++
Thyroid diseases are among the most common endocrine disorders encountered during pregnancy. They are challenging both because of pregnancy-related changes in thyroid physiology that make diagnosis of thyroid disorders difficult and because of the limited number of medications used to treat mother and fetus. Screening for subclinical thyroid disorders remains a highly debated topic.
+++
Thyroid Function during Normal Pregnancy
++
The thyroid, a gland that functions to provide thermal and metabolic regulation, develops from the third week in gestation from the primitive pharynx. The gland then migrates to the neck and starts to produce thyroid hormone by 10–12 weeks' gestation.
++
Maternal thyroid physiology is altered during normal pregnancy. There is glandular hyperplasia with thyroid enlargement. Thyroid volume is increased on ultrasound examination, but the echostructure is unchanged. The normal increase in the renal glomerular filtration rate causes an increase in urinary iodide clearance, necessitating increased intake of dietary iodine in order to make and maintain thyroid hormone concentrations. Both total thyroxine (T4) and triiodothyronine (T3) levels increase because the level of their carrier, thyroxine-binding globulin (TBG), becomes elevated. Estrogen causes increased TBG synthesis with decreased TBG clearance. Because of the similar subunits of chorionic gonadotropin and thyrotropin (thyroid-stimulating hormone [TSH]), crossover between these 2 peptides can lead to an increase in free thyroxine (fT4) in the first trimester. The TSH level is lowest and fT4 level highest when human chorionic gonadotropin (hCG) levels peak. Elevated fT4 causes suppression of TSH, which, in turn, causes barely detectable levels of maternal thyrotropin-releasing hormone (TRH). Overall, the demand for T4 increases by an estimated 1–3% above daily nonpregnant needs. The increased demand starts very early, reaching a plateau at 16–20 weeks. These normal physiologic changes make diagnosis of thyroid disease during pregnancy difficult.
++
Studies from animal models have helped to elucidate the role of maternal T4 in the fetus. T3 is made by conversion of maternal T4. It has been demonstrated that if maternal T4 is low, fetal T3 levels in the brain will be low even in the presence of normal maternal and fetal serum T3, suggesting that both T3 and T4 in the fetal brain are maternal T4 dependent. Further evidence of a maternal source of T3 in the fetal brain is that by midgestation, fetal concentration of T3 is 34% of adult levels. This is much higher than would be expected considering the low circulating fetal serum levels. It is during midgestation that initial growth velocity of the fetal brain occurs, and animal data suggest that the thyroid hormone necessary for this development is primarily maternally derived. Toward the end of the first trimester, the fetal hypothalamic–pituitary–thyroid axis becomes active. By 14 weeks' gestation, fetal production of T4 is detectable. Normal thyroid hormones levels in the fetus and newborn are crucial for subsequent brain maturation and intellectual development.
+++
Essentials of Diagnosis
++
- Elevated free T4 and T3 levels; suppressed TSH levels
- Signs and symptoms of hyperthyroidism include heat intolerance, fatigue, anxiety, diaphoresis, tachycardia, and a widened pulse pressure
++
The prevalence of hyperthyroidism (also known as thyrotoxicosis) during pregnancy ranges from 0.05 to 0.2%. The most common cause of hyperthyroidism during pregnancy is Graves' disease. Graves' disease is caused by thyroid-stimulating antibody (TSAb) belonging to the immunoglobulin (Ig) G class, which binds with high affinity to the TSH receptor. TSAb may cross the placenta, bind to fetal TSH receptors, and cause fetal or neonatal hyperthyroidism. However, the placenta acts as a partial barrier, so usually only those with high titers are likely to be affected. Other causes of hyperthyroidism include thyroiditis, thyroid adenoma, and multinodular goiter.
++
The signs and symptoms of hyperthyroidism—heat intolerance, fatigue, anxiety, diaphoresis, tachycardia, and a widened pulse pressure—can all be found during normal pregnancy. Signs specific to hyperthyroidism would be pulse >100 bpm, goiter, and exophthalmos, but these may not be present. Gastrointestinal symptoms such as severe nausea and vomiting may also be present, but these can be related to β-hCG elevations. Laboratory tests will confirm elevated T4, fT4, T3, and free T3 (fT3) levels and a suppressed or undetectable TSH level. TSAb titers will be elevated in a significant number of patients. Other laboratory findings may include a normocytic, normochromic anemia, mild neutropenia, and elevated liver enzymes.
