Thyroid disease in pregnancy

01OverviewDefinition, clinical context and the essential points that orientate the chapter.

Maternal thyroid hormone supports pregnancy and fetal neurodevelopment, particularly before the fetal thyroid is fully functional. Both under-treatment and excessive treatment can harm pregnancy, so RCOG recommends care involving clinicians with appropriate obstetric and endocrine experience. Pre-conception optimisation is preferable, but a new diagnosis during pregnancy still requires prompt action.

Physiology changes interpretation. Early hCG stimulation can lower TSH, binding proteins raise total T4, and reference intervals vary by assay and gestation. Hyperemesis-related gestational transient thyrotoxicosis is usually distinguished from Graves' disease by context, goitre or eye signs, antibodies and persistence rather than by one suppressed TSH.

Management includes the fetus and the postpartum period. TSH-receptor antibody concentration, uncontrolled maternal thyrotoxicosis and antithyroid medicines may prompt fetal growth, heart-rate and goitre surveillance. After birth, maternal doses often change rapidly and neonatal clinicians need advance notice when fetal or neonatal thyroid dysfunction is plausible.

Key points

Pregnancy raises thyroxine-binding globulin and changes total hormone concentrations; interpret TSH and free T4 using gestation- and assay-appropriate reference ranges whenever the laboratory supplies them.
Human chorionic gonadotrophin can suppress TSH in early pregnancy. A low TSH alone is not Graves' disease: examine the clinical picture, free hormones, TSH-receptor antibodies and trajectory.
Established hypothyroidism usually needs an early levothyroxine increase. The patient should contact the maternity/endocrine team promptly after a positive test rather than wait for routine booking.
Levothyroxine is safe and should not be stopped in pregnancy. Separate it from iron, calcium and pregnancy multivitamins because these can reduce absorption.
For Graves' hyperthyroidism, use the lowest effective antithyroid medicine exposure that controls maternal disease while avoiding fetal hypothyroidism; drug choice can change across gestation under specialist supervision.
Carbimazole is associated with congenital malformations, particularly in the first trimester, while propylthiouracil carries important hepatic toxicity. Pre-conception counselling permits a planned, individualised strategy.
Radioiodine is contraindicated during pregnancy and breastfeeding. If surgery is essential, timing and preparation are agreed jointly by obstetric, endocrine, anaesthetic and thyroid surgical teams.
TSH-receptor antibodies cross the placenta and can affect the fetus even after maternal thyroidectomy or radioiodine. A past Graves' history remains obstetrically relevant.
Postpartum immune rebound may trigger Graves' disease or a transient destructive thyroiditis. The hyperthyroid phase of postpartum thyroiditis is not treated with antithyroid medicines because hormone synthesis is not increased.

02AetiologyUnderlying causes, associations and risk factors, with why each one matters.

Pre-existing autoimmune thyroid disease

Hashimoto or Graves disease may predate conception, with pregnancy changing hormone requirements, antibody activity and maternal or fetal monitoring needs.

New pregnancy-associated dysfunction

Gestational transient thyrotoxicosis, postpartum thyroiditis and newly recognised hypothyroidism can emerge through pregnancy-specific immune and hormonal physiology.

Treatment-related thyroid imbalance

Inadequate or excessive levothyroxine and antithyroid medicine exposure can affect both maternal physiology and the fetal thyroid.

03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.

1
Pregnancy changes thyroid tests
Human chorionic gonadotrophin can lower TSH early, while binding proteins raise total hormone and assay-specific gestational ranges alter interpretation.
2
Maternal hormone supports the fetus
Maternal thyroid hormone contributes to pregnancy and early fetal neurodevelopment before fetal thyroid function is fully established.
3
Antibodies and medicines cross the placenta
TSH-receptor antibodies and antithyroid medicines can alter fetal thyroid activity, growth, heart rate and gland size.
4
Requirements change after delivery
Loss of placental physiology and postpartum immune change can rapidly alter maternal replacement or antithyroid needs and reveal thyroiditis.

04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.

Overt maternal hypothyroidism

Raised gestation-adjusted TSH with low free T4 supports overt primary hypothyroidism. Symptoms such as fatigue, constipation and cold intolerance overlap with pregnancy, so biochemical confirmation and timely levothyroxine are essential.

Graves' hyperthyroidismRed flag

Persistent biochemical thyrotoxicosis with goitre, bruit, orbitopathy, prior Graves' disease or positive TSH-receptor antibodies favours Graves' disease over transient hCG-mediated suppression. Maternal tachycardia, weight loss and heart failure indicate severity.

Gestational transient thyrotoxicosis

Early pregnancy, hyperemesis, high hCG states, absent Graves' stigmata and subsequent improvement suggest a transient process. Supportive treatment is often sufficient, but severe dehydration and electrolyte disturbance still need urgent obstetric care.

Fetal thyroid effectRed flag

Persistent fetal tachycardia, growth restriction, fetal goitre, hydrops or abnormal bone maturation can reflect fetal hyper- or hypothyroidism. Maternal antibodies and antithyroid exposure guide specialist interpretation.

