Pregnancy with graves disease

Graves’ Disease and Pregnancy

Treating Graves’ Disease During Pregnancy

The treatment of Graves’ disease during pregnancy will depend on your individual symptoms, the severity of the condition, as well as how far your pregnancy has progressed. Women with Graves’ disease are often advised to postpone conception and use contraception until the disease is controlled. Women with difficult to control Graves’ who are on high doses of antithyroid medications often choose definitive therapy, such as surgery to remove the thyroid gland, prior to conception.

Anti-Thyroid Medications

Your doctor may prescribe antithyroid medications if the benefits of taking them appear to outweigh the risks. Tapazole (methimazole) and propylthiouracil (PTU) are the two antithyroid drugs used in the United States to treat hyperthyroidism. Both of these medications can cross the placenta and potentially cause birth defects and hypothyroidism in the fetus. (2) Doctors often recommend the lowest possible dose of antithyroid medication to minimize the risks.

“We used to think that the antithyroid drug methimazole caused birth defects and that PTU didn’t,” says Douglas Ross, MD, a professor of medicine at Harvard Medical School and co-director of thyroid associates at Massachusetts General Hospital. “A few years ago, a large study from Denmark also showed that PTU does cause birth defects, although they are much less severe than methimazole birth defects.” (5)

Birth defects caused by methimazole are often life-threatening and can include choanal atresia (blockage of the nasal passage), esophageal atresia (the upper part of the esophagus does not connect with the lower part), aplasia cutis (absence of skin), umbilical cord defects, or omphalocele (abdominal organs outside the body).

Birth defects caused by PTU can include anatomical anomalies (abnormalities) in the face or neck region and in the urinary system. Such abnormalities generally require surgical treatment but are less severe than the defects caused by methimazole. (6)

“At least in my practice, this information has led most women to decide that they don’t want to take antithyroid drugs at all if they have Graves’ disease and they want to get pregnant,” says Dr. Ross. “And so they choose to do definitive therapy — more frequently the surgery, because they’re in a hurry to get pregnant, than radioactive iodine — to definitively get rid of their thyroid.”

Beta-Blockers

Beta-blockers, a class of drugs commonly used to lower blood pressure, are also used to control the so-called hyperadrenergic symptoms of Graves’ disease, such as anxiety, irritability, rapid heart rate, tremors, and sweating.

While beta-blockers are commonly used during pregnancy, there’s conflicting evidence regarding the risks associated with taking them. If you are prescribed a beta-blocker during pregnancy or are already taking one when you become pregnant, discuss the relative risks and benefits of these drugs with your doctor.

Surgery

A thyroidectomy (surgery to remove all or part of the thyroid gland) is sometimes performed to treat Graves’ disease. After surgery, patients may be prescribed thyroid hormones, as most people will develop hypothyroidism (underactive thyroid) after the surgery. Some women opt to have a thyroidectomy prior to trying to conceive. Surgery poses risks if performed at different points in a pregnancy, so talk to your doctor about the risks and alternatives.

Radioactive Iodine

Radioactive iodine treatment is not recommended for pregnant or nursing women, although some women choose to undergo radioactive iodine treatment before they try to conceive. People who choose radioactive iodine therapy will develop hypothyroidism, which is easier to treat and causes fewer health complications than hyperthyroidism.

If you’re a woman of childbearing age and are considering radioactive iodine treatment, make sure to take a pregnancy test before you begin it, and ask your doctor how long you should wait after the treatment is complete before you try to conceive.

No Treatment

While treating Graves’ disease during pregnancy comes with risks, so does foregoing treatment during pregnancy. Women who do not control their Graves’ disease are almost 10 times more likely to have a baby with low birth weight. They are also 16 times more likely to deliver preterm and 5 times more likely to develop preeclampsia and experience stillbirth.

If you have Graves’ disease and want to have a baby, speak to your doctor about the best way to have a healthy pregnancy while also managing your disease.

  1. 1

    Mestman JH (1997) Hyperthyroidism in pregnancy. Clin Obstet Gynecol 40: 45–64

    • CAS
    • Article
    • Google Scholar
  2. 2

    Burrow GN (1993) Thyroid function and hyperfunction during gestation. Endocr Rev 14: 194–202

    • CAS
    • Article
    • Google Scholar
  3. 3

    Casey BM et al. (2006) Subclinical hyperthyroidism and pregnancy outcomes. Obstet Gynecol 107: 337–341

    • Article
    • Google Scholar
  4. 4

    Davis LE et al. (1989) Thyrotoxicosis complicating pregnancy. Am J Obstet Gynecol 160: 63–70

    • CAS
    • Article
    • Google Scholar
  5. 5

    Millar LK et al. (1994) Low birth weight and preeclampsia in pregnancies complicated by hyperthyroidism. Obstet Gynecol 84: 946–949

    • CAS
    • PubMed
    • Google Scholar
  6. 6

    Anselmo J et al. (2004) Fetal loss associated with excess thyroid hormone exposure. JAMA 292: 691–695

    • CAS
    • Article
    • Google Scholar
  7. 7

    Momotani N et al. (1984) Maternal hyperthyroidism and congenital malformation in the offspring. Clin Endocrinol (Oxf) 20: 695–700

