33 year old gravida 2 para 1 was referred by her general practitioner at 6 weeks of gestation with severe nausea and vomiting. She was dehydrated, unable to tolerate fluids orally and had diminished urine output with ketonurea. There was no abdominal pain, bowel or urinary symptoms. Thyroid function tests showed TSH<0.5 (normal 0.4-6) and elevated free T3 and T4. Full blood count, and urea and electrolytes were within normal limits. Ultrasound scan showed a singleton pregnancy consistent with her dates. She was clinically euthyroided. Thyroid peroxidase antibodies were normal. She was managed with intravenous fluids and antiemetics. The medical team advised conservative management of her hyperthyroidism. Despite a further admission, which was managed conservatively, by 10 weeks gestation her thyroid function tests returned to normal.

A symposium of her thyroid function tests is given below:

Hyperemesis gravidarum is a severe and intractable form of nausea and vomiting in pregnancy. It may result in weight loss; nutritional deficiencies; and abnormalities in fluids, electrolyte levels, and acid-base balance. The peak incidence is at 8-12 weeks of pregnancy, and symptoms usually resolve by week 16. Hyperemesis gravidarum occurs in 0.5-10 cases per 1000 pregnancies. The prevalence increases in molar pregnancies and multiple pregnancies. The cause of severe nausea and vomiting in pregnancy has not been identified. Extreme nausea and vomiting may be related to elevated levels of estrogens or human chorionic gonadotrophin. Hyperemesis is associated with hyperthyroidism, pyridoxine deficiency, and psychological factors.¹

Thyroid function tests change during normal pregnancy due to the influence of two main hormones, estrogen and human chorionic gonadotrophin. HCG is produced in large quantities during pregnancy, particularly at the end of the first trimester. Due to its molecular similarities with TSH, Hcg weakly stimulates the maternal gland to increase its hormone production and slightly suppress TSH in the first trimester. Estrogen increases the amount of thyroid hormone binding protein in the serum which increases the total thyroid hormone levels in the blood, however free hormone levels usually remain normal.²

Assessment of thyroid function during pregnancy should be done with a careful clinical evaluation of the patient's symptoms as well as measurement of TSH and free, not total, thyroid hormones.

Measurement of thyroid autoantibodies may also be useful in selected cases to detect maternal Graves disease or Hashimoto thyroiditis and to assess risk of fetal or neonatal consequences of maternal thyroid dysfunction.³

B hcg exists as several isoforms depending on carbohydrate content. Desialated isoforms, which are produced more abundantly in cases of b hcg induced hyperthyroidism, have greater thyrotrophic activity than the commoner sialated isoforms. Therefore, the quality rather than quantity of b hcg is important in the development of b hCG induced hyperthyroidism. This also explains why pregnancy, with high bhCG concentrations comparable to those reported in this case, is not usually associated with thyrotoxicosis.⁴

The incidence of hyperthyroidism in pregnant women has been estimated at 0.2%. Most women have symptoms before pregnancy, but some will demonstrate symptoms for the first time during pregnancy.

The most common cause of hyperthyroidism during pregnancy is Graves disease, which accounts for 85-90% of all cases. Other causes include Sub-acute thyroiditis, Toxic multinodular goiter, Toxic adenoma, TSH-dependent thyrotoxicosis, Exogenous T3 or T4, Iodine-induced hyperthyroidism, and Pregnancy-specific associations: Hyperemesis gravidarum and Hydatidiform mole.⁵

Diagnosis of hyperthyroidism during pregnancy is important because untreated or poorly treated hyperthyroidism can lead to adverse obstetrical outcomes. These include first-trimester spontaneous abortions, high rates of still births and neonatal deaths, two- to threefold increases in the frequency of low birth weight infants, preterm delivery, fetal or neonatal hyperthyroidism, and intrauterine growth retardation. Diagnosis of Graves disease can be difficult because healthy pregnant women may exhibit tachycardia, palpitations, mild heat intolerance, emotional lability, diaphoresis, and warm, moist skin.⁶

For these reasons, diagnosis of hyperthyroidism during pregnancy needs to be made on careful clinical observations and well-conceived laboratory testing.

As most cases of hcg induced hyperthyroxinemia are transient, the thyroid function tests usually return to normal by the second trimester without treatment. However in those women with persistent hyperemesis and hyperthyroxinemia in the second half of pregnancy, antithyroid drug therapy should be considered.⁷

Thyrotoxicosis can exacerbate and mimic the symptoms of hyperemesis. Thyroid function tests should be measured in all pregnant women with hyperemesis and the results should be carefully interpreted.