A recent article in the New England Journal of Medicine reported the successful diagnosis and treatment of fetal goitrous hypothyroidism in a mother with Graves' disease. The fetus is being recognized as an important patient in its own right in terms of thyroid disease. The fetal thyroid system develops independently of the normal maternal thyroid axis. Presence of feedback suppression of TSH by T4 has been demonstrated in a 35-week fetus. Information learned from congenital hypothyroidism suggests that lack of fetal thyroid hormones may have a negative impact on the developing fetal brain with lack of normal myelination. It is uncertain at what gestational age the fetus and the developing central nervous system become adversely affected by thyroid hormone deficiency. Since congenital hypothyroidism is sporadic and since there is no current method for easily screening all pregnancies for hypothyroidism, the thrust in fetal diagnosis and therapy has been in those pregnancies suspected of having a hypothyroid fetus when a fetal goiter is detected by ultrasonography or in a hyperthyroid mother who may be on antithyroid therapy. Intraamniotic injections of L-thyroxine have proven successful for fetal therapy. Amniotic fluid TSH may prove useful in the diagnosis and treatment of a hypothyroid fetus. Previous studies have suggested that the period of thyroxine dependency of the fetal central nervous system is limited predominantly to the last 4-8 weeks of gestation. Fetal hyperthyroidism due to transplacental transmission of thyroid-stimulating immunoglobulins may occur in a mother with a history of hyperthyroidism due to Graves' disease.(ABSTRACT TRUNCATED AT 250 WORDS)