MATERNAL HYPERTHYROIDISM

• Complicates 0.2% of all pregnancies.
• Associated with an increased risk of severe preeclampsia, hyperemesis gravidarum, low birth weight, prematurity, intrauterine growth restriction and perinatal mortality (1-3).
• Most common cause is Graves’ disease:
• Autoimmune disorder characterized by the presence of IgG antibodies directed towards thyroid-stimulating hormone (TSH, thyrotropin) receptor that induce the production of excess thyroid hormone (4).
• Transplacental passage of these thyroid- stimulating immunoglobulins (TSI) can activate the fetal and neonatal thyroid gland. TSH does not cross the placenta, whereas thyroxine demonstrates limited transport ability (1,5).
• The main risk to the fetus is thyrotoxicosis, which occurs in 1% of pregnancies complicated by autoimmune thyroiditis, and is dependent on both the maternal antibody levels and the response of the fetal cells.
• A functional TSH receptor appears by gestational week 12, concomitant with the beginning of fetal thyroid hormone synthesis between weeks 10 and 12 (1,6).
• The mortality of fetal and neonatal thyrotoxicosis is as high as 30%, and is usually caused by cardiac failure (3).
• Fetal manifestations include tachycardia, arrhythmia and cardiac insufficiency. Tachycardia is typically the first manifestation of fetal hyperthyroidism, usually arising after 25 weeks of gestation (2,4).
• Monitoring a fetus at risk for hyperthyroidism can be challenging because:
• Maternal thyroid levels are not necessarily reflective of fetal levels.
• Few studies have identified a reliable maternal TSI that confers fetal risk, but TSI levels 2.5-5 times greater than normal levels in the third trimester is of concern (6-8).

ULTRASOUND

• Scans of the fetal neck may demonstrate thyroid size, and to detect dorsiflexion of the fetal neck if a goiter is present.
• There may be generalized thyroid enlargement or less commonly thyroid cysts.
• Doppler has been used to evaluate regression of fetal goiter after medical treatment (9) .
• Fetal tachycardia (>160 bpm after 28 weeks).
• IUGR.
• Link to Fetal Goiter

REFERENCES

1. Davis LE, Lucus MJ, Hankins GDV et.al. Thyrotoxicosis complicating pregnancy. Am J Obstet Gynecol 1989;160:63.

2. Masiukiewicz US, Burrow GN. Hyperthyroidism in pregnancy: Diagnosis and treatment. Thyroid 1987;9:647.

3. Mestman JH. Hyperthyroidism in pregnancy. Endocrinol Metab Clin North Am 1998;27:127.

4. Polak M. Hyperthyroidism in early infancy: Pathophysiology, clinical features, and diagnosis with a focus on neonatal hyperthyroidism. Thyroid 1998;8:1171.

5. Krude H, Bierbermann H, Krohn HP et.al. Congenital hyperthyroidism. Exp Clin Endocrinol Diabetes 1997;195(S4):6.

6. Mestman JH, Goodwin M, Montoro MM. Thyroid disorders of pregnancy. Endocrinol Metab Clin North Am 1995;24:41.

7. McKenzie JM, Zakarija M. Clinical review 3: The clinical use of thyrotropin receptor antibody measurements. J Clin Endocrinol Metab 1989;69:1093.

8. Zimmerman D. Fetal and neonatal hyperthyroidism. Thyroid 1999;9:727.

9. Luton D, Fried D, Sibony O et.al. Assessment of fetal thyroid function by colored doppler echography. Fetal Diagn Ther 1997;12:24.