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As with diabetes mellitus, thyroid disease may predate pregnancy or may initially manifest during pregnancy. Obstetric conditions, such as gestational trophoblastic disease or hyperemesis gravidarum, may themselves affect thyroid function. All neonates of women with thyroid dis-ease are at risk for neonatal thyroid dysfunction. For this reason, the neonate’s pediatrician should be informed about the maternal diagnosis.
Thyrotoxicosis is the condition that results from excessproduction of and exposure to thyroid hormone from any cause. Hyperthyroidism is thyrotoxicosis caused by hyper-functioning of the thyroid gland. Graves disease is an auto-immune disease characterized by abnormal production of thyroid-specific immunoglobulins that either stimulate or inhibit thyroid function. Exacerbation of the signs and symptoms of hyperthyroidism is called a thyroid storm.Hypothyroidism is caused by inadequate thyroid hormoneproduction. Postpartum thyroiditis is an autoimmune inflammation of the thyroid gland that presents as new-onset, painless hypothyroidism, transient thyrotoxicosis, or thyrotoxicosis followed by hypothyroidism within 1 year postpartum.
Levels of thyroid-binding hormone (TBG) normally increase in pregnancy. Test results that change significantly in pregnancy are those influenced by TBG concentra-tion, including total thyroxine (TT4), total triiodothy-ronine (TTd) and resin triiodothyronine uptake (TR3U). A transient increase may also occur in free thyroxine (FT4) and free thyroxine index (FTI) levels in the first trimester (Fig. 14.3).
Plasma iodide levels decrease during pregnancy, and this change may cause a noticeable increase in thyroid gland size (approximately 18% change) in 15% of women. How-ever, in most women, the thyroid returns to normal size postpartum.
There is insufficient evidence to warrant routine screening of asymptomatic pregnant women for hypothyroidism.
Testing should be performed in women with a prior his-tory of thyroid disease or symptoms of thyroid disease. Thyroid function is evaluated by measuring thyroid-stimulating hormone (TSH) levels. TSH does not cross the placenta, so this test is an accurate measure of hor-mone function during pregnancy. In pregnant women suspected of being hyperthyroid or hypothyroid, FT4 and FTI levels should be measured in addition to TSH.
Hyperthyroidism in pregnancy is treated with thioamides, specifically propylthiouracil (PTU) and methimazole. Thegoal of treatment during pregnancy is to maintain the FT4 or FTI in the high normal range using the lowest possible dosage of thioamides to minimize fetal exposure. Thioamide treat-ment for Graves disease in pregnancy may suppress fetal and neonatal thyroid function and has also been associated with fetal goiter. Neonatal hypothyroidism is usually tran-sient and does not require treatment.
Thyroid storm is a medical emergency characterized by an extreme hypermetabolic state. Although rare (it occurs in 1% of pregnancy patients with hyperthyroidism), it carries a high risk of maternal heart failure. It is often precipitated by infection,surgery, labor, or delivery. Thyroid storm must be diag-nosed and treated quickly in order to prevent shock, stupor, and coma (Box 14.1). Treatment of thyroid storm consists of a standard series of drugs, each of which plays a role in suppressing thyroid function. The underlying precipitating event should also be treated. The fetus should be appropri-ately evaluated with ultrasonography, biophysical profile, or nonstress test, depending on the gestational age.
Treatment of hypothyroidism in pregnant women is the same as for nonpregnant women and involves administration of levothy-roxine at sufficient dosages to normalize TSH levels. Maternalthyroxine requirements increase in women with hypothy-roidism diagnosed before pregnancy. Levothyroxine levels should be adjusted at 4-week intervals until TSH levels are stable. Thereafter, levels should be checked once per trimester.
Severe nausea and vomiting of pregnancy (hyperemesisgravidarum) may cause biochemical hyperthyroidism, inwhich levels of TSH are undetectable, or FTI levels are elevated, or both. This condition resolves spontaneously by 18 weeks of gestation. Routine measurements of thyroid function are not recommended in patients with hyperemesis gravidarum unless other overt signs of hyperthyroidism are evident.
Postpartum thyroiditis occurs in 5% of women who have no prior history of thyroid disease. Postpartum thyroiditisalso may occur after pregnancy loss and has a 70% risk of recurrence. Almost half of women with postpartum thyroiditis have hypothyroidism, while the remaining women are evenly split between thyrotoxicosis and thyro-toxicosis followed by hypothyroidism. Postpartum thyro-toxicosis usually resolves on its own without treatment. Of those with hypothyroidism, approximately 40% of women require treatment for extremely high TSH levels or an increasing goiter size. Only 11% of women diag-nosed with postpartum hypothyroidism develop perma-nent hypothyroidism.
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