hCG increases thyroxine and therefore suppresses TSH
Both hCG and hyperthyroidism result in high free T4 and low TSH
In hyperemesis gravidarum, patients will have high hCG and 50% have low TSH (+/- increased fT4)
To distinguish gestational hCG-associated throtoxicosis from hyperthyroidism:
Hyperemesis gravidarim - ↑hCG, ↓TSH
Not TRab antibody positive
Resolves by 20 weeks gestation
Only treat if no improvement > 20 weeks
Hyperthyroidism in pregnancy
Causes
Most common cause in this age group (fertile women) is Graves' disease
Other causes include TMNG, toxic adenoma and thyroiditis
Complications
Infertility/ammenorhoea
Spontaneous miscarriage
Stillbirth
Thyroid crisis in labour
Transient neonatal thyrotoxicosis
Management
Wait and see (supportive management)
If hyperemesis, will settle
Graves may settle as pregnancy suppresses autoimmunity
Check TRAb antibodies - if present alert neonatologist as TRAb antibodies can cross the placenta and cause neonatal transient hyperthyroidism
β-blockers if needed
LOW DOSE antithyroid drugs - wait as late as possible due to side effects on foetus
Propylthiouracil 1st trimester
Carbimazole 2/3rd trimester
Post-partum thyroiditis
Aetiology
Affects 5% postpartum women (25% in T1DM)
Occurs within 6 months of giving birth
In the postpartum phase there is exacerbation of all autoimmune diseases
Clinical presentation
After delivery, the mother develops transient over-active thyroid, classically at around 6 weeks, and then at around 3 months has an underactive thyroid
Will develop small, diffuse, nontender goitre
Hypothyroid phase associated with neonatal depression
Can persist up to 1 year post partum
25-50% will have persistent hypothyroidism beyond 1 year
Investigations
Thyroid function tests
Thyroid antibody tests
Scintigraphy scan
Management
No treatment for hyperthyroid phase, if symptomatic hypothyroid treat with thyroxine
Should eventually be able to stop thyroxine but if patient is still on thyroxine after a year it is likely they will need it long term