid dysfunction during pregnancy and postpartum recommends targeted screening for the following individuals: history of thyroid disorder, family history of thyroid disease, goiter, thyroid autoantibodies, clinical signs or symptoms of thyroid disease, autoimmune disorders, infertility, head and/or neck radiation, and preterm delivery (373). The American Congress of Obstetricians and Gynecologists accepted these recommendations for TSH testing (374). Because of the (i) potentially significant neurologic affects on the fetus and other adverse pregnancy events; (ii) physiologic rise in TBG and the TSH-like activity of hCG in pregnancy, and (iii) potential for the targeted screening groups to have overt or subclinical hypothyroidism defined by the reference ranges for pregnancy (TSH <2.5, 3.1, and 3.5 μIU/mL for the first, second, and third trimesters, respectively), targeted maternal testing for hypothyroidism is encouraged. The targeted screening protocol allows that 30% of subclinical hypothyroidism cases may be missed. According to these recommendations, preconceptionally diagnosed hypothyroid women (overt or subclinical) should have their T4 dosage adjusted such that the TSH value is less than 2.5 μIU/mL before pregnancy. The T4 dosage in women already on replacement will routinely require a dose escalation (30% to 50%) at 4 to 6 weeks gestation in order to maintain a TSH value less than 2.5 μIU/mL. Pregnant women with overt hypothyroidism should be normalized as rapidly as possible to maintain TSH at less than 2.5 and 3 μIU/mL in the first, second, and third trimesters, respectively. Euthyroid women with thyroid autoantibodies are at risk of hypothyroidism and should have TSH screening in each trimester. After delivery, hypothyroid women need a reduction in T4 dosage used during pregnancy. Because subclinical hypothyroidism is associated with adverse outcomes for mother and the fetus, T4 replacement is recommended.
Figure 31.11 Types of autoimmune injury found in Hashimoto thyroiditis. A: Complement-mediated cytotoxicity, which can be abolished by inactivating the complement system. B: Antibody-dependent cell-mediated cytotoxicity (ADCC) function through killer T cells, monocytes, and natural killer cells that have immunoglobulin G fragment receptors. C: Stimulation of blockade of hormone receptors leading to hyperfunction or hypofunction or growth, depending on the types of immunoglobulins acting on the target cell. TBII, TSH-binding inhibitor immunoglobulin; TGI, thyroid growth–promoting immunoglobulin; TSAb, thyroid-stimulating antibodies; TSH, thyroid-stimulating hormone. (From Coulam CB, Faulk WP, McIntyre JA. Immunologic obstetrics. New York: Norton Medical Books, 1992:658, with permission.)