hyperthyroidism

1. THYROTOXICOSIS
IN
PREGNANCY
Hamad Emad H. Dhuhayr

2. PHYSIOLOGIC CHANGES IN THYROID FUNCTION
DURING PREGNANCY
• Thyroid binding globulin (TBG) increases due to reduced
hepatic clearance and estrogenic stimulation of TBG synthesis.
• The test results that change in pregnancy are influenced by
changes in TBG concentration.
• Plasma iodide levels decrease due to fetal iodide use and
increased maternal clearance -> leads to notable increase in
gland size in 15% of women (without abnormal TFTs)

3. PHYSIOLOGIC CHANGES IN THYROID FUNCTION
DURING PREGNANCY
Maternal
Status
TSH
**initial
screening
test**
Free T4 Free
Thyroxine
Index
(FTI)
Total T4 Total T3 Resin
Triiodo-thyronine
Uptake
(RT3U)
Pregnancy No
change
No
change
No
change
Increase Increase Decrease
Hyperthyroidism Decrease Increase Increase Increase Increase
or no
change
Increase
Hypothyroidism Increase Decrease Decrease Decrease Decrease
or no
change
Decrease

4. FETAL THYROID
7-9 weeks formation of thyroid gland
10 weeks TSH and thyroxine deteable
17 weeks maturation of the gland
>18weeks response to TSH stimulation

5. HYPERTHYROIDISM
• Occurs in 0.2% of pregnancies; graves’
disease accounts for 95% of cases
Look for:
-Nervousness
-Tremor
-Tachycardia
-Frequent stools
-Sweating
-Heat intolerance
-weight loss
-Goiter
-Insomnia
-Palpitations
-Hypertension
-Lid lag/lid retraction
-Pretibial myxedema

6. CAUSES & DIAGNOSIS OF HYPERTHYROIDISM
• Most common cause of hyperthyroidism is graves’
disease
• Document elevated FT4 or elevated FTI with suppressed TSH,
in absence of goiter/mass
• Most patients have antibodies to TSH receptor,
antimicrosomal, or antithyroid peroxidase antibodies, but
measurement of these is not required (though some
endocrinologists recommend measuring TSI, which are
stimulatory antibodies to TSH receptor)
• Other causes:
• Excess TSH production, gestational trophoplastic disease,
hyperfunctioning thyroid adenoma, toxic goiter, subacute
thyroiditis, extrathyroid source of “TH”

7. GUIDELINES FOR CLINICAL MANAGEMENT OF MATERNAL
HYPERTHYROIDISM DURING PREGNANCY
• 1. Use the lowest dosage of thionamide (preferably PTU) to maintain
maternal total T4 concentrations in the upper one third of normal to
slightly elevated range for pregnancy.
• Normal range of total t4 during pregnancy is estimated to be 1.5
times the nonpregnant state
• 2. Monitor maternal total T4 serum concentration every 2–4 weeks,
and titrate thionamide as necessary.
• Monitoring serum tsh may become useful later.

8. GUIDELINES FOR CLINICAL MANAGEMENT OF MATERNAL
HYPERTHYROIDISM DURING PREGNANCY
• 3. Measure TSH receptor antibodies (thyroid-stimulating
immunoglobulins or TSH receptor binding inhibitory
immunoglobulins) at 26–28 weeks to assess risk of
fetal/neonatal hyperthyroidism.
• Tsh receptor antibody measurement is crucial in
hypothyroid levothyroxine-treated women with a prior
history of graves’ disease, who do not appear thyrotoxic.
• 4. Perform fetal ultrasound at weeks 26–28 to assess potential
fetal response to thionamide treatment and effect of TSH
receptor antibodies on fetal thyroid function

9. GUIDELINES FOR CLINICAL MANAGEMENT OF MATERNAL
HYPERTHYROIDISM DURING PREGNANCY
• 5. Consider thyroidectomy if persistently
high doses of thionamide (PTU > 600 mg/d
or MMI > 40 mg/d) are required,or if the
patient cannot tolerate thionamide therapy.
• 6. Β-adrenergic blocking agents and low
doses of iodine may be used perioperatively
to control hyperthyroid state.
• 7. Check fetal cord blood at delivery for TSH
and T4.

10. TREATMENT
• Thionamides
• Propylthiouracil (PTU) and
methimazole(mmi)
• Both cross the placenta with equal transfer
kinetics.
• Both can cause fetal goiter and
hypothyroidism, usually mild and transient &
dose-dependent
• Median time to normalization of maternal
thyroid function
• 7 weeks with PTU and 8 weeks with MMI
• PTU more highly bound to albumin

11. TREATMENT
Thionamides
• Maternal :rash
• Rare birth defects in MMI: aplasia cutis, choanal
atresia,esophageal atresia, and minor dysmorphic
features
• Low thyroid function at birth ½ neonates whose mothers received PTU
or MMI and had serum T4 concentrations within the normal (non-pregnant)
range
• Normal IQ scores
• Graves’ disease may ameliorate
• Thionamide discontinued in 30% during the final weeks
• Fall in serum TSH receptor-stimulating antibody concentrations
and a rise in TSH receptor-blocking antibodies.
• Graves' hyperthyroidism can worsen postpartum
• Do not recommend the use of t4 with thionamide therapy
during pregnancy.

12. TREATMENT
• Β-adrenergic blockers
• Weaned as soon as the hyperthyroidism is
controlled
• Occasional cases of neonatal growth restriction,
hypoglycemia, respiratory depression, and
bradycardia
• Increased frequency of first-trimester miscarriages
• Avoiding in the first trimester
• Iodides
• Past reports of neonatal hypothyroidism after
exposure to iodine
• Low-dose potassium iodide may be considered
• Preparation for thyroidectomy
• Thionamide-intolerant patients refusing surgery.

13. TREATMENT
• Surgery
• Subtotal thyroidectomy :
• Persistently high dosages of thionamides (PTU > 600
mg/d, MMI > 40 mg/d) are required to control maternal
disease
• Allergic or intolerant of both thionamides
• Noncompliant with medical therapy
• Compressive symptoms
• Second trimester, before gestational week 24
• Prepared with a β-adrenergic blocking agent and a 10- to 14-
day course of potassium iodide

14. TREATMENT
• Radioactive iodine therapy
• Contraindicated
• Fetal thyroid gland begins to concentrate iodine
after gestational week 10, fetal thyroid tissue is
present by 10 to 12 weeks
• Predisposing to congenital hypothyroidism
• Nursing
• Breast feeding in mothers taking PTU or MMI is safe
• Thyroid function in newborn infants is unaffected
• PTU is preferred because it is less concentrated in
breast milk

15. REFFRENCES
• KUMAR
• CECIEL
• WEBSITE UP TO DATE