    • CAS
    • Article
    • Google Scholar
  8. 8

    Phoojaroenchanachai M et al. (2001) Effect of maternal hyperthyroidism during late pregnancy on the risk of neonatal low birth weight. Clin Endocrinol (Oxf) 54: 365–370

    • CAS
    • Article
    • Google Scholar
  9. 9

    Mitsuda N et al. (1992) Risk factors for developmental disorders in infants born to women with Graves disease. Obstet Gynecol 80: 359–364

    • CAS
    • PubMed
    • Google Scholar
  10. 10

    Burrow GN (1985) The management of thyrotoxicosis in pregnancy. N Engl J Med 313: 562–565

    • CAS
    • Article
    • Google Scholar
  11. 11

    Demers LM and Spencer CA (2003) Laboratory medicine practice guidelines: laboratory support for the diagnosis and monitoring of thyroid disease. Clin Endocrinol (Oxf) 58: 138–140

    • CAS
    • Article
    • Google Scholar
  12. 12

    Sapin R et al. (2004) Free thyroxine measured with equilibrium dialysis and nine immunoassays decreases in late pregnancy. Clin Lab 50: 581–584

    • CAS
    • PubMed
    • PubMed Central
    • Google Scholar
  13. 13

    Spencer CA et al. (2005) Thyroid reference ranges in pregnancy: studies of an iodine-sufficient pregnant cohort . Thyroid 15 (Suppl 1): S-16

    • Google Scholar
  14. 14

    Panesar NS et al. (2001) Reference intervals for thyroid hormones in pregnant Chinese women. Ann Clin Biochem 38: 329–332

    • CAS
    • Article
    • Google Scholar
  15. 15

    Casey BM et al. (2005) Subclinical hypothyroidism and pregnancy outcomes. Obstet Gynecol 105: 239–245

    • Article
    • Google Scholar
  16. 16

    Haddow JE et al. (2004) The reference range and within-person variability of thyroid stimulating hormone during the first and second trimesters of pregnancy. J Med Screen 11: 170–174

    • CAS
    • Article
    • Google Scholar
  17. 17

    Glinoer D et al. (1993) Serum levels of intact human chorionic gonadotropin (HCG) and its free α and β subunits, in relation to maternal thyroid stimulation during normal pregnancy. J Endocrinol Invest 16: 881–888

    • CAS
    • Article
    • Google Scholar
  18. 18

    Goodwin TM et al. (1992) Transient hyperthyroidism and hyperemesis gravidarum: clinical aspects. Am J Obstet Gynecol 167: 648–652

    • CAS
    • Article
    • Google Scholar
  19. 19

    Amino N et al. (1982) Aggravation of thyrotoxicosis in early pregnancy and after delivery in Graves’ disease. J Clin Endocrinol Metab 55: 108–112

    • CAS
    • Article
    • Google Scholar
  20. 20

    Marqusee E et al. (1997) Thyroiditis after pregnancy loss. J Clin Endocrinol Metab 82: 2455–2457

    • CAS
    • PubMed
    • Google Scholar
  21. 21

    Tan JY et al. (2002) Transient hyperthyroidism of hyperemesis gravidarum. BJOG 109: 683–688

    • Article
    • Google Scholar
  22. 22

    Luton D et al. (2005) Management of Graves’ disease during pregnancy: the key role of fetal thyroid gland monitoring. J Clin Endocrinol Metab 90: 6093–6098

    • CAS
    • Article
    • Google Scholar
  23. 23

    Amino N et al. (2003) No increase of blocking type anti-thyrotropin receptor antibodies during pregnancy in patients with Graves’ disease. J Clin Endocrinol Metab 88: 5871–5874

    • CAS
    • Article
    • Google Scholar
  24. 24

    Zakarija M and McKenzie JM (1983) Pregnancy-associated changes in the thyroid-stimulating antibody of Graves’ disease and the relationship to neonatal hyperthyroidism. J Clin Endocrinol Metab 57: 1036–1040

    • CAS
    • Article
    • Google Scholar
  25. 25

    Wing DA et al. (1994) A comparison of propylthiouracil versus methimazole in the treatment of hyperthyroidism in pregnancy. Am J Obstet Gynecol 170: 90–95

    • CAS
    • Article
    • Google Scholar
  26. 26

    Marchant B et al. (1977) The placental transfer of propylthiouracil, methimazole and carbimazole. J Clin Endocrinol Metab 45: 1187–1193

    • CAS
    • Article
    • Google Scholar
  27. 27

    Mortimer RH et al. (1997) Methimazole and propylthiouracil equally cross the perfused human term placental lobule. J Clin Endocrinol Metab 82: 3099–3102

    • CAS
    • PubMed
    • Google Scholar
  28. 28

    Gardner DF et al. (1986) Pharmacology of propylthiouracil (PTU) in pregnant hyperthyroid women: correlation of maternal PTU concentrations with cord serum thyroid function tests. J Clin Endocrinol Metab 62: 217–220

    • CAS
    • Article
    • Google Scholar
  29. 29

    Momotani N et al. (1997) Effects of propylthiouracil and methimazole on fetal thyroid status in mothers with Graves’ hyperthyroidism. J Clin Endocrinol Metab 82: 3633–3636

