As soon as pregnancy is established, several physiological changes occur, leading ultimately to a progressive increase in hormone demand that can only be met by a very marked augmentation in maternal thyroid output. This end-point is ensured by physiological adaptations of the thyroidal economy, provided that the thyroid gland is fully operative and iodine intake adequate (1). Whenever the integrity of the maternal thyroid is either anatomically or functionally compromised (i.e. thyroid surgery, autoimmune thyroiditis) or iodine supply is not sufficient for pregnancy, variable degrees of maternal thyroid insufficiency may occur over the course of gestation. These include either overt or subclinical hypothyroidism, the prevalence of which in Western countries is estimated to be 0.3-0.5 and 2-3, respectively (2). Furthermore, epidemiological data from either moderately or mildly iodine-deficient areas, have shown that pregnant women may experience another thyroid function abnormality, namely isolated hy-pothyroxinemia (IH).
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