Thyroid disease in pregnancy

Thyroid dysfunction in pregnancy has consequences for both mother and baby, including pre-eclampsia, prematurity and congenital abnormality. Most of it is managed in general practice, with specialist input for hyperthyroidism and for nodules.

Physiology — why the numbers change

The gland enlarges and becomes more vascular, circulating iodine falls, and thyroid-binding globulin rises.

Beta-hCG shares structural similarity with TSH and directly stimulates the TSH receptor in the first trimester. Free T4 and free T3 rise and TSH is suppressed. A serum TSH below 0.1 mIU/L may be present in 5% of women by the 11th week of pregnancy. TSH then normalises as beta-hCG falls in the second and third trimesters.

The fetal thyroid starts functioning at 10–12 weeks but does not fully mature until the third trimester; before then fetal requirements are met by maternal thyroxine.

Prevalence in screened pregnancies: overt hypothyroidism 0.3–0.5%, subclinical hypothyroidism 2–3%, overt hyperthyroidism 0.1–0.4% (Graves’ disease accounts for 85%), hCG-mediated hyperthyroidism 1–3%, thyroid nodules 3–21%.

Iodine

Iodine requirement rises in pregnancy and lactation because of increased hormone production, increased renal excretion and fetal demand. The NHMRC recommends a daily supplement of iodine 150 micrograms; recommended total daily intake in pregnancy is 250 micrograms. Most pregnancy multivitamins already contain that dose. Offer supplementation to women with normal thyroid function and to those with overt or subclinical hypothyroidism, but do not give iodine supplements to a woman with hyperthyroidism.

Screening

Universal screening is not currently recommended. Screen women at higher risk of thyroid dysfunction:

• symptoms of hypothyroidism
• family or personal history of thyroid disease, or of thyroid peroxidase antibodies
• type 1 diabetes, or another autoimmune disease (coeliac disease, pernicious anaemia, Addison’s disease, lupus, rheumatoid arthritis)
• history of head and neck radiation
• recurrent miscarriage or impaired fertility
• morbid obesity
• residence in an area of moderate to severe iodine insufficiency
• hyperemesis gravidarum with clinical features suggestive of hyperthyroidism
• molar pregnancy

The local (HNE HealthPathways) high-risk list adds several triggers worth knowing, because they widen who gets a TSH: age over 30, two or more prior pregnancies, goitre, obesity III (BMI >40), and amiodarone, lithium or a recent high iodine load such as iodinated contrast. Write “gestation” on the pathology request so the laboratory applies pregnancy ranges.

Which follow-on tests to add depends on the history: TSH, free T4, free T3 and TRAb if there is a personal history of hyperthyroidism; TSH, free T4 and TPO antibodies if the history is of hypothyroidism.

Targeted screening misses cases — one Sydney obstetric series found 9.6% of subclinical hypothyroidism would have been missed by a targeted approach. Retest later in pregnancy if symptoms or signs develop, even after a normal early result.

Interpreting the TSH

Use population and trimester-specific reference ranges wherever the laboratory provides them. Where they are unavailable, the ATA advises reducing the lower TSH limit by 0.4 mU/L and the upper limit by 0.5 mU/L relative to the non-pregnant range.

Where the laboratory gives no trimester-specific range, HNE HealthPathways treats these as normal in pregnancy: first trimester 0.1–2.5 mIU/L, second trimester 0.2–3.0 mIU/L, third trimester 0.3–3.5 mIU/L. Confirm the ranges with your own laboratory — assays and populations differ.

If the TSH is in range and there is no pre-existing thyroid disease, only repeat thyroid function if symptoms or signs develop later in pregnancy.

A TSH above 4 mIU/L in the first trimester is an agreed threshold for starting levothyroxine. Between 2.6 and 4 mIU/L, treatment is controversial and the evidence for benefit is conflicting; antibody status decides it (see below).

If the TSH is outside the reference range, add free T4, free T3, thyroid peroxidase antibodies, and TRAb where there is a history of Graves’ disease.

Hypothyroidism

Already on thyroxine

Optimise the TSH before conception where pregnancy is planned. Once pregnancy is confirmed, increase the dose straight away — a practical approach is two extra tablets per week, roughly 20–30% of the baseline dose. StatPearls quotes a larger typical increase of 30–50% over the pre-pregnancy dose; either way, titrate to the TSH rather than to a fixed percentage.