    • CAS
    • PubMed
    • Google Scholar
  30. 30

    Momotani N et al. (1986) Antithyroid drug therapy for Graves’ disease during pregnancy. Optimal regimen for fetal thyroid status. N Engl J Med 315: 24–28

    • CAS
    • Article
    • Google Scholar
  31. 31

    Cheron RG et al. (1981) Neonatal thyroid function after propylthiouracil therapy for maternal Graves’ disease. N Engl J Med 304: 525–528

    • CAS
    • Article
    • Google Scholar
  32. 32

    Momotani N et al. (2006) Anti-thyroid drug therapy for Graves’ disease during pregnancy: mildest thyrotoxic maternal free thyroxine concentrations to avoid fetal hypothyroidism . Presented at the 77th Annual Meeting of the American Thyroid Association: 2006 October 11–15, Phoenix, AZ

    • Google Scholar
  33. 33

    Wolf D et al. (2006) Antenatal carbimazole and choanal atresia: a new embryopathy. Arch Otolaryngol Head Neck Surg 132: 1009–1011

    • Article
    • Google Scholar
  34. 34

    Di Gianantonio E et al. (2001) Adverse effects of prenatal methimazole exposure. Teratology 64: 262–266

    • CAS
    • Article
    • Google Scholar
  35. 35

    Clementi M et al. (1999) Methimazole embryopathy: delineation of the phenotype. Am J Med Genet 83: 43–46

    • CAS
    • Article
    • Google Scholar
  36. 36

    Van Dijke CP et al. (1987) Methimazole, carbimazole, and congenital skin defects. Ann Intern Med 106: 60–61

    • CAS
    • Article
    • Google Scholar
  37. 37

    Mujtaba Q and Burrow GN (1975) Treatment of hyperthyroidism in pregnancy with propylthiouracil and methimazole. Obstet Gynecol 46: 282–286

    • CAS
    • PubMed
    • Google Scholar
  38. 38

    Hayashida CY et al. (1990) Neonatal hepatitis and lymphocyte sensitization by placental transfer of propylthiouracil. J Endocrinol Invest 13: 937–941

    • CAS
    • Article
    • Google Scholar
  39. 39

    Eisenstein Z et al. (1992) Intellectual capacity of subjects exposed to methimazole or propylthiouracil in utero. Eur J Pediatr 151: 558–559

    • CAS
    • Article
    • Google Scholar
  40. 40

    Messer PM et al. (1990) Antithyroid drug treatment of Graves’ disease in pregnancy: long-term effects on somatic growth, intellectual development and thyroid function of the offspring. Acta Endocrinol (Copenh) 123: 311–316

    • CAS
    • Article
    • Google Scholar
  41. 41

    Redmond GP (1982) Propranolol and fetal growth retardation. Semin Perinatol 6: 142–147

    • CAS
    • PubMed
    • Google Scholar
  42. 42

    Momotani N et al. (1992) Effects of iodine on thyroid status of fetus versus mother in treatment of Graves’ disease complicated by pregnancy. J Clin Endocrinol Metab 75: 738–744

    • CAS
    • PubMed
    • Google Scholar
  43. 43

    Stoffer SS and Hamburger JI (1976) Inadvertent 131I therapy for hyperthyroidism in the first trimester of pregnancy. J Nucl Med 17: 146–149

    • CAS
    • PubMed
    • Google Scholar
  44. 44

    Brosco JP et al. (2006) Impact of specific medical interventions on reducing the prevalence of mental retardation. Arch Pediatr Adolesc Med 160: 302–309

    • Article
    • Google Scholar
  45. 45

    Rose SR et al. (2006) Update of newborn screening and therapy for congenital hypothyroidism. Pediatrics 117: 2290–2303

    • Article
    • Google Scholar
  46. 46

    Brodsky JB et al. (1980) Surgery during pregnancy and fetal outcome. Am J Obstet Gynecol 138: 1165–1167

    • CAS
    • Article
    • Google Scholar
  47. 47

    Fisher DA (1997) Fetal thyroid function: diagnosis and management of fetal thyroid disorders. Clin Obstet Gynecol 40: 16–31

    • CAS
    • Article
    • Google Scholar
  48. 48

    Szinnai G et al. (2007) Sodium/iodide symporter (NIS) gene expression is the limiting step for the onset of thyroid function in the human fetus. J Clin Endocrinol Metab 92: 70–76

    • CAS
    • Article
    • Google Scholar
  49. 49

    Chopra IJ (1992) Fetal and neonatal hyperthyroidism. Thyroid 2: 161–163

    • CAS
    • Article
    • Google Scholar
  50. 50

    Di Cosmo C et al. (2006) The sodium-iodide symporter expression in placental tissue at different gestational age: an immunohistochemical study. Clin Endocrinol (Oxf) 65: 544–548

    • CAS
    • Article
    • Google Scholar
  51. 51

    Bidart JM et al. (2000) Expression of Na+/I– symporter and Pendred syndrome genes in trophoblast cells. J Clin Endocrinol Metab 85: 4367–4372

    • CAS
    • PubMed
    • Google Scholar
  52. 52

    Mitchell AM et al. (2001) Sodium iodide symporter (NIS) gene expression in human placenta. Placenta 22: 256–258

    • CAS
    • Article
    • Google Scholar
  53. 53

    Vulsma T et al. (1989) Maternal-fetal transfer of thyroxine in congenital hypothyroidism due to a total organification defect or thyroid agenesis. N Engl J Med 321: 13–16

    • CAS
    • Article
    • Google Scholar
  54. 54

    de Escobar GM et al. (2004) Maternal thyroid hormones early in pregnancy and fetal brain development. Best Pract Res Clin Endocrinol Metab 18: 225–248

    • Article
    • Google Scholar
  55. 55

    Gitlin D (1971) Development and metabolism of the immune globulins. In Immunologic Incompetence 3–16, (Eds Kagan BM and Stiehm ER) Chicago: Year Book Medical Publishers, Inc.

