Hypothyroid;25% to 47% average dosage increase during pregnancy
increased serum thyroid stimulating hormone (TSH) and thyroglobulin concentrations, relative hypothyroxinemia, and occasional goiter formation
Esp. from area with borderline iodine sufficiency
associated with increase in thyroid gland size in 15%
EFFECTS OF PREGNANCY ON THYROID PHYSIOLOGY ↑ Basal metabolic rate; ↑ cardiac output ↑ Oxygen consumption by fetoplacental unit, gravid uterus, and mother ↑ T 4 production; fetal T 4 synthesis during second and third trimesters ↑ Iodine requirements ↑ Renal I - clearance ↑ Free T 4 ; ↓ basal thyrotropin; ↑ T 4 production First trimester ↑ in hCG ↑ T 4 production D3 expression in placenta and (?) uterus ↑ T 4 and T 3 pool size; ↑ T 4 production; ↑ cardiac output ↑ Plasma volume ↑ Total T 4 and T 3 ; ↑ T 4 production ↑ Serum thyroxine-binding globulin Thyroid-Related Consequences Physiologic Change
elevated serum TSH concentration:2.5% of pregnancies
In iodine-sufficient environment
prior radioactive iodine treatment
surgical ablation of Graves’ disease
less common causes: overtreatment of hyperthyroidism with thionamides, transient hypothyroidism owing to postpartum thyroiditis, medications that alter the absorption or metabolism of levothyroxine, and pituitary/hypothalamic disease)
Symptoms masked by the hypermetabolic state of pregnancy.
20% to 30% overt hypothyroidism develop symptoms
weight gain, lethargy, decrease in exercise capacity, and intolerance to cold,constipation, hoarseness, hair loss, brittle nails, dry skin, goiter, or delay in the relaxation phase of the deep tendon reflexes
Elevated serum TSH concentration
Central hypothyroidism do not manifest an elevated serum TSH level
Guidelines for clinical management of maternal hypothyroidism during pregnancy
1. Check serum TSH level as soon as pregnancy is confirmed.
2. For newly diagnosed hypothyroid women, initial levothyroxine dosage is based on severity of hypothyroidism. For overt hypothyroidism, administer 2 mcg/kg/d. If TSH is < 10 mU/L, initial dose of 0.1 mg/d may be sufficient.
3. For previously diagnosed hypothyroid women, monitor serum TSH every 3–4 weeks during first half of pregnancy and every 6 weeks thereafter.
2.1.a.4. Subtotal thyroidectomy for maternal Graves’ disease if
1) a patient has a severe adverse reaction to ATD therapy,
2)persistently high doses of ATD are required
3) a patient is not adherent to ATD therapy and has uncontrolled hyperthyroidism.
optimal timing of surgery is in the second trimester.
2.1.a.5. no evidence that treatment of subclinical hyperthyroidism improves pregnancy outcome
2.1.b.1 TRAb (either TSH receptor-stimulating or –binding antibodies) freely cross the placenta and can stimulate the fetal thyroid.
These antibodies should be measured before pregnancy or by the end of the second trimester in mothers with current Graves’ disease, with a history of Graves’ disease and treatment with 131I or thyroidectomy, or with a previous neonate with Graves’ disease.
Women who have a negative TRAb and do not require ATD have a very low risk of fetal or neonatal thyroid dysfunction.
2.1.b.2. 131I should not be given to a woman who is or may be pregnant.
radiation danger to the fetus, including thyroid destruction if treated after the 12th week of gestation.
There are no data for or against recommending termination of pregnancy after 131I exposure
2.1.b.3. In women with elevated TRAb or in women treated with ATD, fetal ultrasound should be performed to look for evidence of fetal thyroid dysfunction
growth restriction, hydrops, presence of goiter, or cardiac failure.
2.1.b.4. Umbilical blood sampling should be considered only if the diagnosis of fetal thyroid disease is not reasonably certain from the clinical data and if the information gained would change the treatment.
2.1.b.5. All newborns of mothers with Graves’ disease should be evaluated for thyroid dysfunction and treated if necessary
3.1. Thyroid function tests should be measured in all patients with hyperemesis gravidarum (5% weight loss, dehydration, and ketonuria)
3.2. Few women with hyperemesis gravidarum will require ATD treatment.
Overt hyperthyroidism believed due to coincident Graves’ disease should be treated with ATD.
Gestational hyperthyroidism with clearly elevated thyroid hormone levels (free T4 above the reference range or total T4 150% of top normal pregnancy value and TSH 0.1 U/ml) and evidence of hyperthyroidism may require treatment as long as clinically necessary
4. AUTOIMMUNE THYROID DISEASE AND MISCARRIAGE
4.1. universal screening for antithyroid antibodies and possible treatment cannot be recommended at this time.
5.3. administer thyroid hormone to achieve a suppressed but detectable TSH in pregnant women with a previously treated thyroid cancer or an FNA positive for or suspicious for cancer and those who elect to delay surgical treatment until postpartum.
High-risk patients benefit from a greater degree of TSH suppression
free T4 or total T4 levels should ideally not be increased above the normal range for pregnancy.
5.4. RAI administration with 131I should not be given to women who are breastfeeding.
pregnancy should be avoided for 6 months to 1 yr in women with thyroid cancer who receive therapeutic RAI doses to ensure stability of thyroid function and confirm remission of thyroid cancer.
7.5. Asymptomatic women with PPT who have a TSH above the reference range but less than 10 U/ml and who are not planning a subsequent pregnancy do not necessarily require intervention but should be remonitored in 4–8 wk.
Symptomatic women and women with a TSH above normal and who are attempting pregnancy should be treated with levothyroxine.
7.6. There is insufficient evidence to conclude whether an association exists between postpartum depression and either PPT or thyroid antibody positivity (in women who did not develop PPT).
women with postpartum depression should be screened for hypothyroidism and appropriately treated.