Clinical Review

What you need to know about thyroid disorders in pregnancy

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Managing overt disorders is straightforward, but even subclinical disease warrants heightened scrutiny



Until recently, thyroid dysfunction was thought to have little influence on pregnancy as long as it was treated, and management was straightforward. That was before case-control studies in prominent journals suggested an association between even subclinical hypothyroidism and impaired neonatal neurodevelopment.1-4

The risk associated with hyperthyroidism in pregnancy is less clear. Currently, it is believed to cause no adverse effects; the low thyroid-stimulating hormone (TSH) resolves in most women within 4 to 12 weeks.

As for the nonpregnant state, there is no agreement between the American College of Physicians and its British counterpart as to whether isolated, subclinical hyperthyroidism leads to morbidity or mortality, although some investigators have found an excess risk of atrial fibrillation and possibly increased bone loss in postmenopausal women. Treatment of hyperthyroidism in non-pregnant women is recommended only if low TSH persists after 4 to 12 weeks and the level is less than 0.1 mIU/L.5

This article discusses the detection and management of thyroid disease in pregnancy, concentrating on 2 representative cases. (See TABLE 1, for a list of the full spectrum of thyroid disorders.)


The spectrum of thyroid disorders is wide

Hashimoto’s or subacute thyroiditis
Subclinical hypothyroidism
Subclinical hypothyroxemia
Postpartum thyroiditis
Secondary hypothyroidism
  • Hypothalamic dysfunction
  • Radioactive iodine therapy
  • Thyroidectomy
  • Iodine deficiency
  • TSH receptor resistance/mutation
Grave’s disease
Subclinical hyperthyroidism
Thyroid storm
Secondary hyperthyroidism
  • TSH-producing pituitary adenoma
  • Toxic multinodular goiter
  • Toxic adenoma
  • Subacute thyroiditis
  • Metastatic follicular thyroid cancer
  • Iodine excess
  • Factitious/iatrogenic
  • Thyroid hormone resistance syndrome
  • Struma ovarii
  • Gestational trophoblastic neoplasia
  • Hyperemesis gravidarum

CASE 1: History of Graves’ disease

S.H., 32, is 6 weeks’ pregnant with her first child. She has a history of Graves’ disease, and underwent radioactive iodine treatment 10 years ago. She then became hypothyroid and has been on levothyroxine replacement for the past 9 years. She visits her endocrinologist annually and reports good control on 125 μg daily of oral levothyroxine sodium.

How should her pregnancy be managed?

When the mother has a history of Graves’ disease, regardless of her current thyroid state, 1% to 5% of newborns develop hyperthyroidism due to transplacental passage of thyroid-stimulating immunoglobulins (TSI). Fetal or neonatal hyperthyroidism is associated with fetal tachycardia (heart rate >160 bpm), poor growth, goiter, craniosynostosis, and advanced bone age. Therefore, fetal growth and heart rate should be monitored throughout pregnancy in these women. Investigators have published monograms on fetal thyroid measurement,6 and even argued that Doppler ultrasonography can differentiate between fetal hypo- and hyperthyroidism caused by drugs or disease processes.7 However, measurement of TSI levels (poor predictive value) and ultrasonography for fetal goiter (low yield) are controversial.

Another important consideration: The requirement for thyroxine hormone increases by approximately 30% in women on thyroid supplementation during pregnancy.8 This has been demonstrated in more than 9 studies, with athyrotic women experiencing greater increases than women with autoimmune hypothyroidism.9 The need for thyroxine increases as early as 5 weeks’ gestation and plateaus by 16 weeks.

Because hypothyroxemia or hypothyroidism (clinical or subclinical) may be associated with adverse neurodevelopment in the newborn, I recommend increasing the dosage of levothyroxine at the first encounter with this patient to 150 μg/day (<25% dosage increase). I also suggest measuring the baseline TSH level, if no reading is available from the past 3 months. If baseline TSH is less than 2.5 mIU/L, the dosage increase is probably adequate. If the TSH exceeds 2.5 mIU/L, however, I would ask the patient to take 1 extra pill (125 μg) on 2 days of the week (>30% dosage increase) and measure TSH again 4 to 6 weeks later (thyroxine takes 5 weeks to equilibrate after a change in dosage). Once the dosage has been adequately adjusted, I would monitor TSH every 6 to 8 weeks until delivery. At that time, the dosage should be reduced to the prepregnancy level, with TSH measured again in 4 to 6 weeks to confirm that the dosage is adequate.

Levothyroxine absorption is hampered by ferrous sulfate, aluminum hydroxide antacids, proton-pump inhibitors, and cholestyramine. Levothyroxine should be ingested at least 4 hours before or after the prenatal vitamin. The metabolism of levothyroxine is altered by phenytoin, carbamazepine, and rifampin.

Subclinical hypothyroidism can progress to overt disease

The majority of women with hypothyroidism are asymptomatic, with only 20% to 30% having any complaints, usually nonspecific (TABLE 2). Women with 1 or 2 symptoms are no more likely to have abnormal thyroid function tests than are asymptomatic women.


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