presentation of hypothyroidism during pregnancy

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INTRODUCTION

The evaluation and treatment of pregnant women with hypothyroidism parallels that of nonpregnant individuals but presents some unique problems. There are several important issues that must be considered when hypothyroidism occurs during pregnancy or when women with preexisting treated hypothyroidism become pregnant. The clinical manifestations, diagnosis, and treatment of hypothyroidism during pregnancy are reviewed here. Other aspects of thyroid disease during pregnancy or in women attempting pregnancy are reviewed elsewhere:

● (See "Overview of thyroid disease and pregnancy" .)

● (See "Hyperthyroidism during pregnancy: Clinical manifestations, diagnosis, and causes" .)

● (See "Hyperthyroidism during pregnancy: Treatment" .)

● (See "Subclinical hypothyroidism in nonpregnant adults", section on 'Reproductive abnormalities' and "Subclinical hypothyroidism in nonpregnant adults", section on 'Fertility' .)

LEO A. CARNEY, DO, JEFF D. QUINLAN, MD, AND JANET M. WEST, MD

This is a corrected version of the article that appeared in print.

Am Fam Physician. 2014;89(4):273-278

Author disclosure: No relevant financial affiliations.

Thyroid disease is the second most common endocrine disorder affecting women of reproductive age, and when untreated during pregnancy is associated with an increased risk of miscarriage, placental abruption, hypertensive disorders, and growth restriction. Current guidelines recommend targeted screening of women at high risk, including those with a history of thyroid disease, type 1 diabetes mellitus, or other autoimmune disease; current or past use of thyroid therapy; or a family history of autoimmune thyroid disease. Appropriate management results in improved outcomes, demonstrating the importance of proper diagnosis and treatment. In women with hypothyroidism, levothyroxine is titrated to achieve a goal serum thyroid-stimulating hormone level less than 2.5 mIU per L. The preferred treatment for hyperthyroidism is antithyroid medications, with a goal of maintaining a serum free thyroxine level in the upper one-third of the normal range. Postpartum thyroiditis is the most common form of postpartum thyroid dysfunction and may present as hyper- or hypothyroidism. Symptomatic treatment is recommended for the former; levothyroxine is indicated for the latter in women who are symptomatic, breastfeeding, or who wish to become pregnant.

Thyroid disease is second only to diabetes mellitus as the most common endocrinopathy that occurs in women during their reproductive years. Symptoms of thyroid disease often mimic common symptoms of pregnancy, making it challenging to identify. Poorly controlled thyroid disease is associated with adverse outcomes during pregnancy, and treatment is an essential part of prenatal care to ensure maternal and fetal well-being. 1 – 3

Thyroid Function Tests in Pregnancy

To understand abnormal thyroid function in pregnancy, a review of normal physiologic changes is warranted ( Table 1 ) . 4 Because of the estrogen-mediated increase in thyroid-binding globulin, the increased volume of distribution of thyroid hormone, and the placental metabolism and transport of maternal thyroxine, there is a 20% to 40% increase in the thyroid hormone requirement as early as the fourth week of gestation. 5

During pregnancy, reference ranges for thyroid-stimulating hormone (TSH) are lower because of the cross-reactivity of the alpha subunit of human chorionic gonadotropin with the TSH receptor. 2 , 3 Changes in serum-binding protein levels can influence measurements of free thyroxine (FT 4 ) that rely on estimates rather than direct measurements, resulting in inaccurate reported values. 6 Physicians should know the limitations of locally available assay methods. When preferred FT 4 assay techniques are unavailable, a serum TSH level is a more accurate assessment of maternal thyroid status, and measurements of total thyroxine and the FT 4 index can be used instead. 3 , 6 Trimester-specific ranges for common serum thyroid studies are shown in Table 2 . 3 , 7 [ corrected ]

The Endocrine Society recommends screening only pregnant women at high risk of thyroid disease using serum TSH measurement ( Table 3 ) . 2 , 3 Although one study found that selectively screening women at high risk would miss 30% of those with overt or subclinical hypothyroidism, 8 a randomized controlled trial of 4,562 women did not show a reduction in adverse outcomes in those who were universally screened vs. case finding. 9

Preconception Counseling

Women with hypothyroidism should be counseled about the importance of achieving euthyroidism before conception because of the risk of decreased fertility and miscarriage. 1 – 3 They must also understand the importance of immediate monitoring at the onset of pregnancy, because by the first prenatal visit, many of these patients will already have an elevated TSH level consistent with uncontrolled hypothyroidism. 5 Euthyroid women who are taking a stable dosage of levothyroxine should be counseled to notify their physician and independently increase their medication by two additional doses per week after a missed menstrual cycle or positive home pregnancy test. 3 In a study of 48 women treated for hypothyroidism with a normal prepregnancy serum TSH level, increasing levothyroxine by two doses per week prevented maternal TSH elevation above 2.5 mIU per L and above 5 mIU per L in 85% and 100% of patients, respectively, with only two patients requiring a subsequent dose reduction. 5

Preconception counseling for women with known hyperthyroidism should include discussion of available treatments and potential adverse effects, as well as the impact on future pregnancies. Standard treatments include long-term antithyroid medication, radioactive iodine ablation, and near-total thyroidectomy. Potential adverse fetal effects of antithyroid medications include congenital abnormalities and neonatal hypothyroidism caused by transplacental transfer. 2 , 3 Although radioactive iodine ablation is not associated with long-term consequences on gonadal function, fertility, or pregnancy outcomes, it is customary to wait six months after the therapeutic dose is administered before attempting conception. 8 Radioactive ablation and surgery can increase the risk of neonatal goiter and hyperthyroidism because of the absence of maternal antithyroid medication, which crosses the placenta and counteracts the stimulatory effect of thyrotropin receptor antibodies on the fetal thyroid. 2 , 3 The importance of achieving and maintaining euthyroidism before conception should be emphasized, because a significant increase in congenital malformations has been reported when hyperthyroidism is not controlled in the first trimester of pregnancy. 10

Hypothyroidism

The incidence of hypothyroidism during pregnancy is estimated to be 0.3% to 0.5% for overt hypothyroidism and 2% to 3% for subclinical hypothyroidism. 11 Overt hypothyroidism is defined as thyroid hormone deficiency with low FT 4 and elevated TSH levels, whereas subclinical hypothyroidism refers to asymptomatic individuals with elevated TSH and normal FT 4 levels.

Worldwide, the most common cause of hypothyroidism is iodine deficiency. In iodine-sufficient regions, the most common causes are autoimmune thyroiditis and iatrogenic hypothyroidism after treatment for hyperthyroidism. 11 Symptoms such as fatigue, weight gain, decreased exercise capacity, and constipation are often confused with common symptoms of pregnancy; other symptoms such as hair loss, dry skin, and bradycardia may be evident only in more symptomatic persons.