++
Subclinical hyperthyroidism, a condition resulting from suppressed levels of TSH and normal levels of T4 and T3, is also seen in pregnancy. It was determined that 1.7% of screened women had subclinical disease. There is no effect of subclinical hyperthyroidism in pregnancy, so screening and treatment for this entity are not warranted.
++
The most common complication of hyperthyroidism in pregnancy is preeclampsia. With large amounts of transplacental transfer of thyroid-stimulating immunoglobulins, thyrotoxicosis could develop in the fetus or newborn. Fetal hypothyroidism may also result from overadministration of thioamides. Poorly controlled hyperthyroidism has also been associated with an increased risk of miscarriage, preterm labor, and low-birth-weight infants.
++
Thyroid storm is a life-threatening complication of women with hyperthyroidism that may result in heart failure if untreated. This complication developed in 8% of women with thyrotoxicosis. Classic findings of thyroid storm include thermoregulatory dysfunction; central nervous system (CNS) effects including agitation, delirium, and coma; gastrointestinal dysfunction; and cardiovascular manifestations such as tachycardia or heart failure. This can be precipitated by labor and delivery, caesarean delivery, infection, or preeclampsia. T4-induced cardiomyopathy, however, is reversible.
++
Treatment during pregnancy almost always consists of antithyroid medications. Surgery is performed in exceptional situations, such as allergic reactions to all drugs available or lack of response to very large doses (“drug resistance”), which in most cases has been the result of noncompliance. The goals of treatment are to rapidly achieve and maintain euthyroidism with the minimum but effective amount of medication, provide symptomatic relief, and keep fT4 levels in the upper third of normal. Thionamides are the most commonly prescribed class of medication used for the treatment of hyperthyroidism. The medications available are propylthiouracil (PTU) and methimazole. Both drugs work by blocking thyroid hormone synthesis; however, PTU also blocks peripheral conversion of T4 to T3. Some physicians prefer PTU, but reports of large numbers of patients indicate that the 2 drugs are equally effective and have similar side effects. PTU is shorter acting, meaning more pills are required more often; therefore, methimazole may be preferable when compliance is a problem. The initial methimazole dose is 20–40 mg/d, and the initial PTU dose is 200–400 mg/d. The dose is gradually reduced as improvement occurs. Most women can be effectively treated on an outpatient basis; however, hospitalization may be considered in severe, uncontrolled cases in the third trimester because of increased risk for complications. Women who have remained euthyroid while taking small amounts of PTU (≤100 mg/d) or methimazole (≤10 mg/d) for 4 weeks or longer can stop taking the medication altogether by 32–34 weeks' gestation under close surveillance. The purpose is to minimize the risk of fetal/neonatal hypothyroidism, which is otherwise uncommon with PTU doses ≤200 mg/d or methimazole ≤20 mg/d. The therapy is resumed if symptoms recur. Women with large goiters, long-standing hyperthyroidism, or significant eye involvement should remain on treatment throughout pregnancy. Other potential side effects of antithyroid medications are pruritus, skin rash, urticaria, fever, arthralgias, cholestatic jaundice, lupus-like syndrome, and migratory polyarthritis. Leukopenia may be a medication effect but is also seen in untreated Graves' disease; therefore, a white blood cell (WBC) count should be obtained before treatment is started. Agranulocytosis is the most severe complication, but fortunately, it is uncommon and found in only 0.1% of patients. Treatment prior to pregnancy is preferred to treatment during pregnancy because outcomes tend to be better. Recently, methimazole has become the treatment of choice for hyperthyroidism in pregnancy. This is because PTU has been found to cause irreversible liver damage, leading potentially to liver failure.
