Athens University School of Medicine, Endocrine Unit, "Evgenidion" Hospital, Athens, Greece
Pregnancy affects thyroid physiology in many ways: (a) The renal
iodide clearance rate is increased, hence iodine requirements
increase. (b) The fetal requirements for thyroid hormones and
iodide are an additional problem. (c) Serum thyroxine-binding
globulin increases, thus producing an increase in the levels
of total T
4 and T
3. (d) Chorionic gonadotropin has a thyroid-stimulating
activity. This may be compensated for by a decrease in TSH,
but in some cases gestational thyrotoxicosis occurs. (e) Thyroid
autoimmunity usually subsides during pregnancy, but may rebound
a few months after parturition, and postpartum thyroiditis may
occur. Because maternal antithyroid autoantibodies cross the
placenta readily, fetal and neonatal hyperthyroidism (or hypothyroidism)
may develop. Pre-existing thyroid diseases are influenced. Nontoxic
goiter increases in size. Iodine and/or thyroxine may be required.
Graves' disease may remit. If present, antithyroid drugs should
be given in small doses, and quite often they may be stopped
altogether. Hypothyroid patients may require a larger T
4 dose.
