Skip to textbook content
Doctor’s PassportTextbook
TopicsAll topics

Loading topic navigation…

Textbook navigation
TopicsAll topics

Loading topic navigation…
← Obstetrics and gynaecology indexChapter sections
OverviewAetiologyPathophysiologyClinical features and red flagsInvestigationsDifferential diagnosisManagementComplicationsMonitoring and follow-upSpecial situationsCommon pitfallsQuestionsSources
Full textbook13 sectionsOpen only what you need
Educational draft · awaiting clinical reviewThe full textbook explains uncertainty but does not replace live national or local guidance, specialist advice, or current prescribing information.

Thyroid disease in pregnancy

Obstetrics and gynaecology · UK scope · Sources checked 7 Sept 2026 · Clinical review pending

RapidFull
!
Thyroid storm or antithyroid toxicity needs urgent care

Marked tachycardia with fever, agitation, heart failure or altered consciousness can indicate thyroid storm; fever or sore throat during thionamide treatment can signal agranulocytosis.

Action: Arrange emergency medical and obstetric assessment for systemic decompensation. With suspected antithyroid-drug agranulocytosis, withhold further doses pending urgent full blood count and specialist advice; jaundice or hepatic pain requires urgent liver assessment.

Overview

Interpret thyroid tests using pregnancy-specific physiology, treat maternal hormone deficiency or excess safely, and recognise antibody-mediated fetal risk and antithyroid-drug emergencies.

Pregnancy changes thyroid hormone production, binding and laboratory interpretation. Oestrogen increases thyroxine-binding globulin, while hCG provides weak thyroid stimulation in early gestation. A low TSH can therefore be physiological or accompany transient hCG-related thyrotoxicosis. Compare both TSH and free T4 with the laboratory's pregnancy and assay reference ranges, establish gestational age and ask about prior thyroid disease, treatment, supplements and symptoms preceding conception.

Maternal hypothyroidism is commonly autoimmune or follows definitive treatment for hyperthyroidism. Fatigue, constipation and dry skin overlap with normal pregnancy and are not adequate diagnostic criteria. Overt hypothyroidism requires prompt levothyroxine treatment. RCOG also recommends treating severe subclinical disease with TSH above 10 mU/L and considering treatment for milder subclinical disease, especially when newly detected in the first trimester. Routine treatment of isolated TPO antibody positivity with normal thyroid function has not shown benefit.

Aetiology

01

Autoimmune thyroid disease

Hashimoto thyroiditis and Graves' disease produce opposite hormone disturbances through autoimmune mechanisms, and a history of either influences pregnancy testing and follow-up.

02

Treatment and hCG effects

Prior thyroidectomy or radioiodine may create lifelong replacement needs, while early-pregnancy hCG stimulation can transiently increase thyroid hormone without persistent gland disease.

Pathophysiology

  1. 1
    Increased hormone demand

    Higher binding-protein concentrations, placental metabolism and fetal needs increase maternal thyroxine requirements, often before the first routine antenatal appointment takes place.

  2. 2
    Antibody transfer

    Maternal TRAb crosses the placenta and can stimulate the fetal thyroid once it becomes functional, even when maternal hormone levels are normal.

  3. 3
    Drug transfer

    Thionamides suppress fetal as well as maternal hormone synthesis, making overtreatment a cause of fetal goitre and hypothyroidism despite apparently controlled maternal disease.

Clinical features and red flags

Hormone deficiency

Cold intolerance, persistent constipation, dry skin and delayed reflex relaxation can support hypothyroidism but require biochemical confirmation.

Graves' features

A diffuse goitre, eye signs or symptoms beginning before pregnancy favour autoimmune hyperthyroidism over transient hCG-mediated changes.

Drug toxicity

A new sore throat or fever during thionamide use should be treated as a possible blood dyscrasia rather than an uncomplicated viral illness.

Fetal thyroid concern

Persistent fetal tachycardia, growth restriction or goitre in a TRAb-positive pregnancy requires fetal-medicine and endocrine input.

Red flags requiring action

  • Fever, confusion, severe tachycardia or pulmonary oedema in a thyrotoxic patient requires emergency treatment for possible thyroid storm.
  • Sore throat, mouth ulcers, fever or unexplained infection while taking carbimazole or propylthiouracil requires immediate blood-count assessment and withholding the medicine until reviewed.
  • Jaundice, dark urine, pruritus or right upper quadrant pain while taking propylthiouracil raises concern for severe hepatotoxicity.