++
β-Blockers (propranolol 20–40 mg every 6–8 hours) can be used for symptomatic relief in severe cases but only for short periods (few weeks) and before 34–36 weeks' gestation. They inhibit conversion from T4 to T3 but may be related to intrauterine growth restriction and hypoglycemia if used for prolonged periods of time.
++
Treatment of thyroid storm is aimed at reducing synthesis of thyroid hormone, minimizing release of thyroid hormone from the thyroid gland, and blocking peripheral effects of thyroid hormone. Aggressive treatment for thyroid storm is critical to the patient's survival. PTU or methimazole is started immediately and may be administered via nasogastric tube if the patient has altered mental status. Iodine solution such as potassium iodide (SSKI) or Lugol's solution may also be given. Iodine solution works by inhibiting thyroid hormone release. If the patient has a history of iodine-induced anaphylaxis, then lithium carbonate is given instead. Fluid hydration and nutritional support are also important. β-Blockers are also given for relief of symptoms such as tachycardia and palpitations, and they may also inhibit peripheral conversion of T4 to T3. Glucocorticoids may also be used in severe cases to reduce peripheral conversion of T4 to T3. Aspirin should be avoided in these patients because it can increase concentrations of fT4 and T3.
++
The maternal and fetal prognosis with hyperthyroidism in pregnancy that is well controlled is generally excellent.
+++
Effect of Hyperthyroidism on Pregnancy
++
Potential complications of hyperthyroidism in the mother include spontaneous abortion, pregnancy-induced hypertension, preterm delivery, anemia, higher susceptibility to infections, placental abruption, and, in severe, untreated cases, cardiac arrhythmias, congestive heart failure, and thyroid storm. In the fetus, possible complications include fetal and neonatal hyperthyroidism, intrauterine growth restriction, stillbirth, prematurity, and morbidity related to antithyroid medications. Most maternal and neonatal complications are seen in cases of uncontrolled or untreated hyperthyroidism.
++
Approximately 1–5% of infants born to women with Graves' disease have hyperthyroidism at birth due to transplacental transfer of TSAbs. The fetal/neonatal risk correlates with maternal TSAb titer level. Signs of fetal hyperthyroidism include fetal tachycardia (heart rate >160 bpm), fetal goiter, and poor growth. High levels of fetal thyroid hormone detected by cordocentesis have been confirmed in a few cases. Tests of fetal well-being are recommended for poorly controlled cases and for patients with high TSAb titers, even if they are euthyroid. Serial ultrasounds are useful for dating and fetal growth evaluation.
++
Breastfeeding is allowed if the total daily dose of PTU is ≤150 mg or daily dose of methimazole is ≤10 mg. The medication should be given immediately after each feeding and the infant monitored periodically.
+++
Effect of Pregnancy on Hyperthyroidism
++
Pregnancy is not thought to alter the course of hyperthyroidism.
+++
Transient Hyperthyroidism of Hyperemesis Gravidarum
+++
Essentials of Diagnosis
++
- Severe nausea and vomiting accompanied by weight loss
- Low serum TSH with mildly elevated fT4
++
Biochemical hyperthyroidism is seen in most women (66%) with hyperemesis gravidarum. The most likely etiology is thyrotropin receptor stimulation from high serum concentrations of hCG.
++
Laboratory abnormalities include low serum TSH and mildly elevated fT4. Serum T3 levels are not elevated in women with transient hyperthyroidism of hyperemesis gravidarum. The degree of thyroid function abnormalities correlates with the severity of vomiting.
+++
Differential Diagnosis
++
Women in early pregnancy with weight loss, tachycardia, vomiting, and laboratory evidence of hyperthyroidism may be difficult to differentiate from early, true thyrotoxicosis. Women with transient hyperthyroidism of hyperemesis gravidarum have no previous history of thyroid disease, no palpable goiter, and, except for tachycardia, no other symptoms or signs of hyperthyroidism. Test results for thyroid antibodies are negative. With transient hyperthyroidism of hyperemesis gravidarum, TSH level may be suppressed and fT4 level elevated, but the T3 level is lower than in true hyperthyroidism. With true hyperthyroidism, both levels are usually elevated.
++
Treatment is symptomatic, and antithyroid medication is not recommended.