Overt and subclinical hypothyroidism have been associated with adverse effects on pregnancy and fetal development ( Table 4 ) . 1 – 3 These maternal conditions contribute to an increased risk of adverse neonatal outcomes, including preterm birth, low birth weight, and increased perinatal morbidity and mortality. 12 Childhood neurodevelopment also seems to be contingent on thyroid hormone regulation; impairment of neuropsychologic developmental indices and school learning abilities has been noted in children whose mothers had poorly controlled hypothyroidism during pregnancy. 2 , 3 , 13

Levothyroxine is the mainstay of treatment for maternal hypothyroidism ( Table 5 ) . 2 , 3 , 14 – 16 The increment of dose adjustment generally is based on the degree of TSH elevation ( Table 6 ) . 17 Serum TSH should be measured every four to six weeks until 20 weeks' gestation and until the patient is on a stable medication dose; it should be measured again at 24 to 28 weeks' and 32 to 34 weeks' gestation. 2 , 3 , 17 Antenatal testing is not recommended in women with well-controlled hypothyroidism, but it should be considered in patients with coexisting maternal or obstetric indications. After delivery, levothyroxine should be decreased to the prepregnancy dosage over a four-week period, and further adjustment should be guided by TSH levels four to six weeks after delivery. 2

Treatment seems to reduce the incidence of miscarriage and preterm birth, and to improve fetal intellectual development; however, it has little impact on hypertensive disorders and placental abruption. 1

Hyperthyroidism

Hyperthyroidism is less common than hypothyroidism, with an approximate incidence during pregnancy of 0.2%. 11 Overt hyperthyroidism is defined as elevated FT 4 and low TSH levels, whereas subclinical hyperthyroidism is defined as asymptomatic low TSH and normal FT 4 levels. Clinical symptoms of hyperthyroidism include tachycardia, nervousness, tremor, sweating, heat intolerance, proximal muscle weakness, frequent bowel movements, decreased exercise tolerance, and hypertension.

Graves disease, which accounts for 95% of cases of hyperthyroidism, is an autoimmune disorder mediated by stimulatory antibodies against the TSH receptor. Other less common causes of hyperthyroidism include gestational trophoblastic disease, nodular goiter or solitary toxic adenoma, viral thyroiditis, and tumors of the pituitary gland or ovary. Transient hyperthyroidism may also be associated with hyperemesis gravidarum and gestational transient thyrotoxicity, most likely resulting from the stimulatory effect of human chorionic gonadotropin on the thyroid. 11 Although the radioactive iodine uptake scan used in the diagnosis of hyperthyroidism is contra-indicated during pregnancy, testing for the presence of antithyroid antibodies can be diagnostically useful.

The natural history of hyperthyroid disorders varies with the underlying etiology. Graves disease is typically characterized by an initial exacerbation of symptoms in the first trimester, and is thought to be caused by the initial stimulatory effect of human chorionic gonadotropin on the thyroid. Symptoms usually improve during the second half of the pregnancy, only to worsen again in the postpartum period. 11 Overt hyperthyroidism that is inadequately treated is associated with an increased risk of adverse maternal and neonatal outcomes ( Table 4 ) . 1 – 3 However, one large prospective study of more than 25,000 pregnant women with subclinical hyperthyroidism showed no increase in adverse pregnancy outcomes; therefore, treatment is not recommended in these cases. 18

Overt hyperthyroidism during pregnancy is treated with methimazole (Tapazole) or propylthiouracil ( Table 5 ) . 2 , 3 , 14 – 16 Because the use of methimazole is associated with birth defects, including aplasia cutis and choanal or esophageal atresia, 16 , 19 propylthiouracil is the preferred medication during the first trimester. 3 However, it is recommended that physicians consider switching to methimazole after the first trimester because the risk of liver failure associated with propylthiouracil use is greater than the risk of congenital abnormalities. 2 , 3

The main concern in women with hyperthyroidism is the potential effect on the fetus. Thyroid receptor antibodies should be measured by the end of the second trimester in women with active Graves disease, a history of Graves disease treated with radioactive iodine or thyroidectomy, or a history of a previous infant with Graves disease. 2 , 3 , 20 In women at high risk, including those receiving antithyroid medication and those with poorly controlled hyperthyroidism or high thyrotoxin receptor antibody levels, fetal ultrasonography should be performed monthly after 20 weeks' gestation to detect evidence of fetal thyroid dysfunction (e.g., growth restriction, hydrops, goiter, cardiac failure). 2 , 3 , 21 These women should also undergo antepartum testing at least weekly beginning at 32 to 34 weeks' gestation (or earlier in particularly high-risk situations). 22

Postpartum Thyroid Dysfunction

The most common cause of postpartum thyroid dysfunction is postpartum thyroiditis, which affects 1.1% to 21.1% of women. 23 Postpartum thyroiditis is defined as an abnormal TSH level within the first 12 months postpartum in the absence of a toxic thyroid nodule or thyrotoxin receptor antibodies. 23 Clinical symptoms can mimic the typical fatigue following delivery, as well as postpartum depression and Graves disease; a thorough assessment is required to differentiate these conditions. A radioactive iodine uptake scan can help distinguish postpartum thyroiditis from Graves disease, but is contraindicated in breastfeeding women. Patients must limit close contact with others for a time after the study.

The clinical course of postpartum thyroiditis varies: approximately 25% of patients present with symptoms of hyperthyroidism, followed by hypothyroidism and then recovery; 43% present with symptoms of hypothyroidism; and 32% present with hyperthyroidism. 3 Because the hyperthyroid phase of postpartum thyroiditis is caused by autoimmune destruction of the thyroid, resulting in release of stored thyroid hormone, antithyroid medications are not typically beneficial and treatment is generally symptomatic, using peripheral beta antagonists. Differentiation of the hyperthyroid phase of postpartum thyroiditis from Graves disease is important because Graves disease requires antithyroid therapy. In contrast, postpartum hypothyroidism should be treated with levothyroxine in women who are symptomatic or breastfeeding, or who wish to become pregnant, and may require lifetime supplementation. 3 , 5

Women with a history of type 1 diabetes and women with thyroglobulin or thyroperoxidase autoantibodies are at increased risk of postpartum thyroiditis. 14 , 15 Asymptomatic women should be screened at three and six months postpartum using serum TSH measurement. 2 Additionally, women with a history of postpartum thyroiditis are at increased risk of permanent hypothyroidism and should be screened annually thereafter. 2 , 3 , 24

Data Sources : Essential Evidence Plus was searched using PubMed, and OVID was searched. Key words were thyroid disease and pregnancy. Article selection was limited to human studies, original research, systematic reviews, and current clinical practice guidelines. Search date: August 22, 2013.

Reid SM, Middleton P, Cossich MC, Crowther CA. Interventions for clinical and subclinical hypothyroidism in pregnancy. Cochrane Database Syst Rev. 2010(7):CD007752.

De Groot L, Abalovich M, Alexander EK, et al. Management of thyroid dysfunction during pregnancy and postpartum: an Endocrine Society clinical practice guideline. J Clin Endocrinol Metab. 2012;97(8):2543-2565.

Stagnaro-Green A, Abalovich M, Alexander E, et al.; American Thyroid Association Taskforce on Thyroid Disease During Pregnancy and Postpartum. Guidelines of the American Thyroid Association for the diagnosis and management of thyroid disease during pregnancy and postpartum. Thyroid. 2011;21(10):1081-1125.

American College of Obstetrics and Gynecology. ACOG practice bulletin no. 37. Thyroid disease in pregnancy. Obstet Gynecol. 2002;100(2):387-396.

Yassa L, Marqusee E, Fawcett R, Alexander EK. Thyroid hormone early adjustment in pregnancy (the THERAPY) trial. J Clin Endocrinol Metab. 2010;95(7):3234-3241.

Lee RH, Spencer CA, Mestman JH, et al. Free T4 immunoassays are flawed during pregnancy. Am J Obstet Gynecol. 2009;200(3):260.e1-260.e6.

Abbassi-Ghanavati M, Greer LG, Cunningham FG. Pregnancy and laboratory studies: a reference table for clinicians [published correction appears in Obstet Gynecol . 2010;15(2 pt 1):387]. Obstet Gynecol. 2009;114(6):1326-1331.

