for clear knowledge about thyroid disorder in pregnancy

1. THYROID DISEASES IN
PREGNANCY
Capt. ZWE YAN NAING

2. INTRODUCTION TO PHYSIOLOGY
Effects of pregnancy on thyroid
• Increased demand of thyroid hormones to maintain the requirements of fetus
• Total serum T3 T4 levels increase 50% during pregnancy
• thyroid hormones transfer to fetus during 1st trimester, later iodine only
• Iodine excretion in urine increased in pregnancy due to increased GFR
• Good intrathyroid store cope with this demand, but in deficient reserved women,
thyroid hormone level fall and stimulate TSH, make goitre

3. Maternal
• More than 1% occur, most common endocrine disorder in pregnancy
• TSH release 1-2 hrly cycle which increase synthesis & release of T3, T4 from thyroid
• Unbound hormones have biologically active, 75% bound to TBG, albumin
• In pregnancy, TBG production increase due to oestrogen in first 2 weeks
• HCG and TSH share common alpha subunit and similar beta subunits
• Increased thyroid activity found in molar pregnancy, multiple pregnancy and
hyperemesis gravidarum

4. Fetal
• Require maternal T4 during first trimester for brain development
• Fetal thyroid is independent of mother, require only transplacental iodine
• Fetal level of thyroid hormone reach those of adult by 36 weeks
• Congenital hyperthyroidism can occur when TSH receptor stimulating antibodies
cross placenta

5. AETIOLOGY AND MANAGEMENT OF
THYROID DISEASES
• Iodine
• Women in area of iodine deficiency may have goiters and reduced reproductive
success
• Iodine deficiency is the leading preventable cause of learning disability worldwide
• Fetal cochlea, cerebral neocortex and basal ganglia are particularly sensitive to
iodine deficiency

6. HYPERTHYROIDISM
• Commonest cause in pregnancy is Graves’ disease, almost 90%
• It is an autoimmune disorder caused by TSH receptor-stimulating anntibodies
• Complicates about 1 in 500 pregnancies
• 50% affected women have positive family history of autoimmune thyroid disease
• Most cases already been diagnosed will already treated
• Other causes multinodular, toxic goiter, acute viral thyroiditis(de Quervains)
carcinoma, drug induced(amiodarone or lithium)

7. • Diagnosis
• Similar symptoms like normal pregnancy such as palpitation, tachycardia,
irritability, heat intolerance and fatigue
• Eye signs include diplopia, photophobia
• A diffuse swelling in thyroid area which move with deglutition may be due to
physiology, Graves’ disease and thyroiditis
• TFT should be request, if facilities available, TRAb should be tested
• Raised free T3, T4 , TSH is suppressed

8. • Effect of pregnancy on thyrotoxicosis
• Immprove in 2nd and 3rd trimester
• Lower requirement of antithyroid drugs
• Exacerbations usually occur in 1st trimester (HCG) and puerperium

9. • Effects of thyrotoxicosis on pregnancy
• Inhibition of ovulation and infertility( severe or untreated cases)
• Increased rate of miscarriage, IUGR, Preterm birth, pernatal mortality if those
become pregnant.
• Thyroid crisis may occur at the time of delivery if poorly controlled

10. • Management
• Carbimazole, propylthiouracil most common used drugs
• Both drugs cross the placenta, so in high dose amy cause fetal hypothyroid and
goiter
• Aplastic cutis( carbimazole in 1st trimester)
• 2-4% congenital anomalies
• Therefore, switching carbimazole to PTU before or in early pregnancy

11. • Management (contd)
• Newly diagnosed thyrotoxicosis in pregnancy should be aggressively treated with
PTU 450-600 mg daily for 4-6 week
• Almost 30% can stop all medication in the last weeks of pregnancy
• Graves’ disease can relapse postnatally as maternal antibody level rise postpartum
• 𝛽 blockers- early symptomatic management like tachycardia, sweating, tremor
• They also reduce peripheral comnversion of T4 to T3
• They are discontinued once the antithyroid drugs take effect(3 weeks)
• Propranolol 40 mg tds does not harm to fetus

12. • Surgery is rare, if required perform in 2nd trimester
• It usually made where dysphagia, stridor, comfirm or suspected carcinoma or allergy
to drugs
• 25-50% become hypothyroid after surgery
• Radioactive iodine is contraindicated in pregnancy and breastfeeding

13. HYPOTHYROIDISM
• Incidence – much more common in women than men
• 1% of pregnancy, most cases already been diagnosed and will be on replacement
therapy
• As hyperthyroidism, features are common in normal pregnancy such as weight gain,
hair loss, lethargy, tiredness constipation, dry skin, goiter and fluid retention
• Discriminated feature is delayed relaxation of tendon ( ankle)
• Associated with other autoimmune like pernicious anaemia, vitiligo and diabetes
mellitus type 1

14. • Pathogenesis
• most cases are due to autoimmune destruction of thyroid gland associated with
microsomal autoantibodies
• Mostly two types- atrophic thyroiditis, Hashimoto’s thyroiditis
• May also be due to iatrogenic following radiotherapy, thyroidectomy, or drugs (
amiodarone, lithium, iodine, anti-thyroid)
• Commonest cause encountered during pregnancy are treated Graves’ disease

15. • Diagnosis
• Low level of free T4, raised TSH
• Finding of thyroid autoantibodies
• Normal pregnant range for each trimester must be used

16. Effect of pregnancy on hypothyroidism
• 25% women require increased level of thyroxine in pregnancy
Effect of hypothyroidism on pregnancy
• Inhibit ovulation and infertility if untreated or severe
• Present with oligomenorrhoea or menorrhagoia
• Increased rate of miscarriage, anaemia, fetal loss, pre-eclampsia, low birth weight
• Neurodevelopmental delay in her offspring
• Severe maternal iodine deficiency may cause permanent brain damage ( deaf
mutism, spasmodic motor disorder and hypothyroidism)

17. Management
• Maintainance dose thyroxine 100-200ug/day
• TFT should be checked once in each trimester
• Starting thyroxine dose of 100ug/day for newly diagnosed hypothyroid in pregnancy
if there is no history of heart disease

18. POSTPARTUM THYROIDITIS
Incidence -1-17%
More common in women with family history of hypothyroidism and those with thyroid
peroxidase antibodies, in whom about 50%
Most of them asymptomatic, present between 3-4 months postpartum
Monophasic (may be hypo or hyper) 40%, biphasic 20%
Represent an activation of previously subclinical thyroiditis

19. • Diagnosis
• Test TFT 2-3 months postpartum to the patients whose already have thyroid
peroxidase antibody
• Also common in type1 diabetes patients
• Almost 75-85% have positive antithyroid antibodis
• Radioactive iodine test can be performed to distinguish with flare up post partum
Graves’ disease, because Graves’ need antithyroid drugs

20. Management
Mostly recover spontaneously without requiring treatment
Treatment is determine by symptoms rather than biochemical abnormal
Betablocker for hyperthyroid, cause antithyroid reduce thyroxine synthesis
Thyroxine need in hypothyroid and withdrawn after 6-8 months
3-4% remain hypothyroid (recurrence)
10-25% recurrence in future pregnancies
Postpartum depression is more common in antibody positive women

21. REFERENCES
• Handbook of Obstetric medicine.Catherine N Piercy 6th ed
• Ian Donald
• Obstetrics & Gynaecology. An evidence-based Text for the MRCOG