++
The mild hyperthyroidism associated with transient hyperthyroidism of hyperemesis gravidarum usually resolves by 20 weeks' gestation. The time to resolution is widely variable (1–10 weeks).
+++
Essentials of Diagnosis
++
- Elevated TSH and low free T4 levels
- Symptoms: modest weight gain, fatigue, sleepiness, lethargy, decreased exercise capacity, depression, and cold intolerance (very unusual in normal pregnancy)
++
Overt hypothyroidism (elevated TSH, low free T4) has been reported in 1 in 1000 to 1 in 2000 deliveries. A study by Casey and colleagues found that the incidence of overt hypothyroidism in pregnant women was 1.8 per 1000. Subclinical hypothyroidism (elevated TSH, normal fT4) is more common, with an incidence of 23 per 1000 in pregnancy. This makes the overall incidence of hypothyroidism 2.5%.
++
The most common cause of hypothyroidism is Hashimoto's thyroiditis, which is found in 8–10% of women of reproductive age. Less common causes are transient hypothyroidism in silent (painless) and subacute thyroiditis, drug induced, high-dose external neck radiation, congenital hypothyroidism, inherited metabolic disorders, and thyroid hormone resistance syndromes. Secondary hypothyroidism may occur in pituitary or hypothalamic disease. Drugs that may cause hypothyroidism by interfering with thyroid hormone synthesis and/or its release include antithyroid drugs (PTU, methimazole), iodine, and lithium. Increased T4 clearance is caused by carbamazepine, phenytoin, and rifampin. Amiodarone decreases T4 to T3 conversion and inhibition of T3 action. Interference with intestinal absorption is seen with aluminum hydroxide, cholestyramine, ferrous sulfate, calcium, vitamins, soy, and sucralfate. Many pregnant women take ferrous sulfate, and it is important to ensure that T4 is taken at least 2 hours before (sometimes even 4 hours is recommended) because insoluble ferric–T4 complexes may form, resulting in reduced T4 absorption.
++
The clinical diagnosis is difficult and frequently unsuspected except in advanced cases. Symptoms are insidious and may be masked by the hypermetabolic state of pregnancy. Symptoms include modest weight gain, fatigue, sleepiness, lethargy, decreased exercise capacity, depression, and cold intolerance (very unusual in normal pregnancy). Signs include general slowing of speech and movements, dry and pale or yellowish skin, sparse thin hair, hoarseness, bradycardia (also unusual in pregnancy), myxedema, hyporeflexia, prolonged relaxation of reflexes, carpal tunnel syndrome, and a diffuse or a nodular goiter.
++
The best laboratory test is the TSH level; current sensitive assays allow very early diagnosis and accurate treatment monitoring. Other useful tests include fT4 and antibody titers. A low fT4 with an elevated TSH is diagnostic of hypothyroidism. A macrocytic or normochromic, normocytic anemia may be present as well. It usually results from decreased erythropoiesis, but it may result from vitamin B12, folic acid, or iron deficiency. Levels of lipids and creatine phosphokinase (of muscle origin) may be elevated. Hypothyroidism may be seen more commonly in women with type 1 diabetes.
+++
Effect of Hypothyroidism on Pregnancy
++
Some studies have reported a 2-fold increased rate of spontaneous abortion in women with elevated levels of thyroid antibodies, even if they are euthyroid, but this finding is not universally confirmed. These antibodies (antiperoxidase [TPO], antimicrosomal antibody [AMA], and antithyroglobulin [ATG]) may cross the placenta and cause neonatal hypothyroidism, which, if untreated, may lead to serious cognitive deficiencies. Lower IQs in infants of even very mildly hypothyroid women have been reported. There is an increased risk of preeclampsia, placental abruption, intrauterine growth restriction, prematurity, and intrauterine fetal demise. The severity of the hypertension and other perinatal complications is greater in the more severely hypothyroid woman. Early treatment and close monitoring to ensure euthyroidism will prevent or decrease perinatal complications.