    • Google Scholar
  56. 56

    Nachum Z et al. (2003) Graves’ disease in pregnancy: prospective evaluation of a selective invasive treatment protocol. Am J Obstet Gynecol 189: 159–165

    • Article
    • Google Scholar
  57. 57

    Polak M et al. (2004) Fetal and neonatal thyroid function in relation to maternal Graves’ disease. Best Pract Res Clin Endocrinol Metab 18: 289–302

    • CAS
    • Article
    • Google Scholar
  58. 58

    Wallace C et al. (1995) Fetal thyrotoxicosis: a case report and recommendations for prediction, diagnosis, and treatment. Thyroid 5: 125–128

    • CAS
    • Article
    • Google Scholar
  59. 59

    Polak M et al. (2006) Congenital hyperthyroidism: the fetus as a patient. Horm Res 65: 235–242

    • CAS
    • PubMed
    • Google Scholar
  60. 60

    Cohen O et al. (2003) Serial in utero ultrasonographic measurements of the fetal thyroid: a new complementary tool in the management of maternal hyperthyroidism in pregnancy. Prenat Diagn 23: 740–742

    • Article
    • Google Scholar
  61. 61

    Van Loon AJ et al. (1995) In utero diagnosis and treatment of fetal goitrous hypothyroidism, caused by maternal use of propylthiouracil. Prenat Diagn 15: 599–604

    • CAS
    • Article
    • Google Scholar
  62. 62

    Ochoa-Maya MR et al. (1999) Resolution of fetal goiter after discontinuation of propylthiouracil in a pregnant woman with Graves’ hyperthyroidism. Thyroid 9: 1111–1114

    • CAS
    • Article
    • Google Scholar
  63. 63

    LeBeau SO and Mandel SJ (2006) Thyroid disorders during pregnancy. Endocrinol Metab Clin North Am 35: 117–136

    • Article
    • Google Scholar
  64. 64

    McNab T and Ginsberg J (2005) Use of anti-thyroid drugs in euthyroid pregnant women with previous Graves’ disease. Clin Invest Med 28: 127–131

    • PubMed
    • Google Scholar
  65. 65

    Bruinse HW et al. (1988) Fetal treatment for thyrotoxicosis in non-thyrotoxic pregnant women. Fetal Ther 3: 152–157

    • CAS
    • Article
    • Google Scholar
  66. 66

    Serup J and Petersen S (1977) Hyperthyroidism during pregnancy treated with propylthiouracil. The significance of maternal and foetal parameters. Acta Obstet Gynecol Scand 56: 463–466

    • CAS
    • Article
    • Google Scholar
  67. 67

    Davidson KM et al. (1991) Successful in utero treatment of fetal goiter and hypothyroidism. N Engl J Med 324: 543–546

    • CAS
    • Article
    • Google Scholar
  68. 68

    Kilpatrick S (2003) Umbilical blood sampling in women with thyroid disease in pregnancy: is it necessary? Am J Obstet Gynecol 189: 1–2

    • Article
    • Google Scholar
  69. 69

    Skuza KA et al. (1996) Prediction of neonatal hyperthyroidism in infants born to mothers with Graves disease. J Pediatr 128: 264–268

    • CAS
    • Article
    • Google Scholar
  70. 70

    Matsuura N et al. (1988) TSH-receptor antibodies in mothers with Graves’ disease and outcome in their offspring. Lancet 1: 14–17

    • CAS
    • Article
    • Google Scholar
  71. 71

    Peleg D et al. (2002) The relationship between maternal serum thyroid-stimulating immunoglobulin and fetal and neonatal thyrotoxicosis. Obstet Gynecol 99: 1040–1043

    • PubMed
    • Google Scholar
  72. 72

    Kempers MJ et al. (2003) Central congenital hypothyroidism due to gestational hyperthyroidism: detection where prevention failed. J Clin Endocrinol Metab 88: 5851–5857

    • CAS
    • Article
    • Google Scholar

Thyroid conditions during pregnancy

What is the thyroid?

The thyroid is a tiny, butterfly-shaped gland in your neck. A gland is an organ that makes substances that help your body work. The thyroid makes hormones (chemicals) that play a big role in your health. For example, thyroid hormones can affect your heart rate (how fast your heart beats) and your metabolism (how well and fast your body processes what you eat and drink).

Sometimes the thyroid gland makes too much or too little of certain hormones. When this happens, you have a thyroid disorder. Some women have a thyroid disorder that begins before pregnancy (also called a pre-existing condition). Others may develop thyroid problems for the first time during pregnancy or soon after giving birth.

With treatment, a thyroid condition may not cause any problems during pregnancy. But untreated thyroid conditions can cause problems for you and your baby during pregnancy and after birth.