Vaidya B, Anthony S, Bilous M, et al. Detection of thyroid dysfunction in early pregnancy: universal screening or targeted high-risk case finding?. J Clin Endocrinol Metab. 2007;92(1):203-207.

Negro R, Schwartz A, Gismondi R, Tinelli A, Mangieri T, Stagnaro-Green A. Universal screening versus case finding for detection and treatment of thyroid hormonal dysfunction during pregnancy. J Clin Endocrinol Metab. 2010;95(4):1699-1707.

Momotani N, Ito K, Hamada N, Ban Y, Nishikawa Y, Mimura T. Maternal hyperthyroidism and congenital malformation in the offspring. Clin Endocrinol (Oxf). 1984;20(6):695-700.

Neale DM, Cootauco AC, Burrow G. Thyroid disease in pregnancy. Clin Perinatol. 2007;34(4):543-557.

Stagnaro-Green A. Overt hyperthyroidism and hypothyroidism during pregnancy. Clin Obstet Gynecol. 2011;54(3):478-487.

Rovet JF. Neurodevelopmental consequences of maternal hypothyroidism during pregnancy. In: Program and abstracts from the 76th annual meeting of the American Thyroid Association; September 30 – October 3, 2004; Vancouver, British Columbia. Thyroid. 2004;14(9):710. Abstract 88.

Männistö T, Vääräsmäki M, Pouta A, et al. Thyroid dysfunction and autoantibodies during pregnancy as predictive factors of pregnancy complications and maternal morbidity in later life. J Clin Endocrinol Metab. 2010;95(3):1084-1094.

Mamede da Costa S, Sieiro Netto L, Coeli CM, Buescu A, Vaisman M. Value of combined clinical information and thyroid peroxidase antibodies in pregnancy for the prediction of postpartum thyroid dysfunction. Am J Reprod Immunol. 2007;58(4):344-349.

Di Gianantonio E, Schaefer C, Mastroiacovo PP, et al. Adverse effects of prenatal methimazole exposure. Teratology. 2001;64(5):262-266.

Mandel SJ. Hypothyroidism and chronic autoimmune thyroiditis in the pregnant state: maternal aspects. Best Pract Res Clin Endocrinol Metab. 2004;18(2):213-224.

Casey BM, Dashe JS, Wells CE, McIntire DD, Leveno KJ, Cunningham FG. Subclinical hyperthyroidism and pregnancy outcomes. Obstet Gynecol. 2006;107(2 pt 1):337-341.

Wing DA, Millar LK, Koonings PP, Montoro MN, Mestman JH. A comparison of propylthiouracil versus methimazole in the treatment of hyperthyroidism in pregnancy. Am J Obstet Gynecol. 1994;170(1 pt 1):90-95.

Mitsuda N, Tamaki H, Amino N, Hosono T, Miyai K, Tanizawa O. Risk factors for developmental disorders in infants born to women with Graves disease. Obstet Gynecol. 1992;80(3 pt 1):359-364.

Luton D, Le Gac I, Vuillard E, et al. Management of Graves' disease during pregnancy: the key role of fetal thyroid gland monitoring. J Clin Endocrinol Metab. 2005;90(11):6093-6098.

ACOG practice bulletin. Antepartum fetal surveillance. Number 9, October 1999 (replaces Technical Bulletin Number 188, January 1994). Clinical practice management guidelines for obstetrician-gynecologists. Int J Gynaecol Obstet. 2000;68(2):175-185.

Muller AF, Drexhage HA, Berghout A. Postpartum thyroiditis and autoimmune thyroiditis in women of childbearing age: recent insights and consequences for antenatal and postnatal care. Endocr Rev. 2001;22(5):605-630.

Azizi F. The occurrence of permanent thyroid failure in patients with subclinical postpartum thyroiditis. Eur J Endocrinol. 2005;153(3):367-371.

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StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan-.

StatPearls [Internet].

Thyroid disease and pregnancy.

Shikha Singh ; Sartaj Sandhu .

Affiliations

Last Update: July 17, 2023 .

• Continuing Education Activity

Thyroid disease is the second most common endocrine disorder after diabetes in pregnancy. Thyroid disease poses a substantial challenge on the physiology of pregnant women and has significant maternal and fetal implications. During pregnancy, thyroid hormone production increases by around 50% along with a similar increase in total daily iodine requirements. Thyroid dysfunction in pregnant women including hypothyroidism and hyperthyroidism requires close monitoring and treatment as warranted. This activity reviews thyroid disease in pregnancy and its management. This activity will review the most common causes of thyroid disease in pregnancy and outline the treatment approach according to current evidence. This activity will highlight the role of the interprofessional team in recognizing and treating thyroid disease in pregnancy.

• Recall the presentation of thyroid disease in pregnancy.
• Describe the workup of thyroid disease in pregnancy.
• Summarize the treatment options for thyroid disease in pregnancy.
• Explain how the facilitation of interprofessional team education and discussion can optimize the effective detection of thyroid disease in pregnancy and monitor the subsequent evaluations.
• Introduction

Thyroid disease is the second most common endocrine disorder after diabetes in pregnancy. Thyroid disease poses a substantial challenge on the physiology of pregnant women and has significant maternal and fetal implications. Research shows during pregnancy, the size of the thyroid gland increases by 10% in countries with adequate iodine stores and by approximately 20% to 40% in countries with iodine deficiency. [1]  During pregnancy, thyroid hormone production increases by around 50% along with a similar increase in total daily iodine requirements. Thyroid dysfunction in pregnant women including hypothyroidism and hyperthyroidism requires close monitoring and treatment as warranted. Occasionally, pregnancy may be complicated by thyroid nodules and thyroid cancer requiring further intervention. This article reviews thyroid disease in pregnancy and its management.

Hypothyroidism

The most common cause of hypothyroidism during pregnancy in iodine replenished areas is chronic autoimmune thyroiditis (Hashimoto thyroiditis). [2]  Worldwide, endemic iodine (I-) deficiency is commonly associated with hypothyroidism in pregnant women.

Hyperthyroidism

Graves disease is the most common cause of overt hyperthyroidism during pregnancy. [3]  Other less common causes include toxic multinodular goiter, toxic adenoma, and thyroiditis. A frequent cause of hyperthyroidism during pregnancy is transient gestational thyrotoxicosis (hCG mediated hyperthyroidism) which affects 1% to 3% of pregnancies in the first half of pregnancy and is due to elevated hCG levels. [4]

• Epidemiology

During pregnancy, spontaneous hypothyroidism has a prevalence of about 2% to 3% with 0.3% to 0.5% women presenting with overt hypothyroidism and 2% to 2.5% with subclinical hypothyroidism. [5]

On the other hand, overt hyperthyroidism can affect up to 0.1% to 0.4% of the pregnancies. [6]

• Pathophysiology

Normal Thyroid Physiology During Pregnancy

During pregnancy, there are increased metabolic needs of the maternal body resulting in changes in thyroid physiology. These changes in thyroid physiology reflect in altered thyroid function tests. The different changes occurring in thyroid physiology are as follow:

• An increase in serum thyroxine-binding globulin (TBG) leading to an increase in the total T4 and total T3 concentrations. Their levels peak by approximately week 16 of gestation and remain high until delivery. [7]  
• Stimulation of the thyrotropin (TSH) receptor by human chorionic gonadotropin (hCG) which increases thyroid hormone production and subsequently reduces serum TSH concentration. [4]

Therefore, compared to the non-pregnant state, women tend to have lower serum TSH concentrations during pregnancy. Studies have shown that 15% of healthy women during the first trimester of pregnancy have TSH below the non-pregnant lower limit of 0.4 mU/L. [8]