+++
Effect of Pregnancy on Hypothyroidism
++
Pregnancy is known to cause increasing requirement of thyroid hormone. That is the reason for evaluation of maternal TSH levels every trimester, with more frequent evaluation every 4 weeks if changes to dosing are deemed necessary. Requirements usually return to prepregnancy levels postpartum, and dosing can also be adjusted on a monthly schedule after that time.
++
l-Thyroxine has long been the treatment drug of choice. The hormonal content of the synthetic drugs is more reliably standardized, and they have replaced desiccated thyroid as the mainstay of therapy. Administration of T4 alone is recommended. In the normal physiologic process, T4 is deiodinated to T3 in the extrathyroidal tissues. In addition, during early pregnancy, the fetal brain is unable to use maternal T3. The best time to take L-thyroxine is early in the morning, on an empty stomach. Women experiencing nausea and vomiting should be allowed to take it later in the day until they improve. Numerous reports indicate that T4 requirements increase during pregnancy. TSH levels should be checked every 4 weeks, with adjustments made until the TSH is at the lower end of the normal range. The initial dose should be 2 μg/kg of actual body weight. Further adjustments are made according to the TSH level. If the TSH level is elevated but <10 μU/mL, add 25–50 μg/d; if the TSH level is >10 but <20, add 50–75 μg/d; and if the TSH level is >20, add 75–100 μg/d. Changes made at less than 4-week intervals may lead to overtreatment. Up to 85% of women receiving T4 replacement before pregnancy will require higher doses while they are pregnant. The levels should be checked early in pregnancy and then every trimester to maintain euthyroidism. After delivery, the dosage is reduced to the prepregnancy amount, and the TSH level is measured 4–8 weeks postpartum. In women with pituitary disease, the TSH level cannot be used to guide therapy. In these cases, the fT4 level should be kept in the upper third of normal.Casey BM, Leveno KJ. Thyroid disease in pregnancy. Obstet Gynecol 2006;108:1283–1292.[PubMed: 17077257].
+++
Subclinical Hypothyroidism
+++
Essentials of Diagnosis
++
- Elevated serum TSH with normal fT4 levels
++
Subclinical hypothyroidism is a condition characterized by an elevated TSH with a normal fT4. The incidence of this finding is approximately 2.5% in pregnant women and 5% in women of reproductive age. The causes of subclinical hypothyroidism are thought to be the same as overt hypothyroidism.
++
Subclinical hypothyroidism is diagnosed when women are found to have elevations in TSH and normal fT4 levels. Women are asymptomatic for thyroid disease.
++
The interest in subclinical hypothyroidism and intellectual development in offspring was reignited after several recent publications addressed a possible relationship between the two. Haddow and colleagues performed a study comparing pregnant women with hypothyroidism to pregnant controls with normal thyroid function. They found that children of women with hypothyroidism scored 4 points lower on a standard IQ test when compared to controls (P = 0.06). In addition, 15% of cases had an IQ score of 85 or less compared to 5% of controls (P = 0.08). Although neither of these values is statistically significant, when the results were sub-analyzed for those women with untreated hypothyroidism, as opposed to those on medication, they found that the IQ scores were 7 points lower in cases than controls (P = 0.005), and 19% had IQ scores <85 compared with 5% of controls (P = 0.007), suggesting that the greater effect on pediatric neurodevelopment is in the untreated mothers with hypothyroidism. Pop and colleagues had similar results when they studied pediatric neurodevelopment at 10, 12, and 24 months in children of mothers with abnormal thyroid function at 12 weeks' gestation. Note that neither of these studies evaluated infants of women with subclinical hypothyroidism. Haddow evaluated infants of mothers with overt hypothyroidism, whereas Pop evaluated infants of women with hypothyroxinemia, thought to be the more clinically relevant deficiency.
