Pregnancy and iodine

Hormonal changes and metabolic demands during pregnancy result in profound alterations in the biochemical parameters of thyroid function. For thyroid economy, the main events occurring during pregnancy are a marked increase i n serum thyroxine-binding globulin levels; a marginal decrease in free horm one concentrations tin iodine-sufficient areas) that is significantly ampli fied when there is iodine restriction or overt iodine deficiency; a frequen t trend toward a slight rise in basal thyrotropin (TSH) values between the first trimester and term; a transient stimulation of the maternal thyroid g land by elevated levels of human chorionic gonadotropin (hCG) resulting in a rise in free thyroid hormones and decrement in serum TSH concentrations d uring the first trimester; and finally, modifications of the peripheral met abolism of maternal thyroid hormones. Together, metabolic changes associate d with the progression of gestation in its first half constitute a transien t phase from preconception steady state to pregnancy steady state. In order to be met, these metabolic changes require an increased hormonal output by the maternal thyroid gland. Once the new equilibrium is reached, increased hormonal demands are maintained until term, probably through transplacenta l passage of maternal thyroid hormones and increased turnover of maternal t hyroxine (T-4), presumably under the influence of the placental (type 3) de iodinase. For healthy pregnant women with iodine sufficiency, the challenge of the maternal thyroid gland is to adjust the hormonal output in order to achieve the new equilibrium state, and thereafter maintain the equilibrium until term. In contrast, the metabolic adjustment cannot easily be reached during pregnancy when the functional capacity of the thyroid gland is impa ired because of iodine deficiency. The ideal dietary allowance of iodine re commended by World Health Organization (WHO) is 200 mug of iodine per day f or pregnant women. In conditions with iodine restriction, enhanced thyroida l stimulation is revealed by relative hypothyroxinernia and goitrogenesis. Goiters formed during gestation may only partially regress after parturitio n. Pregnancy, therefore, represents one of the environmental factors that m ay help explain the higher prevalence of goiter and thyroid disorders in wo men compared with men. An iodine-deficient status in the mother also leads to goiter formation in the progeny and neuropsycho-intellectual impairment in the offspring. When adequate iodine supplementation is given early durin g pregnancy, it allows for the correction and almost complete prevention of maternal and neonatal goitrogenesis. In summary, pregnancy is accompanied by profound alterations in the thyroid economy, resulting from a complex co mbination of factors specific to the pregnant state, which together concur to stimulate the maternal thyroid machinery. Increased thyroidal stimulatio n induces, in turn, a sequence of events leading from physiological adaptat ion of the thyroidal economy observed in healthy iodine-sufficient pregnant women to pathological alterations affecting both thyroid function and the anatomical integrity of the thyroid gland, when gestation takes place in co nditions with iodine restriction or deficiency: the more severe the iodine deficiency, the more obvious, frequent, and profound the potential maternal and fetal repercussions.