Trimester-Specific Ranges

The serum TSH concentration is the initial and most reliable measure of thyroid function during pregnancy. [9]  As elaborated above, there are physiologic changes in TSH levels during pregnancy which warrants close monitoring of TSH levels. As per the latest American Thyroid Association (ATA) guidelines, serum TSH levels during pregnancy should be defined using population and trimester-specific based reference ranges. When population and trimester-specific normal ranges are not available, the ATA guidelines recommend reducing the lower limit of TSH by 0.4 mU/L and the upper limit by 0.5 mU/L. It would correspond to the TSH reference range of 0.1 to 4.0 mU/L during the first trimester with a gradual return of TSH towards the non-pregnant normal range during second and third trimesters. [1]  The free T4 levels measured by immunoassays are not very reliable during pregnancy due to changes in binding proteins. Alternatively, measurement of total T4 levels or free T4 index may be more reliable. [10]

Iodine Requirement During Pregnancy

There is an increase in iodine requirement during pregnancy due to an increase in maternal thyroid hormone production as well as an increase in renal iodine clearance. Along with the above two factors, there is also a fetal iodine requirement; therefore, dietary iodine requirements are higher during pregnancy. [11]  Women with sufficient iodine intake before and during pregnancy can easily adapt to the increased demand for thyroid hormone during pregnancy. However, in the areas of iodine deficiency, where iodine requirements are not optimally replenished, it frequently results in maternal iodine deficiency. It has adverse effects on the fetus including poor neurological and cognitive development. The World Health Organization (WHO) recommends 250 mcg of iodine intake daily during pregnancy and lactation. [12]  The ATA guidelines recommend all pregnant women should consume approximately 250 mcg iodine daily. In the United States, women who are planning a pregnancy or are currently pregnant should supplement their diet with a daily oral supplement containing 150 mcg of iodine in the form of potassium iodide which should be started 3 months in advance of a planned pregnancy. It is important to note that excessive iodine intake should be avoided during pregnancy which is also harmful and causes fetal hypothyroidism and goiter. As per WHO, maximum permissible intake of iodine during pregnancy is 500 mcg daily. [13]

• History and Physical

History and physical examination in pregnant women with hypothyroidism are similar to those with hypothyroidism in non-pregnant adults. Many women are asymptomatic while others may have fatigue, constipation, weight gain, and cold intolerance. 

Physical examination findings may include dry skin, puffy faces, periorbital edema, delayed relaxation of deep tendon reflexes and bradycardia. 

Similarly, history and physical examination in pregnant women with thyrotoxicosis are identical to hyperthyroidism in non-pregnant adults. Some symptoms of hyperthyroidism may include palpitations, excessive sweating, heat intolerance, anxiety, insomnia, weight loss, and tremors.

Physical examination findings may include tachycardia, lid lag and stare, diaphoresis, and hyperreflexia. Findings specific to Graves disease include diffuse goiter, ophthalmopathy (exophthalmos), and pretibial myxedema.

Hypothyroidism during pregnancy is defined as elevated TSH levels above the population and trimester-specific reference range. When it is not available, an upper reference range above 4.0 mU/L should be used. Hypothyroidism during pregnancy can present as overt hypothyroidism defined as increased trimester-specific TSH and low  free T4 levels or subclinical hypothyroidism defined as   increased trimester specific TSH and normal  free T4 levels.

Overt hyperthyroidism during pregnancy is characterized by decreased TSH and increased free T4 levels. Subclinical hyperthyroidism is characterized by decreased TSH and  normal free T4 levels. It is important to remember transient subclinical hyperthyroidism can be seen during the first trimester of pregnancy due to adaption in thyroid physiology as discussed above. In gestational thyrotoxicosis, there is a physiological decrease in TSH levels during the first trimester due to hCG mediated stimulation of the TSH receptor. It peaks between 7 to 11 weeks of gestation. [14]  Gestational thyrotoxicosis can be differentiated from Graves disease by careful history and examination. Additionally, in Graves disease, TSH receptor antibodies are elevated on the blood test.

• Treatment / Management

Hypothyroidism 

Overt hypothyroidism warrants treatment with thyroid hormone replacement with the goal to keep TSH level in trimester specific range. There is ample research demonstrating the detrimental effects of untreated overt hypothyroidism on maternal and fetal health. On the other hand, there is insufficient evidence about the treatment of subclinical hypothyroidism during pregnancy. ATA guidelines recommend subclinical hypothyroidism should be treated in females with positive TPO antibodies and TSH greater than 2.5 mU/L. [1]  The thyroid function tests should be checked every 4 to 6 weeks until week 20 and at least once around the 30th week of gestation.  Most women (50% to 85%) with pre-existing hypothyroidism before pregnancy have an increased demand for thyroid hormone requirements during pregnancy which increases with progression of pregnancy by approximately 30%. [15]

Hyperthyroidism 

The treatment goals for hyperthyroidism during pregnancy is to maintain mild maternal hyperthyroidism while avoiding fetal hypothyroidism. [16]  To maintain mild maternal hyperthyroidism, maternal free T4/total T4 should be maintained at the upper limit of normal of the reference range using the lowest effective dose of antithyroid drugs. The treatment for hyperthyroidism during pregnancy is indicated based on etiology as well as the severity of hyperthyroidism.

Graves disease is the most common cause of thyrotoxicosis during pregnancy. The management of Graves disease complicating pregnancy is as follow:

• Antithyroid drugs : The thionamides – methimazole (MMI) and propylthiouracil (PTU) – are most commonly used for the treatment of hyperthyroidism during pregnancy. [17]  MMI is contraindicated in the first trimester of pregnancy due to potential teratogenic effects; therefore, PTU is recommended as the first line drug in the first trimester. [18]  It is recommended to switch to MMI during the second trimester due to a risk of rare but severe risk of hepatotoxicity associated with PTU. [19]
• Beta blockers: Short-term treatment with beta-blockers such as propranolol and metoprolol can be used for symptomatic control. However, long-term treatment with beta-blockers should be avoided due to the risk of intrauterine fetal growth retardation. [20]
• Surgery: Thyroidectomy is rarely needed and only reserved for the patients who cannot tolerate thionamides due to severe side effects or when euthyroidism cannot be achieved despite using large doses of thionamides. When indicated, it should be performed during the second trimester.

Radioactive iodine ablation is contraindicated during pregnancy.

Subclinical hyperthyroidism, as well as  gestational thyrotoxicosis , do not require treatment during pregnancy and rather observation is recommended with periodic monitoring of thyroid function tests every 4 to 6 weeks.

• Differential Diagnosis

The differential diagnosis for hypothyroidism as well as hyperthyroidism during pregnancy are similar to those with non-pregnant adults. Detailed discussion is beyond the scope of this review. 

• Medical Oncology

Thyroid Nodules and Thyroid Cancer During Pregnancy 

The prevalence of thyroid nodules during pregnancy varies between 3% and 21%. [21] [22]  The evaluation and management of thyroid nodules during pregnancy are similar to those with non-pregnant patients. Thyroid ultrasound should be performed and indications to perform a fine needle aspiration (FNA) are similar as in non-pregnant patients. FNA is safe to be performed during pregnancy. All women with thyroid nodules should have a TSH level measured to rule out toxic adenoma.