Aim for a TSH of 0.5–2.5 mIU/L, or the lower half of the trimester-specific range. Check TSH every four weeks through the first trimester, then six to eight weekly, and four weeks after any dose change. Locally the schedule is four-weekly until the TSH is stable, then six- to eight-weekly with a final check at 28–32 weeks, and again at six weeks postpartum. Adjust the levothyroxine dose by about 10% when the TSH falls outside the trimester-specific range.

A practical alternative to a percentage increase: if the same dose is taken every day, double the dose on two days of the week until an early-pregnancy TSH can be checked and the dose individualised.

If a woman stays hypothyroid on an apparently adequate dose, think adherence and absorption. Thyroxine is taken on an empty stomach before breakfast, with a 4–5 hour gap before vitamins, calcium or iron. Pregnancy multivitamins interfere with levothyroxine absorption — the simplest instruction is levothyroxine in the morning and all pregnancy supplements, iron and calcium at night.

After delivery, drop back to the pre-conception dose and recheck thyroid function at 4–6 weeks.

Where the hypothyroidism was first diagnosed in pregnancy, the local rule is to cease levothyroxine after delivery in every woman except two groups: those contemplating another pregnancy within 12 months, and those whose TSH was above 10 mIU/L before treatment started — continue in those cases and review annually. Repeat free T4 and TSH at six weeks postpartum in all women. Strongly TPO-antibody-positive women who cease levothyroxine have a higher risk of permanent overt hypothyroidism, so monitor them two to three times a year.

New diagnosis in pregnancy

Overt hypothyroidism warrants immediate thyroxine plus antibody testing (anti-TPO, anti-thyroglobulin, and TRAb if previously treated Graves’ disease). Usual starting dose is at least 50 micrograms daily, maintenance typically 100–150 micrograms daily, adjusted for the degree of hypothyroidism and the woman’s size. Recheck at four weeks and up-titrate to a TSH below 2.5 mIU/L as quickly as possible.

The local threshold differs from the 4 mIU/L figure above. HNE HealthPathways starts levothyroxine 50 micrograms daily at a TSH above 5.1 mIU/L and arranges urgent maternity referral within two weeks, with the TPO antibody titre chased. Below 5.1 mIU/L but above the reference range, check the TPO antibody titre and manage on antibody status while awaiting review. Follow whichever threshold your maternity service uses — check the current pathway, since this is exactly the kind of local figure that moves.

Subclinical hypothyroidism

Associated with recurrent miscarriage, intrauterine growth restriction, preterm birth, low birth weight, perinatal mortality and pre-eclampsia. Always test antithyroid antibodies, since they change both the management and the postpartum risk.

• Antibody positive with TSH 2.5–4 mIU/L — start thyroxine.
• TSH 4 mIU/L or above — start thyroxine regardless of antibody status.
• Antibody negative with TSH below 4 mIU/L — no data support treating.

Starting dose is 50 micrograms daily, with thyroid function checked within four weeks.

Reassess the need for thyroxine postpartum. If it was started for antibodies with a TSH below 4 mIU/L, cease and recheck at six weeks. If the TSH was above 4 mIU/L on antibodies, continue; if it was above 4 mIU/L without antibodies, cease and recheck at six weeks.

Refer urgently if secondary hypothyroidism (e.g. pituitary dysfunction) is suspected.

Hyperthyroidism

Arrange emergency assessment and notify the maternity team for any of these:

• agranulocytosis or neutropenic sepsis in a woman taking carbimazole or propylthiouracil
• hyperthyroidism with cardiac or respiratory compromise, or other markers of severe illness (fever, vomiting, labile blood pressure, altered mental state)
• hyperthyroidism with hypokalaemia and paralysis
• reduced visual acuity in Graves’ disease
• suspected myxoedema, or a thyroid mass with obstructive symptoms

Refer any woman with a current or new diagnosis of hyperthyroidism for specialist review. TRAb distinguishes Graves’ disease from hCG-mediated hyperthyroidism, which matters because the fetal risk and the management differ. Radioiodine scanning is contraindicated in pregnancy.

hCG-mediated hyperthyroidism (TRAb negative) is transient and generally needs no treatment; there is likewise no evidence supporting treatment of subclinical hyperthyroidism. Observe with TSH and free T4 every four to six weeks. Transient mild hyperthyroidism is common — locally quoted at 10–20% of normal pregnancies, apparent after 6 weeks and peaking at 9–12 weeks. If the TSH is below 0.1 mIU/L with a raised free T4 or free T3 or a positive TRAb, seek advice while awaiting review; if free T4, free T3 and TRAb are normal or only mildly raised, recheck TRAb and thyroid function in two weeks. Persistent mild hyperthyroidism beyond 15 weeks is not the expected hCG pattern — refer.

