The systematic screening and management of hypothyroidism and hyperthyroidism during pregnancy.

Altogether, thyroid function abnormalities during pregnancy can affect up to 10% of all women. The high prevalence of both hypo- and hyperthyroidism, the obstetrical repercussions associated with thyroid dysfunction in the mothers, as well as the potential role of maternal thyroid dysfunction as an influence on fetal development constitute solid arguments for a further increase of our knowledge of the pathophysiological processes underlying the alterations of thyroid function related to the pregnant state. In this review, the focus will be on the most clinically relevant aspects associated with hypothyroidism [autoimmune thyroid disorders (AITDs), subfertility, risk of miscarriage, risk of hypothyroidism in women with AITD and treatment of hypothyroid women] and with hyperthyroidism (clinical presentations during pregnancy, Graves' disease and its management, fetal hyperthyroidism in women with antithyroid-stimulating hormone receptor antibodies and gestational transient thyrotoxicosis associated with human chorionic gonadotropin stimulation of the maternal thyroid gland).

The importance of iodine nutrition during pregnancy.

Objective: To examine the importance of iodine nutrition during pregnancy.

Design: Review of existing literature of iodine in pregnancy.

Setting: Population surveys and metabolic studies.

Clinical and biological consequences of iodine deficiency during pregnancy.

The main change in thyroid function associated with the pregnant state is the requirement of an increased production of thyroid hormone that depends directly upon the adequate availability of dietary iodine and integrity of the glandular machinery. In healthy pregnant women, physiological adaptation takes place when the iodine intake is adequate, while this is replaced by pathological alterations when there is a deficient iodine intake. Pregnancy acts typically, therefore, as a revelator of underlying iodine restriction.

The regulation of thyroid function during normal pregnancy: importance of the iodine nutrition status.

The main change in thyroid function associated with the pregnant state is the requirement of an increased production of thyroid hormone that depends directly upon the adequate availability of dietary iodine and integrity of the glandular machinery. Physiologic adaptation takes place when the iodine intake is adequate, while this is replaced by pathologic alterations when there is a deficient iodine intake. Pregnancy acts typically, therefore, as a revelator of underlying iodine restriction.

Acute increase in goiter size during a normal pregnancy: an exceptional case report.

This case report illustrates an exceptional clinical situation in which a pregnant woman abruptly presented, at 5 months' gestation, with major swelling of the thyroid gland that led to respiratory symptoms and emergency hospitalization. The medical condition was shown to be caused by acute intrathyroidal hemorrhage within a preexisting-albeit until then unnoticed-multinodular goiter. The cause of the intrathyroidal hemorrhage could not be firmly delineated, although it remains possible that an unusual extraneous cause constituted a "trauma" that triggered this rare medical condition.

Management of hypo- and hyperthyroidism during pregnancy.

Pregnancy has profound effects on the regulation of thyroid function, and on thyroidal functional disorders, that need to be recognized, carefully assessed and correctly managed. Relative hypothyroxinemia and goitrogenesis may occur in healthy women who reside in areas with restricted iodine intake, strongly suggesting that pregnancy constitutes a stimulatory challenge for the thyroid. Overt thyroid dysfunction occurs in 1-2% of pregnant women, but mild forms of dysfunction (both hyper- and hypothyroidism) are probably more prevalent and frequently remain unrecognized.

Feto-maternal repercussions of iodine deficiency during pregnancy. An update.

The main changes in thyroid function associated with the pregnant state are increased thyroid hormone requirements. These increased requirements can only be met by a proportional increase in hormone production, that directly depends upon the availability of dietary iodine. When the iodine intake is adequate, normal "physiological" adaptation takes place.

Potential consequences of maternal hypothyroidism on the offspring: evidence and implications.