What are the main kinds of thyroid conditions?

There are two main kinds of thyroid conditions:

  1. Hyperthyroidism (“hyper” means too much). This is when the thyroid is overactive and makes too much thyroid hormone. This condition can cause many of your body’s functions to speed up. Hyperthyroidism during pregnancy usually is caused by an autoimmune disorder called Graves’ disease. Autoimmune disorders are health conditions that happen when antibodies (cells in the body that fight off infections) attack healthy tissue by mistake. If you have Graves’ disease, your immune system makes antibodies that cause your thyroid to make too much thyroid hormone. In rare cases, hyperthyroidism is linked to a severe form of morning sickness called hyperemesis gravidarum (excessive nausea and vomiting during pregnancy). Also in rare cases, hyperthyroidism can be caused by thyroid nodules. These are lumps in your thyroid that make too much thyroid hormone.
  2. Hypothyroidism (“hypo” means too little or not enough). This is when the thyroid is underactive and doesn’t make enough thyroid hormones, so many of your body’s functions slow down. Hypothyroidism during pregnancy usually is caused by an autoimmune disorder called Hashimoto’s disease. When you have Hashimoto’s disease, your immune system makes antibodies that attack your thyroid and damage it so it can’t produce thyroid hormones.

If you have a thyroid condition during pregnancy, treatment can help you have a healthy pregnancy and a healthy baby.

How are thyroid conditions during pregnancy diagnosed?

Health care providers don’t usually test your thyroid before or during pregnancy unless you’re at high risk of having a thyroid condition or you have signs or symptoms of one. If you have signs or symptoms of a thyroid condition, especially during pregnancy, tell your provider. Signs of a condition are things someone else can see or know about you, like that you have a rash or you’re coughing. Symptoms are things you feel yourself that others can’t see, like having a sore throat or feeling dizzy. Signs and symptoms of thyroid conditions may appear slowly over time. Many are signs and symptoms of other health conditions, so having one doesn’t always mean you have a thyroid problem.

Your provider gives you a physical exam and a blood test to check for thyroid conditions. The blood test measures the levels of thyroid hormones and thyroid stimulating hormone (also called TSH) in your body. TSH is a hormone that tells your thyroid gland to make thyroid hormones. If you think you may have a thyroid condition, ask your provider about testing.

Are you at risk for having a thyroid condition during pregnancy?

You’re at higher risk for a thyroid condition during pregnancy than other women if you:

  • Are currently being treated for a thyroid condition or you have thyroid nodules or a goiter. A goiter is a swollen thyroid gland that can make your neck look swollen.
  • Have had a thyroid condition in the past (including after giving birth), or you’ve had a baby who had a thyroid condition
  • Have an autoimmune disorder or you have a family history of autoimmune thyroid disease, like Graves’ disease or Hashimoto’s disease. Family history means that the condition runs in your family (people in your family have or have had the condition). Use the March of Dimes family health history form and share it with your provider. The form helps you keep a record of any health conditions and treatments that you, your partner and everyone in both of your families has had. It can help your provider check for health conditions that may affect your pregnancy. If you have a family history of thyroid or autoimmune conditions, ask your provider about testing.
  • Have type 1 diabetes. Diabetes is a condition in which your body has too much sugar (called glucose) in the blood. Type 1 diabetes is a kind of preexisting diabetes, which means you have it before you get pregnant. If you have type 1 diabetes, your pancreas stops making insulin. Insulin is a hormone that helps keep the right amount of glucose in your body.
  • Have had high-dose neck radiation or treatment for hyperthyroidism. Radiation is a kind of energy. It travels as rays or particles in the air.

If you’ve had a thyroid condition or think you’re at risk for having a thyroid condition, ask your provider about testing.

What are signs and symptoms of hyperthyroidism?

Hyperthyroidism that’s untreated or not treated correctly is linked to problems for women and babies during pregnancy and after birth.

Problems for women can include:

  • Preeclampsia. This is a serious blood pressure condition that can happen after the 20th week of pregnancy or after giving birth (also called postpartum preeclampsia). It’s when a woman has high blood pressure and signs that some of her organs, like her kidneys and liver, may not be working normally. Blood pressure is the force of blood that pushes against the walls of your arteries. Arteries are blood vessels that carry blood away from your heart to other parts of the body. High blood pressure (also called hypertension) is when the force of blood against the walls of the blood vessels is too high. It can stress your heart and cause problems during pregnancy.
  • Pulmonary hypertension. This is a kind of high blood pressure that happens in the arteries in your lungs and on the right side of your heart.
  • Placental abruption. This is a serious condition in which the placenta separates from the wall of the uterus before birth. The placenta grows in your uterus (womb) and supplies the baby with food and oxygen through the umbilical cord.
  • Heart failure. This is when your heart can’t pump enough blood to the rest of your body.
  • Thyroid storm. This is when your symptoms suddenly get much worse. It’s a rare, but life-threatening condition during pregnancy. Pregnant women who have thyroid storm are at high risk of heart failure.