Postpartum dysfunction

Postpartum thyroiditis often produces a hyperthyroid phase followed by hypothyroidism; Graves' may also relapse. Pain is unusual, and antibody pattern, Doppler findings and time course help avoid inappropriate antithyroid treatment.

05InvestigationsWhat to request, why it matters and how to interpret it.

Investigation order

Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.

01
Serum TSH and free T4First step
Why
Define maternal thyroid status using pregnancy-appropriate laboratory interpretation.
Interpretation and limitations
Use trimester- and assay-specific intervals when available. Repeat after treatment changes at the interval agreed by the maternity/endocrine pathway; do not diagnose overt disease from TSH alone when free hormone and clinical context disagree.
02
TSH-receptor antibodies
Why
Distinguish autoimmune hyperthyroidism and estimate fetal/neonatal risk in current or previous Graves' disease.
Interpretation and limitations
A positive or substantially raised result supports Graves' activity and can cross the placenta. Timing of repeat testing and fetal surveillance follows the specialist obstetric guideline, including after definitive maternal treatment.
03
Thyroid peroxidase antibodies
Why
Identify autoimmune thyroid disease where this changes risk discussion or treatment thresholds.
Interpretation and limitations
Positivity increases future hypothyroidism and postpartum thyroiditis risk but is not itself proof that symptoms require thyroid hormone; interpret alongside TSH, free T4 and pregnancy history.
04
Full blood count and liver tests
Why
Provide a clinical baseline and investigate antithyroid medicine toxicity when symptoms occur.
Interpretation and limitations
Fever or sore throat requires urgent neutrophil assessment and medicine interruption advice; jaundice, dark urine, pruritus or severe abdominal symptoms require prompt hepatic evaluation, especially with propylthiouracil.
05
Fetal ultrasound surveillance
Why
Assess growth, amniotic fluid, fetal heart rate and thyroid size when maternal disease or treatment creates fetal risk.
Interpretation and limitations
A fetal goitre can reflect either stimulation by maternal antibodies or excessive antithyroid exposure. Interpretation and any maternal dose adjustment require fetal-medicine and endocrine input.
06
Postpartum thyroid function
Why
Reassess maternal requirements after delivery and investigate new postpartum symptoms.
Interpretation and limitations
Return toward the pre-pregnancy levothyroxine plan when appropriate, then recheck at the guideline-defined interval. A biphasic course suggests thyroiditis; persistent synthesis-driven thyrotoxicosis favours Graves' relapse.

06Differential diagnosisRealistic alternatives and the features that help distinguish them.

Gestational transient thyrotoxicosis

Hyperemesis, early gestation and absent goitre, eye signs or receptor antibodies favour hCG-related physiology over Graves disease.

Graves disease

Persistent hormone excess, goitre, eye disease and TSH-receptor antibodies support autoimmune synthesis and identify fetal surveillance implications.

Normal gestational adaptation

A mildly suppressed early TSH with appropriate gestational free-hormone interpretation may be physiological rather than pathological thyrotoxicosis.

Postpartum thyroiditis

A painless release phase followed by temporary hypothyroidism after delivery differs mechanistically from recurrent Graves disease.

07ManagementImmediate care, first-line treatment, alternatives and escalation.

01HypothyroidismConception to postpartum replacementFirst stepKnown levothyroxine-treated disease, or new raised TSH with biochemical hypothyroidism in pregnancy.

1At pregnancy confirmation, contact the endocrine/maternity team promptly and implement the pre-agreed levothyroxine increase or urgent clinician-directed adjustment; check TSH and free T4 without waiting for routine booking.
2Titrate using pregnancy-specific targets and repeat tests regularly through gestation. Check administration, missed doses and separation from iron or calcium before assuming pharmacological failure.
3After delivery, reduce toward the pre-pregnancy dose when appropriate and recheck thyroid function around the locally specified postpartum interval; do not abandon follow-up when treatment began only during pregnancy.

02HyperthyroidismControl Graves' disease with minimal fetal exposureOvert synthesis-driven thyrotoxicosis rather than isolated low TSH or transient hCG effect.

1Assess severity, obtain TSH-receptor antibodies and discuss immediately with obstetric-endocrine specialists. Treat thyroid storm or heart failure as a maternal emergency in a monitored setting.
2Select propylthiouracil versus carbimazole by gestation, prior reaction and individual risk; use the lowest effective dose and avoid block-and-replace during pregnancy unless a highly specialist indication exists.
3Monitor maternal free hormone and clinical status, arrange fetal surveillance when antibody or treatment risk warrants it, and plan postpartum dose review plus neonatal communication before delivery.

03Low TSHSeparate physiology from pathologySuppressed TSH detected in early pregnancy, often during hyperemesis assessment.

1PreferredCheck free T4 or the locally preferred pregnancy assay, gestational age, symptoms, goitre/eye signs, medication and hCG context rather than labelling Graves' from TSH alone.
2Support hydration, antiemesis and electrolyte correction for hyperemesis. Request TSH-receptor antibodies and specialist review when Graves' remains plausible or biochemical abnormality is marked or persistent.
3Repeat thyroid tests to document resolution or evolution. Do not use radioiodine scanning in pregnancy and do not expose transient thyrotoxicosis to unnecessary antithyroid medicine.