The prevalence of thyroid cancer varies widely due to differences in study design and patient population. The prognosis of differentiated thyroid cancer (DTC) is not largely influenced by pregnancy. [23]  Given the slow growth of DTC, definitive management (thyroidectomy) can usually be delayed up until after delivery. The biopsy proven thyroid cancer nodules should be monitored with thyroid ultrasound every trimester. In rare circumstances, such as rapidly growing thyroid nodules or in the presence of metastases, surgery is indicated during pregnancy. In such cases, the second trimester is the safest period for performing the surgery. [1] [24]

• Complications

Untreated hypothyroidism during pregnancy may result in adverse maternal and fetal outcomes including preterm labor, preeclampsia, preterm delivery, gestational hypertension, postpartum hemorrhage, low birth weight, neuropsychological and cognitive impairment in the fetus, and increased perinatal morbidity and mortality. [25]

Similarly, untreated or inadequately treated hyperthyroidism during pregnancy is associated with an increased risk of preterm labor, spontaneous abortion, intrauterine growth restriction, pre-eclampsia, low birth weight, stillbirth, and fetal malformations. [26]

• Pearls and Other Issues

Thyroid Antibodies in Euthyroid Pregnant Women

Studies have shown an overall prevalence of thyroid peroxidase antibody (TPO Ab) in women of childbearing age is 6% to 20%. [27]  These women are at higher risk of developing hypothyroidism during pregnancy, and therefore thyroid function should be monitored in these women. Additionally, studies have shown TPO Ab positivity has been associated with spontaneous pregnancy loss as well as increased risk of preterm delivery. [28]  

At present, there is not sufficient evidence to warrant supplementation of levothyroxine in euthyroid pregnant women with TPO Ab positivity. A small dose of LT4 25 to 50 mcg daily can be considered in TPO Ab-positive euthyroid pregnant women with a prior history of miscarriage.

• Enhancing Healthcare Team Outcomes

Thyroid disease in pregnancy can lead to serious maternal and fetal implications if not adequately diagnosed and treated. It is vital to follow an interprofessional approach when treating pregnant women with thyroid disease. It should be managed by a team of healthcare professionals including an endocrinologist, obstetrician, primary medical doctor, nurse practitioner, and pharmacist. The team should work closely in monitoring thyroid function tests and titrating medications in pregnant women with thyroid disease (including hypothyroidism and hyperthyroidism). There is clear evidence of adverse pregnancy outcomes in cases of untreated overt hypothyroidism and hyperthyroidism in pregnant women. (Level III)

It is equally important for health care providers to understand normal thyroid physiology during pregnancy. It would help them to interpret thyroid function tests accurately and avoid incorrect diagnosis and treatment in pregnant women.

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Disclosure: Shikha Singh declares no relevant financial relationships with ineligible companies.

Disclosure: Sartaj Sandhu declares no relevant financial relationships with ineligible companies.

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• Cite this Page Singh S, Sandhu S. Thyroid Disease and Pregnancy. [Updated 2023 Jul 17]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan-.

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Home » Thyroid Disease in Pregnancy

WHAT ARE THE MOST COMMON CAUSES OF HYPERTHYROIDISM DURING PREGNANCY?

Overall, the most common cause of hyperthyroidism in women of childbearing age is Graves’ disease (see Graves’ Disease brochure ), which occurs in 0.2% of pregnant patients. In addition to other usual causes of hyperthyroidism (see Hyperthyroidism brochure ), very high levels of hCG, seen in severe forms of morning sickness (hyperemesis gravidarum), may cause transient hyperthyroidism in early pregnancy. The correct diagnosis is based on a careful review of history, physical exam and laboratory testing. Go to the Hyperthyroidism in Pregnancy Brochure   >>

WHAT ARE THE MOST COMMON CAUSES OF HYPOTHYROIDISM DURING PREGNANCY?

Overall, the most common cause of hypothyroidism is the autoimmune disorder known as Hashimoto’s thyroiditis (see Hypothyroidism brochure ). Hypothyroidism can occur during pregnancy due to the initial presentation of Hashimoto’s thyroiditis, inadequate treatment of a woman already known to have hypothyroidism from a variety of causes, or over-treatment of a hyperthyroid woman with anti-thyroid medications. Approximately, 2.5% of women will have a TSH of greater than 6 mIU/L (slightly elevated) and 0.4% will have a TSH greater than 10 mIU/L during pregnancy. Go to the Hypothyroidism in Pregnancy Brochure >>

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Pediatric thyroid information, printable brochures.

Hyperthyroidism in Pregnancy Brochure PDF

Hyperthyroidism in Pregnancy FAQ

Hypothyroidism in Pregnancy Brochure PDF

Hypothyroidism in Pregnancy  FAQ

Clinical Thyroidology ® for the Public – Highlighted Article

Thyroid health – management of hypothyroidism during pregnancy: when and how to treat, disorders of thyroid function presentations at american thyroid association: 88 th annual meeting, further information.

For information on thyroid patient support organizations, please visit the Patient Support Links section on the ATA website at www.thyroid.org

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Thyroid Disorders in Pregnancy

Thyroid disorders may predate or develop during pregnancy. Pregnancy does not change the symptoms of hypothyroidism and hyperthyroidism.

Fetal effects vary with the disorder and the medications used for treatment. But generally, untreated or inadequately treated hyperthyroidism can result in

Fetal growth restriction

Preeclampsia

Untreated hypothyroidism can cause

Intellectual deficits in offspring

Miscarriage

The most common causes of maternal hypothyroidism are Hashimoto thyroiditis and treatment of Graves disease.

If women have or have had a thyroid disorder, thyroid status should be closely monitored during and after pregnancy in the women and in their offspring. Goiters and thyroid nodules discovered during pregnancy should be evaluated as they are in other patients (see Approach to the Patient With a Thyroid Nodule and Simple Nontoxic Goiter/Diagnosis ).

Graves disease

Maternal Graves disease is monitored clinically and with free T4 and high-sensitivity thyroid-stimulating hormone (TSH) assays.

In centers with experienced thyroid surgeons, a 2nd-trimester thyroidectomy, although very uncommon, may be considered after medications restore euthyroidism. After thyroidectomy, women are given full replacement of L-thyroxine (0.15 to 0.2 mg orally once a day), beginning 24 hours later.

Radioactive iodine (diagnostic or therapeutic) and iodide solutions are contraindicated during pregnancy because of adverse effects on the fetal thyroid gland. Beta-blockers are used only for thyroid storm or severe maternal symptoms.

If pregnant women have or have had Graves disease, fetal hyperthyroidism may develop. Whether these women are clinically euthyroid, hyperthyroid, or hypothyroid, thyroid-stimulating immunoglobulins (Igs) and thyroid-blocking Igs (if present) cross the placenta. Fetal thyroid function reflects the relative fetal levels of these stimulating and blocking Igs. Hyperthyroidism can cause fetal tachycardia ( > 160 beats/min), growth restriction, and goiter; rarely, goiter leads to decreased fetal swallowing, polyhydramnios, and preterm labor. Ultrasonography is used to evaluate fetal growth, thyroid gland, and heart.

Congenital Graves disease

Maternal hypothyroidism.

Women with mild to moderate hypothyroidism frequently have normal menstrual cycles and can become pregnant.

During pregnancy, the usual dose of L-thyroxine is continued. As pregnancy progresses, minor dose adjustments may be necessary, ideally based on TSH measurement after several weeks.

If hypothyroidism is first diagnosed during pregnancy, L-thyroxine is started; dosing is based on weight. Usually, pregnant women require a higher dose than nonpregnant women.

Hashimoto thyroiditis

Maternal immune suppression during pregnancy often ameliorates Hashimoto thyroiditis ; however, hypothyroidism or hyperthyroidism that requires treatment sometimes develops.