++
The discrepancy in findings from these 2 studies has led to conflicting position statements regarding the surveillance for hypothyroidism in pregnant women from the American Association of Clinical Endocrinologists, the American Thyroid Association, the Endocrine Society, and the American College of Obstetricians and Gynecologists (ACOG). Current obstetric practice does not involve screening for thyroid disease unless the patient has risk factors, such as pregestational diabetes, or is symptomatic. The most recent joint position statement of the 3 previously mentioned endocrine societies recommends routine TSH evaluation (with fT4 if TSH is abnormal) both preconceptionally or as soon as pregnancy has been diagnosed. However, ACOG does not support the performance of thyroid function tests in asymptomatic pregnant women. ACOG advises that the current data are limited because of their observational nature. To date, there has not been a clinical trial that specifically addresses isolated subclinical hypothyroidism and neurodevelopmental outcomes, making recommendations regarding the management of this mild thyroid dysfunction difficult. Furthermore, the available clinical literature has not shown that the identification and treatment of women with subclinical hypothyroidism prevents the purported neurodevelopmental sequelae. The National Institute of Child Health and Human Development Maternal-Fetal Medicine Units network is currently conducting a clinical trial to help answer these questions.
++
Certain pregnant women are at high risk for hypothyroidism and should undergo screening, including those with previous therapy for hyperthyroidism, high-dose neck irradiation, previous postpartum thyroiditis, presence of a goiter, family history of thyroid disease, treatment with amiodarone, suspected hypopituitarism, and type 1 diabetes mellitus.
++
ACOG does not advocate routine screening and treatment for subclinical hypothyroidism at this time.Haddow JE, Palomaki GE, Allan WC, et al. Maternal thyroid deficiency during pregnancy and subsequent neuropsychological development of the child. N Engl J Med 1999;19:549–555.[PubMed: 10451459]. Pop VJ, Brouwers EP, Vader HL, Vulsma T, van Baar AL, de Vijlder JJ. Maternal hypothyroxinaemia during early pregnancy and subsequent child development: a 3-year follow-up study. Clin Endocrinol 2003;59:282–288.[PubMed: 12919150].
+++
Congenital Hypothyroidism
+++
Essentials of Diagnosis
++
- Elevated serum TSH and low T3 and T4 in the neonate
++
Congenital hypothyroidism is found in 1 in 4000 to 1 in 7000 infants after diagnosis from national screening programs. Congenital hypothyroidism is defined as hypothyroidism in the neonate. Most cases of congenital hypothyroidism are sporadic, resulting from thyroid dysgenesis. However, approximately 15% appear to be hereditary, mostly due to an inborn error in thyroid hormone synthesis. Early and aggressive treatment is critical to improve neonatal outcomes.
++
Transient congenital hypothyroidism has been described in a number of settings, including iodine deficiency and in utero exposure to antithyroid drugs.
++
Low serum T4 and high serum TSH levels in the neonate confirm a diagnosis of congenital hypothyroidism. Most neonates are asymptomatic at birth, mainly because some maternal T4 crosses the placenta. Signs that may present over time include lethargy, slow movement, hoarse cry, poor feeding, and constipation.
++
The first report of a possible correlation between thyroid disease and mental retardation in offspring came from iodine-deficient areas of Switzerland in 1915. Mothers of children with mental retardation were noted to have abnormal thyroid function. Choufoer and colleagues then described the effect of maternal thyroid levels on the newborn in 1965. They described pregnancy outcomes related to endemic goiter in iodine-deficient New Guinea. They found neurologic manifestations of cretinism, or physical stunting and mental retardation, in women who were not clinically hypothyroid, but who had a low concentration of thyroid hormone. In this same decade, Man and Jones evaluated a cohort of 1349 children of mothers with hypothyroxinemia, defined in that time as a low serum butanol-extractable with a normal thyroid-binding globulin. They found an association between low BEI and low infant Bayley scores on mental and motor development. The Bayley Scales of Infant Development were designed to test the cognitive, motor, and behavioral development of infants up to 42 months of age. The test has high validity and reliability. These and other observations of maternal thyroid disease led to the landmark double-blind study by Pharoah and colleagues in 1971. They gave alternate families in New Guinea either 4-mL injections of iodized oil or a saline placebo and then returned a year later to initiate periodic evaluation of any offspring delivered after treatment. They concluded that supplementation of iodine in pregnancy prevented subsequent cretinism.
++
Oral thyroid supplementation, usually T4, is the treatment for congenital hypothyroidism. Treatment is usually starting when screening tests for congenital hypothyroidism return as positive without waiting for result of confirmatory tests.