Investigations

  1. 01
    TSH and free T4First step
    Why
    Classify dysfunction and guide treatment using gestation-appropriate interpretation.
    Interpretation and limitations
    Use trimester and assay ranges; suppressed TSH alone does not prove overt hyperthyroidism and can remain low during successful treatment.
  2. 02
    TSH-receptor antibodies
    Why
    Support Graves' diagnosis and estimate antibody-mediated fetal risk.
    Interpretation and limitations
    Test early with any Graves' history; positivity or antithyroid use prompts repeat testing, and levels above three times the positive threshold increase fetal concern.
  3. 03
    Free T3 and targeted antibody assessment
    Why
    Clarify newly detected thyrotoxicosis when Graves' disease and transient gestational changes are competing explanations.
    Interpretation and limitations
    Raised free T3 and TRAb support Graves' disease, whereas routine TPO screening in euthyroid pregnancy is not recommended.
  4. 04
    Full blood count and liver tests
    Why
    Establish treatment safety and investigate possible thionamide toxicity.
    Interpretation and limitations
    Urgent symptom-triggered testing is essential; a previously normal blood count does not rule out abrupt agranulocytosis.
  5. 05
    Fetal ultrasound and neonatal thyroid testing

Differential diagnosis

01

Transient gestational thyrotoxicosis

High hCG can cause early biochemical thyrotoxicosis without Graves' antibodies or characteristic gland findings; supportive care is usually sufficient as hCG levels decline.

02

Normal pregnancy symptoms

Fatigue, heat intolerance and palpitations overlap with thyroid symptoms, so thyroid tests and specific examination findings are needed before assigning a diagnosis.

03

Postpartum thyroiditis

Autoimmune inflammation after delivery can release stored hormone before a hypothyroid phase, differing from ongoing hormone synthesis in a postpartum Graves' relapse.

Management

01Replacement adjustmentMeet the increased thyroxine requirementFirst stepPregnancy is confirmed in someone with established levothyroxine-treated hypothyroidism.+
  1. 1Activate the agreed empirical dose increase and arrange prompt TSH and free T4 testing rather than waiting for routine antenatal booking.
  2. 2Titrate to the RCOG pregnancy target and check every four to six weeks until 20 weeks, then at 28 weeks.
  3. 3Review iron and calcium timing, vomiting and missed doses, and document the postnatal dose and testing plan.
02Thyrotoxicosis assessmentDistinguish Graves' disease from transient changeTSH is suppressed with a raised free T4 in a pregnant patient.+
  1. 1Assess pre-pregnancy symptoms, goitre, eye disease, medication exposure and hCG-related circumstances, then obtain TRAb and free T3 when needed.
  2. 2

Complications

01

Untreated hormone deficiency

Significant maternal hypothyroidism increases risks of pregnancy loss and impaired fetal development, especially when severe deficiency is present early in gestation.

02

Uncontrolled thyrotoxicosis

Persistent hormone excess can cause maternal arrhythmia or heart failure and is associated with preterm birth, impaired fetal growth and stillbirth.

03

Fetal or neonatal thyroid dysfunction

Maternal antibodies may cause hyperthyroidism while antithyroid drug exposure can suppress the infant thyroid, requiring planned testing after birth in at-risk babies.

Monitoring and follow-up

  • For antithyroid treatment check TSH and free T4 every two to four weeks in the first half of pregnancy, considering fortnightly tests after stopping, switching or changing dose.
  • After 20 weeks, four-to-eight-week thyroid testing may be appropriate when control is stable, with faster reassessment for symptoms.
  • Ensure TRAb results are shared with fetal medicine and neonatology and document which infant tests are required.
  • Review adherence and supplement timing when thyroid results shift unexpectedly instead of repeatedly escalating replacement blindly.
  • Arrange postpartum thyroid tests and reassess new palpitations, depression or fatigue for relapse or postpartum thyroiditis.

Special situations

A thyroidectomy does not remove antibodies

Someone now taking levothyroxine after definitive Graves' treatment can still carry TRAb capable of stimulating the fetal thyroid.

TSH can lag

Persistently low TSH during treated hyperthyroidism does not necessarily justify more thionamide when free T4 is already appropriately controlled.

Avoid routine block and replace

High antithyroid doses with maternal levothyroxine can leave the fetus hypothyroid because placental transfer differs between the medicines.