Acute (subacute) thyroiditis

Common during pregnancy, acute thyroiditis usually produces a tender goiter during or after a respiratory infection. Transient, symptomatic hyperthyroidism with elevated T4 can occur, often resulting in misdiagnosis as Graves disease.

Usually, treatment is unnecessary.

Postpartum maternal thyroid dysfunction

Hypothyroid or hyperthyroid dysfunction occurs in 4 to 7% of women during the first 6 months after delivery. Incidence seems to be higher among pregnant women with any of the following:

A strong family history of autoimmune thyroid disorders

Type 1 ( insulin -dependent) diabetes mellitus

In women with any of these risk factors, TSH and free serum T4 levels should be checked during the 1st trimester and postpartum. Dysfunction is usually transient but may require treatment. After delivery, Graves disease may recur transiently or persistently.

Painless thyroiditis with transient hyperthyroidism is a recently recognized postpartum, probably autoimmune disorder. It occurs abruptly in the first few weeks postpartum, results in a low radioactive iodine uptake, and is characterized by lymphocytic infiltration. Diagnosis is based on symptoms, thyroid function tests, and exclusion of other conditions. This disorder may persist, recur transiently, or progress.

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Updates on thyroid disorders in pregnancy and the postpartum period

Kelly d rosenberger , dnp, aprn-fpa, cnm, whnp-bc, faanp, natalie parker , dnp, aprn, cnm, whnp-bc.

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The authors have disclosed no potential conflicts of interest, financial or otherwise.

Issue date 2024 Feb.

Copyright © 2024 The Author(s). Published by Wolters Kluwer Health, Inc. This is an open-access article distributed under the terms of the Creative Commons Attribution-Non Commercial-No Derivatives License 4.0 (CCBY-NC-ND), where it is permissible to download and share the work provided it is properly cited. The work cannot be changed in any way or used commercially without permission from the journal.

NPs play a pivotal role in caring for pregnant people. This article provides an overview of gestational and postpartum thyroid disorders, including their assessment, management, and indications for referral. The goal of this article is to help providers better assess and manage thyroid disorders during pregnancy and improve patient outcomes.

Keywords: hyperthyroidism, hypothyroidism, postpartum thyroiditis, pregnancy, thyroid disease, thyroid disorders, thyroid function tests

No caption available.

In females and those assigned female at birth who are of reproductive age, thyroid disorders are second only to diabetes mellitus as the most common endocrine disorders. The typical symptoms of pregnancy often emulate symptoms of thyroid dysfunction, creating a significant diagnostic challenge during this time. Poorly managed thyroid disorders during pregnancy are associated with adverse outcomes. Untreated thyroid disease during pregnancy has been associated with increased risk of miscarriage, hypertensive disorders, fetal growth restriction, placental abruption, and several other conditions that are discussed in this article. 1 , 2 Therefore, diagnosis and treatment of thyroid disorders are necessary components of prenatal care to safeguard maternal and fetal well-being.

Thyroid changes in pregnancy

During a typical pregnancy, increased metabolic demands significantly impact maternal thyroid physiology. The major changes in thyroid function include a slight enlargement of the thyroid gland due to hyperplasia and increased vascularity, but the enlargement does not constitute a true goiter or significant thyromegaly. Thyroid function test results change during uncomplicated pregnancies as well as in pregnancies in individuals with thyroid dysfunction; these changes vary by trimester. 3 During typical pregnancy, concentrations of the thyroid hormones thyroxine (T4) and triiodothyronine (T3) increase; the thyroid-stimulating hormone (TSH) slightly decreases, though usually within normal range, due to human chorionic gonadotropin (hCG) cross-reacting with TSH receptors; total T4 (TT4) levels increase while free T4 (FT4) levels remain unchanged. 1 - 3 Worldwide, the most common perinatal thyroid disorders are hypothyroidism, hyperthyroidism, postpartum thyroiditis, and goiter. 4 In the US, where iodine intake among the general population is sufficient, goiter during pregnancy is rare. However, in iodine-deficient regions, goiter is more common during pregnancy.

Hypothyroidism in pregnancy

Overt hypothyroidism is defined as low FT4 and increased TSH levels during pregnancy. 2 , 4 Subclinical hypothyroidism during pregnancy is defined as increased TSH and normal FT4 levels. 1 , 2 , 4 Worldwide, the incidence and prevalence of overt and subclinical hypothyroidism during pregnancy vary greatly due to the different definitions of each condition that have been utilized over the years in numerous studies showing inconsistent results. 2 In the US, the highly variable recognition and treatment of subclinical hypothyroidism in pregnancy has been attributed to geographic location, socioeconomic status, race, and ethnicity. 5 A study by Maraka and colleagues found that most pregnant patients with subclinical hypothyroidism did not receive therapy. This lack of treatment initiation was associated with both clinician and patient factors, including insufficient awareness of evolving guidelines, lack of established treatment practices, confusion due to inconsistent evidence and professional society recommendations, and patients' refusal of therapy. 5

Globally, iodine deficiency is the most common cause of hypothyroidism generally attributed to geographic location. In countries with adequate iodine intake among the general population, the most common causes are autoimmune thyroiditis (Hashimoto thyroiditis) and iatrogenic hypothyroidism after treatment for hyperthyroidism. In the US, the American Thyroid Association (ATA) guidelines recommend supplementation with 150 mcg of iodine daily—the dose in the majority of prenatal vitamins—during pregnancy and lactation. 2 , 6

In pregnancy, hypothyroidism has been associated with an increased risk of several complications, including preeclampsia; gestational hypertension; placental abruption; non-reassuring fetal heart rate tracings; preterm delivery, including very preterm delivery (before 32 weeks); low birth weight; increased rate of cesarean section; postpartum hemorrhage; perinatal morbidity and mortality; and neuropsychological and cognitive impairment in children. 1 - 4 , 7 , 8

It is important for clinicians to determine if presenting signs or symptoms of thyroid disease are present. Hypothyroidism signs and symptoms include weight gain, decreased exercise capacity, constipation, fatigue, dry skin, hair loss, and bradycardia. Differential diagnosis should include depression, myalgic encephalomyelitis/chronic fatigue syndrome, and Addison disease, as these conditions share similar symptoms, such as fatigue, weight fluctuations, and difficulties with concentration, to hypothyroidism. 9 - 11

Hyperthyroidism in pregnancy

The incidence of hyperthyroidism during pregnancy is 0.2%, with overt hyperthyroidism defined as increased FT4 and low TSH and subclinical hyperthyroidism defined as asymptomatic low TSH and normal FT4. 2 , 12 Graves disease is an autoimmune disorder with TSH receptor antibodies accounting for 95% of cases. 2 , 12 Other less common causes of hyperthyroidism include gestational trophoblastic disease, nodular goiter, solitary toxic adenoma, viral thyroiditis, and pituitary or ovarian tumors. 2 In pregnancy, hyperthyroidism has been associated with an increased risk of several complications, including spontaneous abortion, premature labor, low birth weight, stillbirth, preeclampsia, and maternal heart failure. 1 - 4 , 7 - 12

Signs and symptoms of hyperthyroidism include failure to gain weight with adequate food intake, thyromegaly, exophthalmos, tachycardia, elevated resting pulse, nervousness, tremor, sweating, heat intolerance, proximal muscle weakness, increased frequency of bowel movements, decreased exercise tolerance, and hypertension.

