Thyroid disease and pregnancy.
Thyroid disease is common in younger women and may be a factor in reproductive dysfunction. This probably only applies to severe cases of hyper- or hypothyroidism. Once adequately treated, neither of these disorders significantly impacts on fertility. The key is to recognize and to treat thyroid disorders in the reproductive-age woman before conception. Thyroxine therapy and even antithyroid drug therapy should be continued during pregnancy as necessary. Pregnancy is a euthyroid state that is normally maintained by complex changes in thyroid physiology. The fetal and neonatal hypothalamic-pituitary-thyroid system develops independently, but it may be influenced by thyroid disease in the mother. Early pregnancy is characterized by an increase in maternal T4 secretion stimulated by hCG and an increase in TBG, resulting in the elevated total serum T4 in pregnancy. The debate continues as to whether maternal T4 is important in early or late fetal brain development. If so, the physiologic changes in thyroid hormone secretion and transport in early pregnancy would help to ensure that a sufficient amount of thyroid hormone was available. There is new evidence in human subjects that substantial maternal T4 can cross the placenta during pregnancy, and this may be particularly important when fetal thyroid function is compromised as a result of congenital hypothyroidism. Maternal and fetal/neonatal outcomes in pregnancy are adversely affected if severe hypothyroidism is undiagnosed or inadequately treated. Thyroid function tests should be obtained during gestation in women taking T4 and appropriate dose adjustments should be made for TSH levels outside a normal range. The TSH-receptor blocking antibodies from the mother are a recognized cause of congenital hypothyroidism in the fetus and neonate that can be permanent or transient. If neonatal hypothyroidism is detected through neonatal screening programs, and prompt and adequate T4 replacement therapy is instituted as soon as possible following delivery, subsequent growth and development are usually normal. Paradoxically, pregnancy often has a favorable effect on the course of maternal Hashimoto's disease, although there is the risk of relapse postpartum. Pathophysiologic conditions of hCG secretion such as gestational trophoblastic disease and hyperemesis gravidarum may present as thyrotoxicosis in pregnancy, but the main cause of this syndrome is Graves' disease. The mainstay of treatment is antithyroid drugs and either propylthiouracil or methimazole may be used safely. Subtotal thyroidectomy, after medical control, is the alternative treatment, but radioiodine ablation is contraindicated.(ABSTRACT TRUNCATED AT 400 WORDS)
Becks
G P
GP
Department of Health Sciences, University of California School of Medicine-San Diego, LaJolla.
Burrow
G N
GN
D005260:Female; D005315:Fetal Diseases / Q000175:diagnosis / Q000209:etiology / Q000628:therapy; D005333:Fetus / Q000502:physiology; D006801:Humans; D011247:Pregnancy; D011248:Pregnancy Complications / Q000175:diagnosis / Q000503:physiopathology / Q000628:therapy; D011252:Pregnancy Complications, Neoplastic / Q000175:diagnosis / Q000628:therapy; D011644:Puerperal Disorders / Q000175:diagnosis / Q000503:physiopathology / Q000628:therapy; D013959:Thyroid Diseases / Q000175:diagnosis / Q000503:physiopathology / Q000628:therapy; D013961:Thyroid Gland / Q000502:physiology / Q000503:physiopathology; D013964:Thyroid Neoplasms / Q000175:diagnosis / Q000628:therapy