Supportive treatment can be correct

A transient hCG-related biochemical abnormality without Graves' disease often resolves without antithyroid medicine, preventing unnecessary fetal drug exposure.

Common pitfalls

  1. 01

    Applying a non-pregnant TSH range without checking the laboratory's trimester-specific interpretation.

  2. 02

    Waiting until the second trimester to assess known hypothyroidism after a positive pregnancy test.

  3. 03

    Automatically changing every patient from PTU at 16 weeks without reference to the current RCOG recommendation and individual plan.

  4. 04

    Treating euthyroid TPO antibody positivity alone with levothyroxine.

  5. 05

    Missing agranulocytosis because fever and sore throat were attributed to a common infection.

  6. 06

    Assuming normal maternal thyroid tests exclude fetal Graves' disease after definitive maternal treatment.

Practice

Two practice questions

Your practice draft is saved in this browser.

Question 1 of 2
0 correct
Obstetrics and gynaecologyOriginal SBA

A positive test on replacement

A patient with established hypothyroidism takes levothyroxine 100 micrograms daily and has a pre-agreed RCOG pregnancy plan. Her pregnancy test is positive today. Which empirical schedule reflects that plan while thyroid tests are arranged?

Choose one answer, then submit
← Rapid synopsisBack to overviewAll Obstetrics and gynaecology topics →
Sources and review status6 sources · checked 7 Sept 2026 · clinical review pending+
Sources

Sources and review status

National guidance is shown before implementation-dependent detail. Typical adult dose examples remain subject to patient factors, contraindications and the live BNF or specialist protocol. Source check completed 7 Sept 2026; clinical approval remains outstanding.

  • RCOG Green-top 76: Management of thyroid disorders in pregnancy
  • RCOG Green-top 76: May 2026 correction
  • RCOG: Thyroid problems in pregnancy
  • NHS: Levothyroxine medicine information
  • MHRA: Carbimazole congenital-malformation risk
  • Propylthiouracil 50 mg: February 2026 SmPC

Editorial contact: Doctor’s Passport editorial team. Source-check date is separate from clinical approval. Report a content problem · Content changes

Authoring stateComplete draftClinical stateAwaiting reviewJurisdictionUnited Kingdom
A patient already using levothyroxine should have a clear preconception action plan. RCOG recommends an empirical increase at a positive pregnancy test by taking twice the usual daily dose on two days each week, approximately a 29% weekly increase, followed by prompt tests and titration. This is an adjustment to an established replacement dose, not a universal starting dose for newly diagnosed patients. Check adherence, vomiting and co-administration with iron or calcium before attributing an unexpected TSH entirely to disease progression.

Hyperthyroidism needs a causal diagnosis. Graves' disease is suggested by pre-pregnancy symptoms, goitre, eye disease and positive TSH-receptor antibodies. Gestational transient thyrotoxicosis is more likely in early pregnancy with hCG-related illness, no prior thyroid features and negative TRAb. Tremor or palpitations alone do not distinguish them. Supportive management usually suffices for transient disease; antithyroid treatment is reserved for hormone overproduction requiring treatment rather than every low TSH.

Thionamide decisions change with gestation and control. Propylthiouracil is preferred when treatment is needed during early organogenesis; if conception occurs on carbimazole, RCOG recommends switching promptly before 10 weeks when appropriate. Presentation after 10 weeks does not confer the same benefit from switching to PTU. If treatment remains necessary beyond 20 weeks, consider changing PTU to carbimazole to reduce maternal liver-toxicity risk. All switches need dose conversion and closer biochemical monitoring by endocrinology.

Maternal and fetal targets are linked but not identical. Antithyroid medicines cross the placenta and can suppress the fetal thyroid, so excessive treatment to correct a still-low maternal TSH can be harmful. RCOG targets free T4 in the upper half of the pregnancy reference range. Routine block-and-replace regimens are avoided because the antithyroid drug reaches the fetus more readily than replacement thyroxine. Rare isolated fetal disease may require a different specialist strategy.

Check TRAb early in anyone with current or previous Graves' disease, including those now hypothyroid after surgery or radioiodine. Positive antibodies or antithyroid treatment prompt repeat measurements at 20 and 28 weeks. High antibody levels, uncontrolled disease or treatment exposure can warrant fetal growth and thyroid surveillance. The May 2026 correction clarifies that indicated monthly growth and Doppler scans start at 26–28 weeks and continue onwards; this is not a two-week-only scanning window.