Problems for babies can include:

  • Premature birth. This is birth that happen too early, before 37 weeks of pregnancy.
  • Goiter
  • Low birthweight. This is when a baby is born weighing less than 5 pounds, 8 ounces.
  • Thyroid problems. Antibodies that cause Graves’ disease cross the placenta during pregnancy. If you have Graves’ disease during pregnancy, your baby is at risk for thyroid conditions during and after birth. If you had treatment for Graves’ disease with radioactive iodine before pregnancy, your baby is at risk for Graves’ disease.
  • Miscarriage or stillbirth. Miscarriage is when a baby dies in the womb before 20 weeks of pregnancy. Stillbirth is when a baby dies in the womb after 20 weeks of pregnancy.

How can hypothyroidism affect pregnancy?

Untreated hypothyroidism during pregnancy is linked to problems for women and babies during pregnancy and after birth.

Problems for women can include:

  • Anemia. This is when you don’t have enough healthy red blood cells to carry oxygen to the rest of your body.
  • Gestational hypertension. This is high blood pressure that starts after 20 weeks of pregnancy and goes away after you give birth.
  • Preeclampsia
  • Placental abruption
  • Postpartum hemorrhage (also called PPH). This when a woman has heavy bleeding after giving birth. It’s a serious but rare condition. It usually happens within 1 day of giving birth, but it can happen up to 12 weeks after having a baby.
  • Myxedema, a rare condition caused by severe, untreated hypothyroidism that can cause you to go into a coma and can cause death
  • Heart failure. This is when your heart doesn’t pump blood as well as it should. Heart failure cause by hypothyroidism is rare.

Problems for babies can include:

  • Infantile myxedema, a condition that’s linked to severe hypothyroidism. It can cause dwarfism, intellectual disabilities and other problems. Dwarfism (also called little people) is a condition in which a person is very short (less than 4 feet 10 inches as an adult). Intellectual disability causes a lower-than-average intelligence and a lack of skills needed to function in daily life.
  • Low birthweight.
  • Problems with growth and brain and nervous system development. The nervous system is made up of your brain, spinal cord and nerves. Your nervous system helps you move, think and feel. Untreated hypothyroidism, especially when it happens during the first trimester, can cause low IQ in a baby.
  • Thyroid problems. This is rare, but it can happen in babies of women with Hashimoto’s disease because the antibodies can cross the placenta during pregnancy.
  • Miscarriage or stillbirth

What is postpartum thyroiditis?

In about 1 to 21 in 100 women (1 to 21 percent), the thyroid becomes swollen in the first year after giving birth. This is an autoimmune condition called postpartum thyroiditis. It can cause your thyroid to be overactive, underactive and even a combination of both.

How are thyroid conditions treated during pregnancy and while breastfeeding?

Many medicines used to treat thyroid conditions during pregnancy are safe for your baby. Thyroid medicines can help keep the right level of thyroid hormones in your body. Your provider gives you blood tests during pregnancy to check your TSH and T4 levels to make sure your medicine is at the right amount (also called dose). T4 is a hormone made by your thyroid.

If you’re taking medicine for a thyroid condition before pregnancy, talk to your provider before you get pregnant. Your provider may want to adjust or change your medicine to make sure it’s safe for your baby. If you’re already taking thyroid medicine when you get pregnant, keep taking it and talk to your provider about it as soon as possible.

Treating hyperthyroidism. If you have mild hyperthyroidism, you may not need treatment. If it’s more severe, you may need to take an antithyroid medicine. This medicine causes your thyroid to make less thyroid hormone.

Most providers treat pregnant women with an overactive thyroid with antithyroid medicines called propylthiouracil in the first trimester and methimazole in the second and third trimesters. The timing of these medicines is important. Propylthiouracil after the first trimester can lead to liver problems. And methimazole in the first trimester may increase the risk of birth defects. Birth defects are health conditions that are present at birth. They change the shape or function of one or more parts of the body. Birth defects can cause problems in overall health, how the body develops, or how the body works.

Providers sometimes use radioactive iodine to treat hyperthyroidism. Pregnant women shouldn’t take this medicine because it can cause thyroid problems in the baby.

Antithyroid medicines are safe to take at low doses while you’re breastfeeding.

Treating hypothyroidism. Levothyroxine is the most common medicine used to treat an underactive thyroid during pregnancy. Levothyroxine replaces the thyroid hormone T4, which your own thyroid isn’t making or isn’t making enough of. It’s safe to take this medicine during pregnancy. Thyroid medicines that contain the T3 hormone aren’t safe to use during pregnancy.

If you had hypothyroidism before getting pregnant, you most likely need to increase the amount of medicine you take during pregnancy. Talk to your health care provider about your medicine as soon as you find out you’re pregnant. Your provider can check to make sure you’re taking the right dose by checking your TSH levels during pregnancy.

Talk to your provider about taking levothyroxine or other medicine to treat hypothyroidism while breastfeeding.

More information

  • American Thyroid Association
  • MotherToBaby

Last reviewed: February, 2019

See also: Prescription medicine during pregnancy

Thyroid Disease, Pregnancy and Fertility

The immune system, which plays a role in thyroid disease, is suppressed during pregnancy in order to protect the developing fetus. As a result of the loss of this protective effect at the end of pregnancy, there is a tendency for thyroid disease to occur after delivery in those women who have had previous thyroid disease or who are at risk for developing thyroid disease. Silent autoimmune thyroiditis is particularly common after pregnancy. This “postpartum thyroiditis” tends to get better after a few weeks although recurrence in subsequent pregnancies and progression to permanent hypothyroidism is possible.

