Graves Hyperthyroidism and Pregnancy: A Clinical Update

Komal Patil-Sisodia, MD; Jorge H. Mestman, MD


Endocr Pract. 2010;16(1):118-129. 

In This Article

Causes of Hyperthyroidism

Thyrotoxicosis refers to the clinical constellation of symptoms that occur when there is excessive circulating thyroid hormone. Hyperthyroidism is specifically defined as excessive production of thyroid hormone by the thyroid gland and can be divided into 4 groups: (a) intrinsic thyroid disease, (b) immune thyroid disease, (c) gestational thyrotoxicosis, and (d) iatrogenic hyperthyroidism (Table 1).

Gestational Thyrotoxicosis

Gestational thyrotoxicosis is a transient, mild hyperthyroidism that occurs early in pregnancy and is not due to intrinsic thyroid disease. Human chorionic gonadotropin, which peaks during the first trimester, has the ability to stimulate the thyroid TSH receptor.[16] Women with higher levels or enhanced activity of human chorionic gonadotropin have elevated T4 levels and suppressed TSH concentrations. Gestational thyrotoxicosis has been documented in up to 10% to 15% of pregnant women,[17] and it commonly occurs in several situations (Table 1). In most cases, the symptoms of gestational thyrotoxicosis are mild, mainly nausea and sometimes vomiting resolving spontaneously by 20 weeks' gestation. The most severe form of gestational thyrotoxicosis is hyperemesis gravidarum, known as transient hyperthyroidism of hyperemesis gravidarum,[18] characterized by severe nausea and vomiting, dehydration, weight loss of up to 5 kg, and ketonuria. Frequent visits to the emergency department for management of dehydration are common. In very severe cases, hospitalization and parental nutrition are needed. Distinguishing this condition from Graves hyperthyroidism may be challenging to the physician because of the presence of tachycardia, mild shortness of breath, and hand tremors due to severe dehydration and the marked elevation in serum free T4 or free T4 index and suppressed serum TSH (Table 2). Treatment with an antithyroid drug is not indicated because the symptoms subside spontaneously with progression of pregnancy, with normalization of T4 levels by 14 to 20 weeks' gestation.[18] In some patients, serum TSH may remain suppressed or below normal after normalization of serum T4.