Endocrine Abstracts

Hypothyroidism is readily dealt with in pregnancy by ensuring optimal thyroxine replacement as early as possible - recent research suggests increasing the thyroxine by two extra days' dosage a week from the time pregnancy is confirmed is worthwhile (Alexander et al 2004).

Hyperthyroidism in pregnancy is usually caused by molar pregnancy, gestational thyrotoxicosis (GT) or Graves' disease. GT affects 1-3% of pregnancies and is 3 times more common in Asian women. There is a close but imprecise correlation between GT and both the presence of hyperemesis and the level of hCG. Graves' disease and other non-transient forms of hyperthyroidism may affect 0.06 - 4% of all pregnancies and have adverse effects on both the fetus and mother. Fetal goitre, intrauterine growth retardation, prematurity, stillbirth and craniosynostosis are all increased, while in mothers there is an increased risk of hypretension, preterm delivery, heart failure, thyroid storm and placental abruption. Overall mean birth weight may not differ in series of women with and without Graves' disease, but the frequency of low birth weight is up to 2.5 times greater in the presence of active hyperthyroidism. Prematurity may occur in 1 in 5000 to 70000 births. The odds ratio for pre-eclampsia is around 4 in women with active Graves' disease.

Treatment of the mother's thyroid disease is usually with propylthiouracil, as both carbimazole and methimazole have been asssociated with aplasia cutis and choanal atresia in the fetus - even though the strengths of these associations have been disputed. An important recent development has been the recognition of congenital hypothyroidism due to hyperthyroidism in pregnancy, which has a prevalence of 1 in 35000 (Kempers et al 2004). Breast feeding is safe with antithyroid drugs at low to moderate doses.