What happens to the normal thyroid during pregnancy?

Hormonal changes and metabolic demands during pregnancy result in profound alterations in the biochemical parameters of thyroid function. For the thyr oidal economy, the main events occurring during pregnancy are: a marked inc rease in serum thyroxine-binding globulin levels; a marginal decrease in fr ee hormone concentrations (in iodine-sufficient conditions) that is signifi cantly amplified when there is iodine restriction or overt iodine deficienc y; a frequent trend toward a slight increase in basal thyrotropin (TSH) val ues between the first trimester and term; a direct stimulation of the mater nal thyroid gland by elevated levels of human chorionic gonadotropin (hCG), which occurs mainly near the end of the first trimester and can be associa ted with a transient lowering in serum TSH; and finally, modifications of t he peripheral metabolism of maternal thyroid hormones. Together, metabolic changes associated with the progression of gestation in its first half cons titute a transient phase from a preconception steady-state to the pregnancy steady-state. In order to be met, these metabolic changes require an incre ased hormonal output by the maternal thyroid gland. Once the new equilibriu m is reached, increased hormonal demands are maintained until term, probabl y through transplacental passage of thyroid hormones and increased turnover of maternal thyroxine (T-4), presumably under the influence of the placent al (type III) deiodinase. For healthy pregnant women with iodine sufficienc y, the challenge of the maternal thyroid gland is to adjust the hormonal ou tput in order to achieve the new equilibrium state, and thereafter maintain the equilibrium until term. In contrast, the metabolic adjustment cannot e asily be reached when the functional capacity of the thyroid gland is impai red (such as in autoimmune thyroid disease and hypothyroidism) or when preg nancy takes place in healthy women residing in areas with a deficient iodin e intake. The ideal dietary allowance of iodine recommended by the World He alth Organization (WHO) is 200 mu g iodine per day for pregnant women. In c onditions with iodine restriction, enhanced thyroidal stimulation is reveal ed by relative hypothyroxinemia and goitrogenesis. Goiters formed during ge station may only partially regress after parturition. Pregnancy, therefore, represents one of the environmental factors that may explain the higher pr evalence of goiter and thyroid disorders in the female population. An iodin e-deficient status in the mother also leads to goiter formation in the prog eny. When adequate iodine supplementation is given early during pregnancy, it allows for the correction and almost complete prevention of maternal and neonatal goitrogenesis. In summary, pregnancy is accompanied by profound a lterations in the thyroidal economy, resulting from a complex combination o f factors specific to the pregnant state, which together concur to stimulat e the maternal thyroid machinery. Increased thyroidal stimulation induces, in turn, a sequence of events leading from physiological adaptation of the thyroidal economy observed in healthy iodine-sufficient pregnant women, to pathological alterations, affecting both thyroid function and the anatomica l integrity of the thyroid gland, when gestation takes place in conditions with iodine restriction or deficiency: the more severe the iodine deficienc y, the more obvious, frequent, and profound the potential maternal and feta l repercussions.