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Feature Article

Thyroid disorders in pregnancy and postpartum

Senthil Thillainadesan, Ash Gargya
OPEN ACCESS

Iodine supplementation

Severe maternal iodine deficiency is associated with pregnancy loss, increased perinatal mortality, intellectual deficits in children and cretinism. Despite the availability of iodinated salt, mild iodine deficiency persists in Australia although this has possibly improved following iodine fortification of bread.3 

During pregnancy, increased thyroid hormone production and renal losses of iodine necessitate increased iodine intake. The recommended iodine intake during pregnancy and lactation is 250 mcg daily compared with 150 mcg daily for nonpregnant adults. The NHMRC recommends a supplement containing 150 mcg iodine to be taken daily during pregnancy.4 

Hypothyroidism during pregnancy

Untreated overt hypothyroidism (defined as an elevated TSH level with a low free T4 level, or a TSH level of 10 mIU/L or above regardless of the free T4 level) is seen in  0.3 to 0.5% of women of childbearing  age.5 It is associated with adverse outcomes during pregnancy including increased risk of pregnancy loss, premature birth and impaired fetal neurocognitive development. All women with overt hypothyroidism should be treated with levothyroxine.2

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Subclinical hypothyroidism is a milder, more common form of hypothyroidism and is defined as an elevated TSH level with a normal free T4 level. In one Australian study, 8.1% of women in early pregnancy had a TSH level between 2.5 and 5.0 mIU/L and 1.5% had a TSH level between 5 and 10 mIU/L.6 Subclinical hypothyroidism has been associated with subfertility and poor pregnancy outcomes including increased risk of miscarriage, preterm delivery, pre-eclampsia, gestational diabetes, growth restriction and premature rupture of membranes.2 The most common cause of hypothyroidism in developed countries is autoimmune thyroid disease, also known as Hashimoto’s thyroiditis. Women who are TPOAb positive have increased rates of miscarriage and preterm delivery independent of thyroid function. As a result, measurement of TPOAb levels is recommended to assist with decision making on when to treat subclinical hypothyroidism. 

High-quality randomised clinical trials on levothyroxine replacement to treat subclinical hypothyroidism during pregnancy are limited. This remains an area of ongoing research. Clinical guidelines on when to treat subclinical hypothyroidism in pregnancy have changed in the past five to 10 years as more clinical trial information has become available.  

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The results from clinical trials of levothyroxine in pregnancy have been mixed. From an offspring neurocognitive perspective the results have been somewhat reassuring. The Controlled Antenatal Thyroid Screening (CATS)-I and CATS-II trials showed no significant difference in intelligence quotient in children aged 3 and 9.5 years of mothers with subclinical hypothyroidism randomised to levothyroxine treatment or placebo.7,8 A second randomised controlled trial similarly showed no improvement in cognitive outcomes in children of mothers treated for subclinical hypothyroidism at 5 years of age.9 A limitation of both these trials was the late commencement of levothyroxine at 13 weeks and 17 to 18 weeks of gestation, respectively. 

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Dr Thillainadesan is an Advanced Trainee in Endocrinology and Dr Gargya is Staff Specialist in Endocrinology at Royal Prince Alfred Hospital, Sydney, NSW.