It is important to recognize thyroid disorders during pregnancy as untreated hypothyroidism may impair full and normal development of the fetus, to some degree, and may increase maternal complications.

Iodine intake should be increased during pregnancy and breastfeeding of 150 micrograms to 250 micrograms per day, but should not exceed 500 micrograms per day.

Treatment of Graves’ hyperthyroidism during pregnancy is different from that in non pregnant women, since radioactive iodine cannot be given and surgery should be avoided (particularly in the first and third trimesters of the pregnancy for fear of inducing a miscarriage). Because of the immunosuppressive effect of pregnancy, antithyroid drugs can be given in doses lower than with non pregnant patients. Over treatment of the hyperthyroidism with antithyroid drugs can affect the baby’s thyroid since the drugs cross the placenta into the baby’s bloodstream.

While antithyroid drugs (methimazole, propylthiouracil) rarely cause birth defects, the risk of uncontrolled hyperthyroidism is worse than the risk of birth defects from antithyroid drugs. Pregnant women with hyperthyroidism require careful monitoring to minimize the risks of hyperthyroidism and antithyroid drugs.

Thyroxine Treatment in Pregnancy

There is no contra-indication to taking thyroxine throughout pregnancy. If hypothyroidism has been diagnosed before pregnancy The Endocrine Society recommends to adjust the dose to reach a TSH not higher than 2.5 mIU/L before pregnancy. It has been observed that thyroxine requirements increase during the pregnancy so most women with thyroid diseases need dose adjustment and monitoring. The baby’s thyroid becomes functional at approximately 12 weeks of gestation. Thyroid hormones play an important role in fetal brain development, so the thyroid hormones provided by the mother during the first trimester of pregnancy are especially important. Thyroxine treatment is adjusted to obtain TSH levels specific to each trimester (less than 2.5 mIU/L in the first trimester or 3 mIU/L during the second and third trimester.

Screening during Pregnancy for Thyroid Disorders

Screening guidelines for thyroid disease differ among the various associations and expert groups. The Endocrine Society recommends screening for thyroid disorders in women at high risk:

Women with prior thyroid disease or surgery, goitre, family history, positive thyroid antibodies,other autoimmune diseases, symptoms or signs suggestive of thyroid dysfunction, previous head and neck irradiation for other disease. Screening is performed by measuring the TSH level.

Breast Feeding and Thyroid Disease

Radioactive isotopes are secreted in milk therefore no isotope tests or isotope scans should be performed on someone who is breastfeeding. Antithyroid drugs can be used when breast feeding, as only negligible amounts actually get into the milk. Thyroxine is also secreted in the milk, but providing the dosage in the mother is in the physiologic range, it appears to be quite safe for the mother on thyroxine to breast feed.

Infertility

Patients with either hyper- or hypothyroidism can have fertility problems although it is certainly possible to have these diseases and still get pregnant. Sub-clinical hypothyroidism can sometimes cause infertility and miscarriages and is, thus, usually treated in women of childbearing age that desire to become pregnant.

In addition, both men and women with untreated thyroid disease often have decreased sexual desire (libido). Hyper- or hypothyroidism is also a cause for male infertility since sperm development requires normal thyroid hormone levels.

Graves’ disease can be treated with radioactive iodine or by surgery before pregnancy to avoid the use of antithyroid medication during pregnancy. It is generally recommended to wait six months after radioactive iodine treatment before becoming pregnant.

One other cause of infertility in patients with thyroid disease is the uncommon condition of primary ovary failure. This is an autoimmune disorder, like Graves’ disease and Hashimoto’s thyroiditis, caused by proteins and white cells in the blood that attack proteins in the patient’s ovaries. This leads to the decreased size of the ovaries, the failure to ovulate, premature menopause, and infertility.

Menstruation

Menstruation tends to be increased in hypothyroidism and decreased in hyperthyroidism. The effects of thyroid hormones on menstrual periods, ovarian function and the endocrine system in general are complicated but important. With too much or too little thyroid hormone a variety of effects on the reproductive system can occur. Girls who become hyper- or hypothyroid during puberty may have delayed menstrual function.

Updated in November 2015 by Deric Morrison, MD, FRCPC, Div. of Endocrinology, Dept. of Medicine, University of Western Ontario. Original text written by Irving B. Rosen, MD, FRCS(C), FACS, Professor of Surgery, University of Toronto, Department of Surgery, Mount Sinai Hospital; Consultant in Surgery, Princess Margaret Hospital, Ontario Cancer Institute and Paul G. Walfish CM, MD, FRCP(C), FACP, FRSM, Professor of Medicine, Pediatrics and Otolaryngology, University of Toronto; Senior Consultant, Endocrinology and Metabolism and Head and Neck Oncology Program, Mount Sinai Hospital.

Can Graves’ Disease or Hyperthyroidism Affect Fertility?

Do you know someone or have you been diagnosed with hyperthyroidism (high thyroid)? Like hypothyroidism (low thyroid), hyperthyroidism can affect fertility chances for both men and women. While not as common as low thyroid, hyperthyroidism affects 2-3% of the population at some point in their lives. Solving thyroid problems before conceiving is more important than you think!