Maternal TRAb crosses the placenta and can cause fetal hyperthyroidism. Check antibodies when pregnancy is confirmed, at 18–22 weeks, and again at 30–34 weeks; if elevated, the fetus needs serial ultrasound for growth and signs of fetal hyperthyroidism.

Planning a pregnancy on antithyroid drugs? Arrange preconception endocrinology referral at least three months before the planned conception so a definitive plan exists before she conceives. If she is already pregnant and on carbimazole or PTU, enact the plan agreed with her endocrinologist; if there is no plan, seek advice from the treating or on-call endocrinologist the same day.

Antithyroid drugs are specialist-initiated. Propylthiouracil is first line in the first trimester because carbimazole is associated with congenital abnormalities; carbimazole may be used from the second trimester. Dose to keep maternal free T4 at the upper limit of normal — a normalised TSH suggests the fetus is getting too much drug. Both drugs cross the placenta and can cause fetal goitre and transient hypothyroidism, and both can cause maternal agranulocytosis. Propranolol short term helps tachycardia and tremor.

Tell the paediatrician at delivery if the mother has taken antithyroid drugs or carries TRAb, so the neonate’s thyroid function is monitored. Graves’ disease commonly relapses postpartum in women who stopped treatment during pregnancy. Thyroxine and antithyroid drugs are compatible with breastfeeding.

Goitre and thyroid nodules

Mild thyroid enlargement is common in pregnancy and largely reflects reduced circulating iodine. Significant growth during pregnancy is abnormal — refer urgently.

Investigate a palpable nodule with ultrasound; radioiodine imaging (including Tc-99m pertechnetate uptake scanning) is contraindicated.

Arrange urgent endocrine referral, and phone the endocrinology registrar for immediate advice, if a pregnant woman has a nodule with a low or suppressed TSH, or a dominant nodule over 4 cm.

• Solid nodule under 10 mm — can usually wait until after delivery.
• Larger lesions — ultrasound-guided fine-needle aspiration.
• Nodule 5 mm or more with high thyroid cancer risk or suspicious ultrasound features — aspirate.
• Complex nodule 15 mm or larger — also requires fine-needle aspiration.

Near term (delivery within four weeks), aspiration can reasonably be deferred to postpartum. For a papillary or follicular neoplasm without advanced disease, postponing surgery until postpartum is unlikely to change disease-specific survival, though second-trimester surgery can be offered. Operate immediately if the nodule causes tracheal obstruction.

Postpartum thyroiditis

Hypothyroidism, thyrotoxicosis or both developing in the year after delivery in a woman with no clinical thyroid disease before pregnancy. It occurs in 7–10% of postpartum women, varying with iodine intake and genetic factors — locally quoted as 5–10%, rising to up to 25% of women with type 1 diabetes.

Consider it in any woman presenting with depressive symptoms postpartum. Almost 50% of women with anti-TPO antibodies in early pregnancy will develop postpartum thyroiditis, making antibodies the most useful marker of risk — check thyroid function at three and six months postpartum in those women, and in women with known autoimmune disease, previous postpartum thyroiditis or chronic viral hepatitis.

Annual TSH for 5–10 years is recommended after postpartum thyroiditis because of the increased risk of permanent overt hypothyroidism.

Referral

Urgent maternity/endocrine referral:

• current Graves’ disease, or a history of Graves’ disease treated with radioactive iodine or thyroidectomy
• a previous neonate with Graves’ disease, or previously elevated TRAb
• any new diagnosis of hyperthyroidism, or symptomatic hyperthyroidism
• persistent hyperthyroidism beyond 15 weeks gestation
• abnormal TFTs or elevated antibodies in the second or third trimester
• elevated thyroid peroxidase antibodies in the first trimester
• suspected secondary hypothyroidism
• palpable thyroid nodule, or significant goitre growth

Routine maternity referral: personal history of thyroid disease.

Source (local): Thyroid Disease in Pregnancy, Postpartum, and Preconception, Community HealthPathways Hunter New England, last updated 21 July 2026 (registry: hne-healthpathways-thyroid-disease-pregnancy; verified 2026-08-31). Local screening triggers, trimester-specific ranges, the TSH 5.1 mIU/L treatment threshold, titration and monitoring schedule, iodine policy, postpartum cessation rules and referral routes come from this pathway — check it for the current local figures before relying on them.