++
With early diagnosis and initiation of treatment, long-term outcomes are excellent, with normal growth and development.Choufeor JC, Vanrhijn M, Querido A. Endemic goiter in western new guinea. II. Clinical picture, incidence and pathogenesis of endemic cretinism. J Clin Endocrinol Metab 1965;25:385–402.[PubMed: 14264263].Jones WS and Man EB. Thyroid function in human pregnancy. VI. Premature deliveries and reproductive failures of pregnant women with low serum butanol-extractable iodines. Maternal serum TBG and TBPA capacities. Am J Obstet Gynecol 1969;15: 909–914.[PubMed: 4183109].Pharoah PO, Buttfield IH, and Hetzel BS. Neurological damage to the fetus resulting from severe iodine deficiency during pregnancy. Lancet 1971;1:308–310.[PubMed: 4100150].
+++
Postpartum Thyroiditis
+++
Essentials of Diagnosis
++
- Postpartum thyroiditis is diagnosed if the serum TSH is either elevated or depressed in the year after delivery.
- This phenomenon has been noted in 5–10% of women in their first postpartum year.
- Women with high thyroid autoantibodies are generally affected, and women with type 1 diabetes are at high risk to develop this complication.
++
The symptoms involve fatigue, palpitations, heat intolerance, and nervousness. There are 2 distinct clinical phases. The first phase lasts from 1–4 months after delivery and is characterized by destruction-induced thyrotoxicosis. Laboratory findings during this phase demonstrate an elevation in free T4 and suppressed TSH. There is an abrupt onset, and a goiter may be palpable. Approximately two-thirds of these women will become euthyroid. Between 4 and 8 months, the other third will develop hypothyroidism.
++
T4 replacement is helpful, but about 30% of women will go on to develop permanent hypothyroidism. The clinical course may vary, with some patients experiencing only the hyperthyroid phase and others only the hypothyroid phase. Treatment in the immediate postpartum period is limited to symptomatic patients only (β-blockers for the hyperthyroid phase and low-dose levothyroxine or T3 for the hypothyroid phase, which is enough to alleviate symptoms and allows recovery of thyroid function when discontinued). Additionally, there is a positive correlation between postpartum depression and postpartum thyroiditis, so these patients should be screened accordingly.
+++
Solitary Thyroid Nodule during Pregnancy
+++
Essentials of Diagnosis
++
- Thyroid nodule palpable on physical examination
++
Thyroid nodules are frequently first detected during pregnancy when many women see a doctor for the first time. The risk of malignancy for a solitary nodule varies between 5% and 43%, depending on various factors including previous radiation, rate of growth, and patient age.
++
Women with a thyroid nodule diagnosed during pregnancy should undergo fine-needle aspiration of the nodule. Thyroid radionuclide scanning is contraindicated during pregnancy. Women with benign nodules may be followed; in most cases, surgery in these women is deferred until after delivery. Women with thyroid cancer should undergo surgery. Surgery during pregnancy carries a higher risk if it is performed during the first and the third trimesters (miscarriage, premature delivery, and fetal death); surgery during the second trimester reportedly has a lower complication rate. Radioactive iodine should never be given during pregnancy. There is no evidence that thyroid cancer occurs more frequently during pregnancy. However, because of the indolent course of these carcinomas, many practitioners advocate postponing surgery until the postpartum period.
American College of Obstetricians and Gynecologists. ACOG Committee Opinion. Number 381, October 2007. Subclinical hypothyroidism in pregnancy.
Obstet Gynecol 2007;110: 959–960.
[PubMed: 17906045]
.
Cunningham FG, Leveno KJ, Bloom SL, Hauth JC, Gilstrap LC, Wenstrom KD. Williams Obstetrics. 22nd ed. New York, NY: McGraw-Hill; 2005.
Pop VJ, Brouwers EP, Vader HL, Vulsma T, van Baar AL, de Vijlder JJ. Maternal hypothyroxinaemia during early pregnancy and subsequent child development: a 3-year follow-up study.
Clin Endocrinol 2003;59:282–288.
[PubMed: 12919150]
.