Hypothyroidism and pregnancy

摘要

Physiologic changes during pregnancy produce minor fluctuations in maternal thyroid function. Additional stresses, most notably thyroid autoimmunity or iodine deficiency, exacerbate alterations in thyroid function and, in some women, result in maternal and/or fetal hypothyroidism. Maternal hypothyroidism can increase short-term risk to mother and fetus. Recent studies have suggested that long-term intellectual development of the offspring may be compromised, although further research should help clarify a cause and effect relationship. Transplacental transfer of drugs and autoantibodies also can affect fetal thyroid function, as can genetic defects. Screening of women at risk for thyroid disease should improve identification of hypothyroidism. Therapy, usually with circulating thyroxine (LT4), mitigates or eliminates the risk of complications. The LT4 dosage often requires an increase during pregnancy, and all women of childbearing age who use LT4 should receive this warning. Congenital hypothyroidism affects only the fetus. Neonatal screening programs during the past 30 years have dramatically improved the outcomes of these children. Approximately 10% of women, almost all of who have thyroid autoimmunity (specificity of positive TPO antibody = 0.94), are at risk for postpartum thyroid dysfunction. A high index of suspicion and selective laboratory testing of women at risk should improve recognition and permit LT4 therapy of symptomatic individuals. Recurrences after subsequent pregnancies are common and permanent hypothyroidism does occur, necessitating lifelong monitoring of women with this disorder.