The adequate functioning of both the maternal and fetal thyroid glands plays important roles to ensure that the fetal neuropsychointellectual development progresses normally. Three sets of clinical disorders ought to be envisaged, potentially leading to impaired brain development: defective glandular ontogenesis (leading to congenital hypothyroidism), maternal hypothyroidism (usually related to chronic autoimmune thyroiditis), and finally iodine deficiency (affecting both the maternal and fetal thyroid functions). The present review will be focused mainly on maternal hypothyroidism, where both the severity and temporal occurrence of maternal thyroid underfunction drive the resulting repercussions for an impaired fetal neuronal development: such clinical situations may take place during early gestation (in women with known but untreated hypothyroidism) or appear only during later gestational stages (in women with thyroid antibodies, who remain euthyroid during the first half of gestation).

Effects of l-thyroxine administration, TSH-receptor antibodies and smoking on the risk of recurrence in Graves' hyperthyroidism treated with antithyroid drugs: a double-blind prospective randomized study.

Objective: In Graves' hyperthyroidism treated with antithyroid drugs (ATD), the overall relapse rate reaches 30-50% following ATD discontinuation. Conflicting results have previously been reported with regard to the usefulness of combining ATD with thyroxine (l-T4), and thereafter maintaining l-T4 treatment after ATD withdrawal. Also, clinicians are in search of useful parameters to predict the risk of a recurrence of hyperthyroidism after ATD treatment.

The potential repercussions of maternal, fetal, and neonatal hypothyroxinemia on the progeny.

The adequate functioning of both the maternal and fetal thyroid glands play an important role to ensure that the fetal neuropsycho-intellectual development progresses normally. Three sets of clinical disorders are considered, that may eventually lead to impaired brain development. Firstly, in infants with a defect of glandular ontogenesis (congenital hypothyroidism), the participation of maternal thyroid hormones to the fetal circulating thyroxine environment is normal and, therefore, risk of brain damage results exclusively from the insufficient hormone production by the abnormal fetal thyroid gland.

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 thyroidal economy, the main events occurring during pregnancy are: a marked increase in serum thyroxine-binding globulin levels; a marginal decrease in free hormone concentrations (in iodine-sufficient conditions) that is significantly amplified when there is iodine restriction or overt iodine deficiency; a frequent trend toward a slight increase in basal thyrotropin (TSH) values between the first trimester and term; a direct stimulation of the maternal thyroid gland by elevated levels of human chorionic gonadotropin (hCG), which occurs mainly near the end of the first trimester and can be associated with a transient lowering in serum TSH; and finally, modifications of the peripheral metabolism of maternal thyroid hormones. Together, metabolic changes associated with the progression of gestation in its first half constitute a transient phase from a preconception steady-state to the pregnancy steady-state.

Thyroid hyperfunction during pregnancy.

The present report focuses on the two main causes of hyperthyroidism observed in the pregnant state: Graves' disease (GD) and gestational transient thyrotoxicosis. Together, the prevalence of hyperthyroidism may represent 3% to 4% of all pregnancies, and therefore constitutes an important clinical issue. Concerning GD, the variable presentations of the disease (women under treatment, in remission, or considered cured) and specific alterations occurring in pregnancy are discussed: changes in thyrotropin (TSH) receptor antibody titers, the risk of fetal and neonatal thyrotoxicosis, the outcome of pregnancy in relation to the control of hyperthyroidism, and the treatment of active GD during and after pregnancy with antithyroid drugs.

Goiter and pregnancy: a new insight into an old problem.

Evidence is presented that pregnancy constitutes a goitrogenic stimulus, particularly in conditions with a restricted or even a marginally low iodine intake. In a series of studies carried out in a large cohort of pregnancies in the Brussels area, the authors show that an increase in thyroid volume is observed in a majority of pregnant women, leading to goiter formation at delivery in 9% of the cases. Furthermore, increments in thyroid volume were correlated with biochemical evidences of functional stimulation of the thyroid, such as an elevation in serum TG levels, preferential T3 secretion, and slight increases in basal TSH at delivery.