Key medicines and prescribing safety4 treatments · regimens, roles and cautions

First-line replacement for overt maternal hypothyroidism and selected subclinical disease according to antibody status and obstetric-endocrine guidance.

Levothyroxine

Continue the established preparation; increase promptly according to the pre-conception plan or specialist advice, then titrate against gestation-specific tests.

Take consistently on an empty stomach where feasible and separate from iron, calcium or antacids. Avoid iatrogenic thyrotoxicosis and reassess the dose promptly after delivery.

Reduces new thyroid hormone synthesis in maternal Graves' disease while avoiding the characteristic carbimazole embryopathy risk in early organogenesis.

Propylthiouracil

Specialist-selected lowest effective divided regimen, commonly favoured around conception and the first trimester when an antithyroid medicine is required.

Serious hepatic injury can occur; provide liver warning symptoms. It crosses the placenta, so excessive treatment can cause fetal hypothyroidism or goitre, and later switching may be considered.

Controls synthesis-driven maternal hyperthyroidism when benefits outweigh teratogenic and other medicine risks.

Carbimazole

Specialist-selected lowest effective dose, with gestation-specific risk discussion and consideration after the first trimester when continuing antithyroid treatment.

Associated with congenital malformations, especially early in pregnancy. Stop and obtain an urgent blood count for fever, mouth ulcers or sore throat; do not restart after confirmed agranulocytosis.

Reduces troublesome adrenergic symptoms such as tremor or marked palpitations in selected patients with thyrotoxicosis.

Propranolol for short symptomatic control

Use only a short specialist-directed course at the minimum effective dose while definitive control develops; avoid routine prolonged exposure.

Check asthma, bradycardia and heart failure. Prolonged maternal beta-blockade may affect fetal growth and neonatal heart rate or glucose, so obstetric oversight is required.

08ComplicationsImportant consequences, why they occur and why they matter clinically.

Miscarriage and hypertensive disease

Poorly controlled maternal hypothyroidism or thyrotoxicosis increases the risks of pregnancy loss, pre-eclampsia and other placental complications.

Fetal growth and thyroid dysfunction

Maternal antibodies, uncontrolled hormone excess and treatment exposure can cause fetal growth disturbance, tachycardia, goitre or hypothyroidism.

Maternal cardiac decompensation

Severe maternal thyrotoxicosis increases the risk of atrial arrhythmia, heart failure and thyroid storm during infection, labour or surgery.

Postpartum relapse or thyroiditis

Rapid immune and treatment changes after birth can destabilise thyroid function when follow-up and dose plans are unclear.

09Monitoring and follow-upTreatment response, safety checks and longer-term review.

Document the laboratory's pregnancy reference interval and use the same assay when possible; a non-pregnant range can drive unnecessary dose changes.
Recheck TSH and free T4 after levothyroxine or antithyroid adjustment and at planned points through gestation, with frequency increased when control is unstable.
In current or previous Graves' disease, schedule TSH-receptor antibody testing and fetal surveillance according to RCOG and the local maternal-medicine pathway.
Give written antithyroid medicine toxicity advice and respond the same day to fever, sore throat, mouth ulcers, jaundice or dark urine.
Make a delivery and postpartum plan: maternal dose change, timing of repeat tests, breastfeeding-compatible therapy, and neonatal assessment when antibodies or medicines created risk.

10Special situationsVariants, exceptions and circumstances that change the usual approach.

Past Graves still crosses the placenta

Maternal radioiodine or thyroidectomy removes thyroid output but not necessarily TSH-receptor antibodies. Fetal risk assessment therefore depends on history and antibody testing, not current maternal TSH alone.

TSH lags behind treatment

During hyperthyroidism treatment, TSH may remain suppressed after free hormone improves. Escalating antithyroid medicine solely to normalise TSH can over-treat the fetus.

A fetal goitre has two directions

Maternal stimulating antibodies can cause fetal hyperthyroidism, while excessive antithyroid transfer can cause fetal hypothyroidism. Fetal-medicine assessment is needed before changing maternal treatment.

Postpartum thyroiditis is destructive

Stored hormone leaks during the hyperthyroid phase, so antithyroid medicines usually do not help. Symptom control, phase recognition and later hypothyroid testing are more useful.

Tablets compete in the gut

New pregnancy iron or calcium is a common reason for worsening TSH in a previously stable patient. Timing history may solve the problem without an unnecessarily large replacement increase.

11Common pitfallsFrequent interpretation and management errors.

01
Interpreting a low first-trimester TSH with a non-pregnant reference range and diagnosing Graves' disease automatically.
02
Stopping levothyroxine because the patient is pregnant instead of promptly reviewing the higher requirement.
03
Using radioiodine imaging or treatment during pregnancy or breastfeeding.
04
Titrating antithyroid therapy to TSH alone while free hormone is already controlled.
05
Forgetting TSH-receptor antibodies after previous thyroidectomy or radioiodine for Graves' disease.
06
Treating the hyperthyroid phase of postpartum thyroiditis as increased hormone synthesis.