Graves’ disease, an autoimmune disorder where the thyroid overproduces hormones, is the most common cause of hyperthyroidism. It causes many symptoms, tends to run in families, and is more common in women than men. Additionally, some people with thyroid problems flip between low and high thyroid levels, adding more complexity to the problem.

While hyperthyroidism requires medical treatment, natural therapies can be considered to ease symptoms and improve fertility. For your best health, it’s important to work with guidance from a qualified health professional if you’ve been diagnosed.

Thyroid hormone testing is necessary to find out for sure, but here are hyperthyroidism symptoms to watch for:

  • Thyroid nodules (goiter); swollen thyroid
  • Bulging or prominent eyes (Graves Orbitopathy)
  • Menstrual cycle changes: short menstrual cycle (less than 5 days), irregular cycles, light cycles or cycles that are far apart
  • Low sperm count/low testosterone
  • High metabolic rate/sweating
  • Racing or irregular heartbeat
  • Insomnia/mood swings/irritability
  • Unexplained weight loss/diarrhea
  • Bone loss/osteoporosis
  • Family history of hyperthyroidism

Hyperthyroidism & Your Fertility

Hyperthyroidism decreases conception chances in a few ways. In men, hyperthyroidism can lower sperm count and testosterone. It increases the risk for ED (erectile dysfunction). In women, it can lead to irregular cycles and affect ovulation. Hyperthyroidism in pregnancy is serious because it increases the risk of miscarriage, preeclampsia or preterm birth.

If you have hyperthyroidism and plan to conceive, work closely with your doctor to make sure your thyroid levels are properly managed. Having a healthy thyroid improves your chances of a healthy pregnancy and delivery.

Natural Options for Thyroid Balance

Natural therapies can be explored for symptom relief and improved fertility if you have hyperthyroidism, but it is important to continue thyroid monitoring and to have guidance from your doctor or other qualified health practitioners for long term recovery.

Dietary triggers worsen autoimmune thyroid reactions:

  • Watch dietary iodine. Iodine aggravates hyperthyroidism by stimulating thyroid hormone production. Early research links hyperthyroidism to excessive iodine intake in people with preexisting thyroid disease. Limit or avoid iodine-enriched foods like salt, bread and dairy products; and foods high in organic iodine like fish and seaweed.
  • Consider eliminating gluten and get tested for celiac disease. 2012 research published in Polish Journal of Endocrinology finds there is a higher incidence of celiac disease in people who have autoimmune thyroid problems. A report published in BMJ Case Reports suggests untreated celiac disease could make thyroid problems less responsive to medical management. For people with celiac disease or gluten sensitivity, following a gluten-free diet is the best way to encourage better gut and thyroid health. Learn more: Can a Gluten-Free Diet Improve Fertility?
  • Eat calcium and magnesium-rich foods like almonds, dark leafy greens, carrots, legumes, avocado and broccoli for bone health. Graves’ disease makes it harder for the body to absorb bone-building minerals. Add Coral Calcium or another calcium/magnesium supplement for extra bone health support.
  • Ask your doctor about selenium therapy. Research finds selenium improves quality of life, slows the progression of thyroid eye disease (Graves Orbitopathy), and improves outcomes for eye health. Today, the European Thyroid Association recommends a six-month trial of selenium supplementation for people with thyroid eye disease. The safe upper limit dosage for an adult is 400mcg daily (including from food sources). Have your selenium levels evaluated and ask your doctor about the best dosage for your needs.

Calm symptoms with herbs. Try gentle teas or high-quality herbal extracts as directed for the best results.

  • Motherwort (Leonurus cardiaca)- helps relax the heart, ease stress reactions and insomnia.
  • Bugleweed (Ajuga virginicus)- supports normal thyroid function; may help prevent thyroid antibodies from binding to the thyroid.
  • Lemon balm (Melissa officinalis)- supports normal thyroid function; decreases anxiety and sleeplessness.

Rebalance Thyroid Health- Restore Fertility

Having hyperthyroidism can be disrupting to your fertility efforts, but effective treatment options (natural and medical) are available. For some people, hyperthyroidism is a lifelong issue. For others, it’s a transient problem, lasting only a few years. Find out about all your choices for support. Work with your doctor if you suspect hyperthyroidism is affecting your health and fertility.

Hethir Rodriguez is the Founder and President of Natural Fertility Info.com. She has been a Certified Herbalist for over 19 years, holds a Bachelors degree (BS) in Nutrition Sciences and is a Certified Birth Doula. Since founding Natural Fertility Info.com in 2007, Hethir has written and co-authored over 1200+ articles on Fertility; and her research, articles, and guides have been read by over 40,000,000 people. Hethir has dedicated her life to helping provide a source for high quality, research based information and support for those on their journey to becoming parents.

Dr. Christine Traxler M.D., OB/GYN

Dr. Traxler is a University-trained obstetrician/gynecologist, working with patients in Minnesota for over 20 years. She is a professional medical writer; having authored multiple books on pregnancy and childbirth; textbooks and coursework for medical students and other healthcare providers; and has written over 1000 articles on medical, health, and wellness topics. Dr. Traxler attended the University of Minnesota College of Biological Sciences and University of Minnesota Medical School, earning a degree in biochemistry with summa cum laude honors in 1981, and receiving her Medical Doctorate degree (MD) in 1986.

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