Treatment of hyper- and hypothyroidsm in pregnancy

Abstract

In healthy subjects there are changes in thyroid function during pregnancy consequent on the increased synthesis of TBG and the thyroid stimulating effect of hCG. Serum thyroid hormones are elevated in the first trimester but fall during the latter half of pregnancy. Iodine deficiency may accentuate these changes. Hyperemesis gravidarum is associated with elevated thyroid hormone values due to high hCG levels in a third of patients. Hyperthyroidism in pregnancy is usually due to Graves’ disease and is best managed with doses of antithyroid drugs sufficient to maintain euthyroidism. There is no evidence of damage to the fetus by this regime and breast feeding can be allowed. Beta adrenoreceptor blocking agents should not be used on a long-term basis. Hypothyroidism in pregnancy is associated with an adverse outcome in fetal health as well as an increase in obstetric complications. While treatment is eventually the same as for a non-pregnant person, there is evidence that the dose of L-thyroxine may require adjustment during pregnancy. Increasing L-thyroxine requirements, based on measurements of maternal L-T₄ values have been noted by some but not all investigators. Women presenting in pregnancy with untreated hypothyroidism should be allowed to continue to term preferably with L-T₄ replacement. The neonatal thyroid status should be assessed carefully in babies from mothers who have had either hyper- or hypothyroidism in pregnancy. Transplacental passage of maternal antibodies may cause neonatal hyperthyroidism or be associated with transient neonatal hypothyroidism.