Early elevations in hCG during pregnancy stimulate thyroid hormone output, which can lead to gestational transient thyrotoxicosis (GTT), also known as transient gestational hyperthyroidism. Graves disease and GTT have similar signs and symptoms to hyperthyroidism. Therefore, a thorough patient history, a physical exam, and indicated lab tests are imperative for an appropriate diagnosis. 13 The differential diagnosis for hyperthyroidism may include TSH-secreting pituitary adenomas, trophoblastic tumors, hyperemesis gravidarum, multinodular goiter, familial nonautoimmune hyperthyroidism, autoimmune thyroiditis, and de Quervain thyroiditis. 4

Postpartum thyroiditis

The prevalence of postpartum thyroiditis varies greatly between 1.1% and 16.7%, with the condition defined as an abnormal TSH level in the first postpartum year in the absence of a toxic thyroid nodule or thyrotoxin receptor antibodies. 2 , 4 , 8 Postpartum thyroiditis may occur after pregnancy loss (miscarriage, abortion, ectopic pregnancy) or after normal delivery. In postpartum thyroiditis, the clinical course may vary, with 25% of patients presenting with symptoms of hyperthyroidism followed by symptoms of hypothyroidism before then achieving an euthyroid state. Twenty to thirty percent of patients with postpartum thyroiditis go on to have persistent hypothyroidism. 14 Patients with a history of thyroid disease, type 1 diabetes mellitus (T1DM), gestational diabetes, chronic hepatitis C, autoimmune disease, or a family history of thyroid disease are at increased risk of developing postpartum thyroiditis and should undergo TSH testing between 6 and 12 weeks postpartum. 2 , 14 Patients who have postpartum depression, difficulties with milk production, or symptoms of thyroid disease, especially 3 to 6 months postpartum, should be tested for thyroid dysfunction. 1 , 2 , 14 The signs and symptoms of hypothyroidism or hyperthyroidism are often dismissed as part of the normal transition from pregnancy to the postpartum period, which can lead to delays in diagnosis and treatment of postpartum thyroiditis. 13 - 15

Screening recommendations

Universal screening of asymptomatic pregnant patients for thyroid dysfunction is not currently recommended based on the available evidence. 2 , 15 However, since as early as 2007, many experts have contended that targeted screening, which is currently recommended by most professional organizations, fails to identify many cases of thyroid disorders during pregnancy. 1 , 16 - 18 The American College of Obstetricians and Gynecologists (ACOG) and ATA both cite the following as indications for targeted thyroid testing in pregnancy: family history of autoimmune thyroid disease; current thyroid therapy; goiter; and/or personal history of therapy for hyperthyroidism, autoimmune disease, T1DM, neck radiation, or postpartum thyroid dysfunction. 1 , 2 , 15 The ATA also supports targeted thyroid testing for individuals who reside in iodine-deficient areas; have a body mass index (BMI) of 40 or higher, especially paired with other health conditions; are older than age 30 years; have decreased fertility; are using assisted reproductive technology; have had two or more previous pregnancies; have previously delivered an infant with thyroid disease; have previously delivered an infant preterm; and have experienced miscarriage. 19 Preconception screening for thyroid dysfunction is recommended for high-risk patients, including those who are positive for thyroid peroxidase antibodies and patients planning for assisted reproduction. 2

A recent survey of clinical practice patterns among endocrinologists, gynecologists, and obstetricians revealed that practice sometimes is not consistent with established professional guidelines, with 57% of endocrinologists and 71% of obstetricians reporting having conducted universal screening for thyroid disorders during pregnancy. 20 A poster presentation at the 2023 ACOG annual meeting also posited that clinicians are not appropriately screening for thyroid disease regardless of the guidelines published by ATA and ACOG; this study, conducted at an Illinois hospital, showed that less than 50% of pregnant patients who met criteria for screening were appropriately screened for thyroid disease and that patients who were correctly screened per the ATA criteria had improved pregnancy outcomes. 18 In some cases, clinical practices and individual clinicians may choose to screen patients differently than recommended in the guidelines based on their assessment of patient and population risk factors, signs, and symptoms.

Evaluation of suspected thyroid disorders

Physical exam should include assessment of vital signs for tachycardia, bradycardia, and hypertension; assessment of weight and BMI for increase or decrease; observation of general appearance for diaphoresis, tremor, exophthalmos, and/or dry skin; and inspection and palpation of the thyroid gland for enlargement and/or nodules.

In the US, mild thyroid enlargement during pregnancy can be a typical finding; however, a significant goiter or distinct thyroid nodules are potentially abnormal and require assessment with thyroid function tests and thyroid ultrasonography. Although thyroid radionuclide scanning is contraindicated during pregnancy, a fine needle aspiration biopsy is safe if warranted. 2

ACOG and ATA recommend a TSH level test as initial workup for thyroid disorders during pregnancy. 2 , 15 In the presence of elevated TSH, ACOG and ATA next recommend assessment of FT4. In clinical practice, many labs now offer the ability to order a reflex FT4 automatically upon measure of an abnormal TSH, improving efficiency. If TSH is decreased, ACOG and ATA recommend assessment of both FT4 and total T3 (TT3). In the presence of risk factors and/or signs and symptoms, other tests such as free T3 (FT3), TT4, and thyroxine-binding globulin (TBG) may be warranted. 15

Standard reference intervals for thyroid function parameters during pregnancy and postpartum vary greatly due to significant differences among populations studied, with geographic location, race, ethnicity, and socioeconomic status as contributing factors. 2 , 5 The ATA recommends that population- and trimester-specific reference ranges for thyroid tests be used whenever possible. If this is not possible, the ATA advises that reference ranges from similar patient populations be used. 2 Reference ranges also need to be assay-specific. 21

TSH is usually lower during pregnancy, with a reduction of the lower limit of the reference range of about 0.4 mU/L and a reduction of the upper limit of about 0.5 mU/L in the first trimester relative to the typical nonpregnant range, which corresponds to about 0.1 to 4.0 mU/L. 2 , 3 In the second and third trimesters, the TSH should increase, returning to, or close to, nonpregnant reference ranges. The ACOG guideline states that after the first trimester, nonpregnant reference ranges for TSH can be used, although the ATA guideline notes that levels remain lower in pregnant individuals than in nonpregnant individuals for the second and third trimesters. 2 , 15 A study by La'ulu and Roberts found a second-trimester TSH reference interval of 0.15 to 3.11 mIU/L in a study of 3,064 US participants comprised of individuals who were White (42%), Hispanic (23%), Black (22%), and Asian (13%). 22 A study by Dorizzi and colleagues found a second-trimester TSH reference interval of 0.68 to 4.07 mU/L in a study of 139 White women from northeast Italy. 21

Before 16 weeks gestation, TT3, TT4, and TBG gradually increase compared with nonpregnant ranges. After 16 weeks gestation, TT3, TT4, and TBG are about 1.5 times higher than prepregnancy levels. 2 , 15 Although a full discussion is outside of the scope of this article, it is important to note that FT4 test results for pregnant individuals are less reliable than they are for nonpregnant individuals. The ACOG guideline states that measurement of TT3 is preferred to FT3. 15

Limited data are available for postpartum reference ranges in the literature, as many subjects are lost to follow-up; however, the literature states that most return to prepregnant levels. In the study by Dorizzi and colleagues, postpartum data were available for 55 of the participants, and a range of 0.56 to 3.42 mU/L was found. 21

Hypothyroidism

Management of hypothyroidism during pregnancy includes treating with incremental doses of levothyroxine that are adjusted based on the degree of TSH elevation. Serum TSH is measured every 4 weeks until midgestation and at least once around 30 weeks gestation; it is also measured at least every 4 to 6 weeks when medications are adjusted. 2 , 15 Dosing recommendations for use of levothyroxine in overt hypothyroidism in pregnancy can be found in the ATA and ACOG guidelines. 2 , 15 If taking levothyroxine for pregestational hypothyroidism, the dose should be increased by about 20% to 30% upon confirmation of pregnancy. 2 The treatment goal for hypothyroidism in pregnancy is to achieve a TSH level between the lower reference limit and 2.5 mU/L. Antenatal surveillance with fetal nonstress test and biophysical profile is not recommended in pregnant patients with hypothyroidism that is well controlled with medication, but it may be considered in patients with coexisting maternal or obstetric indications.