After birth, review replacement dose and arrange thyroid testing, usually at about six weeks. Graves' disease can relapse postpartum, while postpartum thyroiditis may move from a transient hyperthyroid phase to hypothyroidism. Breastfeeding is generally compatible with levothyroxine and appropriately dosed antithyroid treatment through specialist advice. Infants exposed to maternal Graves' antibodies or antithyroid medicines need a neonatal thyroid-testing plan rather than reliance on routine newborn screening alone.

Key points

  • Interpret TSH and free T4 with trimester-specific and assay-specific reference ranges; normal early-pregnancy physiology may suppress TSH.
  • Established hypothyroidism needs prompt levothyroxine adjustment at a positive pregnancy test, often two extra usual daily doses per week under the pre-agreed plan.
  • RCOG recommends TSH and free T4 every four to six weeks until 20 weeks, then again at 28 weeks for levothyroxine-treated hypothyroidism.
  • For treated hypothyroidism aim for TSH below 2.5 mU/L while keeping free T4 within the appropriate pregnancy reference range.
  • If antithyroid treatment is necessary in early pregnancy, RCOG favours propylthiouracil; a carbimazole-to-PTU switch should occur promptly before 10 weeks when indicated.
  • Use the lowest effective antithyroid dose, targeting free T4 in the upper half of the pregnancy range rather than normalising TSH aggressively.
  • Gestational transient thyrotoxicosis generally needs supportive care, and euthyroid thyroid-peroxidase-antibody positivity alone does not justify levothyroxine.
  • Past Graves' disease still warrants TRAb assessment because antibodies can affect the fetus even after thyroidectomy or radioiodine.
Why
Detect growth effects, fetal thyroid dysfunction and postnatal disease in at-risk infants.
Interpretation and limitations
Plan surveillance according to maternal control, drug exposure and TRAb, including neonatal tests soon after birth and at one to two weeks when indicated.
Use supportive care for transient gestational thyrotoxicosis and specialist antithyroid therapy for active Graves' or toxic nodular disease.
  • 3Choose the thionamide and monitoring interval according to gestation, prior control and risks to both patient and fetus.
    • 03Safety and fetal careRespond to toxicity and antibody riskA treated patient develops infection symptoms or has a high-risk Graves' pregnancy.+
    1. 1EscalationWithhold antithyroid treatment for suspected agranulocytosis pending immediate blood count and clinical advice; escalate hepatic warning symptoms urgently.
    2. 2Arrange serial fetal assessment when disease control, treatment or antibody findings justify it, continuing indicated scans beyond their starting gestation.
    3. 3Notify neonatology of Graves' history, TRAb results and medicine exposure so infant testing and follow-up are explicit.
    Key medicines and prescribing safety3 treatments · regimens, roles and cautions+
    Replaces deficient maternal thyroid hormone and meets the early increase in pregnancy requirement.

    Levothyroxine in established hypothyroidism

    At a positive pregnancy test, take the usual oral daily dose on five days weekly and twice that dose on two days weekly when following the agreed RCOG plan; subsequently individualise against TSH and free T4.

    This schedule modifies an existing dose; newly diagnosed disease needs an individual starting prescription. Separate iron or calcium from levothyroxine and avoid biochemical overtreatment.

    Preferred early-pregnancy thionamide when clinically significant hyperthyroidism requires treatment.

    Propylthiouracil

    Use an endocrinologist-selected oral dose and titrate to maternal free T4 with the lowest effective exposure. The cited SmPC gives a general adult initiation range of 300–600 mg daily, once daily or divided; this is not a recommended pregnancy starting range, and pregnancy treatment may require substantially less.

    Do not automatically use the top of the general adult range. Watch for agranulocytosis, hepatotoxicity and fetal hypothyroidism, and consider carbimazole if ongoing treatment is needed beyond 20 weeks.

    An alternative thionamide when gestation and maternal risk favour it, including continuing treatment later in pregnancy.

    Carbimazole after specialist reassessment

    Prescribe the lowest effective oral daily dose selected by endocrinology; when switching from PTU, RCOG uses an approximate PTU:carbimazole ratio of 20:1, so 200 mg PTU daily corresponds to 10 mg carbimazole daily before biochemical retitration.

    Conversion is a starting estimate, not a fixed equivalence for every patient; first-trimester malformation risk, agranulocytosis and pancreatitis history require explicit review.