A para 2+0 female, 11 weeks gestation presented with vaginal bleeding and hyper-emesis. An ultrasound scan showed a dichorionic pregnancy with one viable foetus and a hydatiform mole. β-human chorionic gonadotrophin (β-hCG) level was elevated at 159845 U/L and subsequent thyroid biochemistry revealed hyperthyroidism. Serum thyrotrophin (TSH) was suppressed at <0.05 mU/L (NR 0.24.5), with a FT4 37 pmol/L (NR 924), and Free T3 of 17.8 nmol/L (NR 2.66.2). She was mildly thyrotoxic with a small smooth goitre. No treatment was suggested as she was asymptomatic and there was a risk of causing hypothyroidism in the viable foetus via placental transfer of anti-thyroid drugs. In view of the high miscarriage risk and risk of very early preterm delivery she opted to terminate the pregnancy.
Approximately 0.2% of pregnancies are complicated by hyperthyroidism, which in 90% of cases is due to Graves disease. Gestational trophoblastic disease is a rare cause of hyperthyroidism in which high levels of hCG cause activation of the thyrotrophin receptor and stimulate supraphysiological secretion of thyroid hormone. hCG levels are particularly high at 1012 weeks gestation, during a twin pregnancy or in trophoblastic disease.
Iodides, thionamides, and thyroid receptor antibodies (TRAbs) readily cross the placenta. There is no significant placental transfer of glycoproteins such as TSH and hCG. Foetal thyroid tissue is not stimulated by the large amount of hCG in the maternal serum in trophoblastic disease, and therefore treatment of the mother with thionamides would result in foetal hypothyroidism.
The risk of persistant gestational trophoblastic disease is approx 20% whether the pregnancy is terminated early or continues to term. Though this patient opted for termination, there have been reports of successful outcomes of pregnancy. In these patients, for the reasons outlined above, it is important to treat symptoms rather than biochemistry.