Thyroid Function during Pregnancy
Pregnancy affects thyroid homeostasis. An increased excretion of iodine in the urine accounts for the increase in thyroid volume even in areas of moderate dietary iodine intake . Some studies, however, do not show an increase in urinary iodine during pregnancy. In either case the increase in thyroid volume is the result of imbalance between the intake and increased requirements of iodine during pregnancy . Iodine deficiency during pregnancy is associated with maternal goitre and reduced maternal thyroxine (T4) level. While thyroid size increases in areas of iodine deficiency it does not do so in those regions that are iodine sufficient; even in moderate iodine-deficient regions urinary iodine excretion is higher in all trimesters than in non-pregnant women and may be causative in maternal goitre formation as assessed by ultrasound. The increase in thyroid volume already referred to is substantially greater in iodine-deficient areas. This gestational goitrogenesis is preventable by iodine supplementation not only in areas of severe iodine deficiency (24-hour urinary iodine less than 50 |xg) but in areas such as Belgium and Denmark  where trials have shown clear beneficial effects on maternal thyroid size. The aim of these studies should be to increase the iodine supply to pregnant and lactating women to at least 250 |xg/day, a level agreed by a recent concensus WHO meeting on iodine requirements in pregnancy and lactation . Clinical studies of children born to mothers with known iodine deficiency clearly showed impaired neurointellec-tual development, sometimes to the extreme of cretinism in severe deficient states. These defects can be corrected by iodine administration before and even during gestation . Urinary iodine excretion in pregnancy is characterised by maximum excretion in the first trimester followed by a decline in the second and third trimesters. Often there is an increase in urinary iodine in the first trimester compared to control non pregnant women but where the population has a high median iodine concentration this difference may not occur.
Thyroid hormone transport proteins particularly TBG (thyroxine-binding globulin) increase due to enhanced hepatic synthesis and a reduced degradation rate due to oligosaccharide modification. Serum concentration of free thyroid hormones has been reported to be decreased, increased or unchanged during gestation by different groups depending on the assays used . However, there is general consensus that there is a transient rise in free thyroxine (FT4) in the first trimester due to the relatively high circulating hCG concentration and a decrease of FT4 in the second and third trimester albeit within the normal reference range. Recently, it has become apparent that there is a need for normative trimester-specific reference ranges for thyroid hormones . Ideally these should be derived from iodine sufficient women who do not have any evidence of thyroid autoimmunity . Changes in free triiodothyronine (FT3) concentration are also seen in which they broadly parallel the FT4, again within the normal range. The precise reason for the decline in free thyroid hormones is not clear. In iodine-deficient areas (including marginal iodine deficiency seen in many European countries) the pregnant woman may become significantly hypothyroxinaemic with preferential T3 secretion. The thyroidal 'stress' is also evidenced by a rise in the median TSH and serum thyroglobulin.
Thus, pregnancy is associated with significant, but reversible changes in thyroid function (table 1). The findings associated with the hypermetabolic state of normal pregnancy can overlap with the clinical signs and symptoms of thyroid disease.
Table 1. Physiologic changes in pregnancy that influence thyroid function tests
Thyroid function test change
TThyroid-binding globulin (TBG) First-trimester hCG elevation TPlasma volume
"tType III 5-deiodinase (inner ring deiodination) due to increased placental mass Thyroid enlargement (in some women) TIodine clearance
TSerum total T4 and T3 concentration TFree T4 and ¿TSH TT4 and T3 pool size
TT4 and T3 degradation resulting in requirement for increased hormone production
4-Hormone production in iodine-deficient areas
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