Levothyroxine is indicated in some individuals with subclinical hypothyroidism in pregnancy; providers should refer to the ATA guideline for more information. 2

After delivery, the levothyroxine dose should be decreased to the prepregnancy dose for patients with pregestational hypothyroidism, and a TSH level should be checked at 6 weeks postpartum. In many, but not all, patients diagnosed with hypothyroidism during pregnancy, thyroid function returns to normal in the postpartum period, and levothyroxine can be discontinued. If it is discontinued, a TSH level should be checked about 6 weeks later. 2 A vast amount of variability in thyroid levels is possible during the postpartum period, especially in patients who are breastfeeding, as prolactin—the most important hormone in lactation—is regulated by the pituitary gland and affected by TSH levels. Exclusivity and duration of breastfeeding are other factors that may also contribute to the variability of thyroid levels in the postpartum period. A recent study by Li and colleagues reported that among patients diagnosed with subclinical hypothyroidism during pregnancy, 38.9% went on to have long-term hypothyroidism, including some who had normal thyroid function at 6 weeks postpartum. 23

Hyperthyroidism

Management of hyperthyroidism includes treating with incremental doses of propylthiouracil in the first trimester, changing to methimazole in the second trimester. Propylthiouracil should be discontinued in the second trimester due to risk of maternal liver damage, whereas methimazole should not be used in the first trimester due to risk of birth defects during that time. 2 , 15 Dosing for both drugs is based on TSH, FT4, and TT3 levels, which should be measured every 2 weeks until stable, with a treatment goal of FT4 in the upper third of the normal range. 4 , 15 Once stabilized in the high normal range, thyroid labs should be checked every 4 weeks. 15 Antenatal testing, such as fetal ultrasonography, should be performed in patients with poorly controlled hyperthyroidism, typically in conjunction with maternal-fetal medicine, to assess for signs of fetal hyperthyroidism, such as fetal growth restriction, hydrops, goiter, and cardiac dysfunction. 4 , 15

Treatment of subclinical hyperthyroidism in pregnancy is generally not recommended. 2 , 15

Providers may consider obtaining TSH levels at 6 to 12 weeks and 3 to 6 months postpartum for patients at high risk for postpartum thyroiditis, such as those with T1DM or previous postpartum thyroiditis. 19 During management of the hyperthyroid phase of postpartum thyroiditis—which is typically caused by autoimmune destruction of the thyroid resulting in release of stored thyroid hormone—antithyroid medications are not beneficial. However, beta-blockers may be used if the patient is symptomatic. 2 , 4 , 15 It is important to differentiate the hyperthyroid phase of postpartum thyroiditis from Graves disease, since Graves disease requires antithyroid therapy. Differentiation is possible with referral for radioactive iodine uptake scan. However, this scan is contraindicated during breastfeeding, and close contact with others must be limited after its performance due to the scan's radioactivity. 2 , 15 In the hypothyroid phase of postpartum thyroiditis, patients may be treated with levothyroxine if symptomatic. 2 , 15 , 19 In most cases of postpartum thyroiditis, thyroid function levels return to normal within 12 to 18 months. However, a small percentage of patients may not recover, leading to permanent hypothyroidism requiring lifelong supplementation. 2 , 15 , 19

Patient education

Patients should be educated on the symptoms of hypothyroidism including lack of energy and feeling fatigued easily; feeling cold easily; developing coarse or thin hair; and constipation. If not treated, hypothyroidism can weaken and slow the heart, often causing patients to feel out of breath or tired when exercising and causing edema in the ankles. 4 Untreated hypothyroidism can also increase BP and raise cholesterol, both of which increase the risk of heart disease. Patients who are prescribed thyroid hormone medication should be educated on the importance of taking it every day. After taking the medication for 4 to 6 weeks, follow-up blood tests are needed to ensure appropriate levels. The medication dose may require adjustment depending on test results. Levothyroxine is the medication of choice; patients should be advised to take this medication by itself on an empty stomach, ideally 1 hour before breakfast daily as well as 4 to 5 hours before or after taking any drugs known to interfere with its absorption, such as certain medications, certain vitamins, calcium, and iron. 24 Most people with permanent hypothyroidism need to be on thyroid medication for the rest of their life, and patients should be counseled accordingly.

Patients should be educated on the common symptoms of hyperthyroidism including feeling tired or weak; losing weight, even when eating normally; having a fast or uneven heartbeat; sweating excessively and having trouble dealing with hot weather; feeling worried; and trembling. There may be a noticeable enlargement of the thyroid gland or palpable nodules on the thyroid. Patients of reproductive potential who have hyperthyroidism should also receive preconception counseling: If hyperthyroidism is present prepregnancy, a euthyroid state should be achieved before trying to conceive to decrease risk to the fetus. 13

Thyroiditis after pregnancy can cause symptoms of hyperthyroidism followed by hypothyroidism; isolated symptoms of hyperthyroidism; or isolated symptoms of hypothyroidism. 2 , 4 Patients with the condition should be educated about the expected clinical course, signs and symptoms, and recommended testing and treatments.

Iodine intake

Patient education should include information on iodine intake. The ATA recommends that all pregnant and breastfeeding women consume 250 mcg of iodine daily, including a daily oral supplement containing 150 mcg of iodine (in the form of potassium iodine). 2 Women planning pregnancy should also consume a daily oral supplement with 150 mcg of iodine. Sufficient iodine intake is also important while breastfeeding to ensure that infants receive iodine in breast milk. Good dietary sources of iodine include dairy, seafood, eggs, meat, poultry, and iodized salt. 6 , 24 Caution patients that too much iodine from diet and dietary supplements such as seaweed during pregnancy or breastfeeding may be harmful and can lead to fetal or infant hypothyroidism and goiter. 2 , 24

Consultation and referral

For the advanced practice provider, consultation with an endocrinology specialist is recommended upon the diagnosis of hypothyroidism, hyperthyroidism, postpartum thyroiditis, or goiter in pregnancy. Referral should be made to the appropriate specialist in the event of poorly controlled thyroid function test levels and/or worsening of symptoms. During pregnancy, referral to and/or comanagement with maternal-fetal medicine as indicated—but especially for patients with elevated TSH receptor antibodies, uncontrolled hyperthyroidism, or a history of irradiation for hyperthyroidism on replacement therapy—are key to improving maternal and fetal outcomes.

Implications and conclusion

As noted, variations in reference intervals for thyroid function parameters are common throughout the literature because of differences in methods used and populations included in these studies. 21 Defining standard population-based trimester-specific reference intervals for thyroid function parameters may be helpful from both academic and clinical points of view and may suggest directions for further research. Although current guidelines recommend the assessment of thyroid function parameters in pregnancy using trimester- and instrumentation reagents-specific reference intervals, such recommendations are rarely implemented in practice, as clinicians usually accept the intervals suggested by the clinical lab manufacturers.

It is also noteworthy that iodine intake has been inadequately evaluated throughout the literature. Urinary iodine concentration to assess the iodine status of the study population has not been measured in many studies, and when it has been measured, it has not been assayed with standard reference technology. 21 Future research should be undertaken to explore this topic.

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